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रविवार, 21 फ़रवरी 2016

Shat-kriyakala - modern time review

Shat-kriyakala - modern time review ;

 Acharya Sushruta has described the concept of Kriyakala which seeks to explain the incident of vrana in terms of dosha disturbance. Vrana in modern parlance may be described as inflammatory process which may lead on to suppuration and ulceration. The concept of Kriyakala describes the mode and stages of the development of diseases. A good understanding of Kriyakala is very essential for early diagnosis, prognosis and for adopting preventive and curative measurement.
The term Kriyakala means the time of action. Kala or time in this context signifies the avastha or stage of the process of diseases.
Kalo hi nityaga avasthika; tatra avasthika vikaram apekshate ||
Ca.Vi.1/229(6)
Kriya or action refer to the resort to measure-aushadha, ahara and charya-with a view to eliminate and correct the doshic disturbance.
Kriyakala therefore, means the (early) recognition of the avastha or the stage of the process of disease and the resort to appropriate measures to correct the same.
As described above shatkriyakala are explained in vrana prashna adhyaya where Dalhan the commentator clarifies vrana in this content is not wound but vatadi humor (dosha) which themselves are cause for dehotpatti (responsible for structural and functional activity of body). They are the one who maintain normalcy. They physiologically go through the phase of chaya prakopa and prashama. This 3 step process is essential for sharira dharan.
The same dosha when get vitiated are cause for destruction of sharir.
Ta eva cha vyapanna pralaya hetava ||
Su.Su.21/3
Destruction (vyapanna) in case of sharir refers to vikruti or disease which undergoes evolution in 6 phase viz chaya, prakopa, prasara, sthanasansraya, vyakti and bhedha.
Inflammation is the local physiological response to tissue injury. It is not in itself, a disease, but is usually a manifestation of disease. Inflammation may have beneficial effect such as the destruction of invading micro-organisms and the walling-off of an abscess cavity to prevent spread of infection. However, may also produce diseases; for example, an abscess in the brain wound act as space occupying lesion compressing vital surrounding structure, or fibrosis resulting from chronic inflammation may destroy tissue permanently.
Inflammation is a protective response that involves immune cells, blood vessels and molecular mediator. It is one among the reason why Acharya Sushruta in this context has accepted rakta (shonita) as fourth dosha. Inflammation is a generic response, and therefore it is considered as a mechanism of innate immunity as compared to adopted immunity specific for each pathogen/hetu. Thus one hetu can cause many diseases and many hetu can cause one disease.
Sanchayam ca prakopam ca prasaram sthana sansrayam II
Vyaktim bhedam ca yo vetti doshanam sa bhaveda bhisaka II
SANCHAYA: It is the first phase of shat kriyakala; it is the stage of accumulation or the stage which represents the inceptive phase of the disease wherein the dosha are stated to have accumulated and stagnated in its own place (Dosha sthanani yesu sanchiyate II Su. Su 21/28), instead of freely circulating as in its normal avastha or phase.
Dosha in this condition are in compact form (Samhati rupa vridhi chaya II Dalhan Su. Su. 21/18). Samhata or compactness can be understood by symptom of vata dosha, vata dosha chaya which is manifested as stabdha purna kostha i.e. stabdha kostha (sense of dullness in abdomen/ sense of reduced intestinal motility) and purna kostha (sense of fullness/ sense of heaviness in abdomen). To fill up the space is normal function of vata which is manifested in excess in sanchaya avastha.
Pitta chaya is manifested with yellow tinge (pittavabhasata). Yellow is normal colour of pitta which is manifested as excess.
Kapha manifest as low body temperature/ reduce temperature (manda ushmata), heaviness of a part or full body (anga gaurav) and languor (alasya). These symptoms are seen in sthan (seat) where chaya rupa vridhi is seen.
The process of acute inflammation is initiated by resident immune cells (sthanik dosha) already present in the involve tissue mainly resident macrophages, dendritic cells, histiocytes, Kupffer cells and mastocytes. Receptors named pattern recognition receptors (PRRs) recognize generic molecules that are broadly shared by pathogens but distinguishable from host molecules, collectively referred to as pathogen associated molecular pattern (PAMPs). Thus cells undergo activation and recognize non self and mechanism of opposition is initiated which is manifested as pradvesho vridhi hetusu i.e. aversion towards similar and attraction towards contraries.
In case of fever it is the pyrogen which may be exogenous (bacterial substance lipopolysaccharide (LPS) present on bacterial cell wall) or endogenous (cytokines, Interleukin-1 and Interleukin-6 etc). These pyrogens enter the body and activate the immune cells (antigen presenting cell) for the formation of cytokines and other factors or due to endogenous cause too activation of immune system takes place.
Atherosclerosis, formally considered a bland lipid storage disease, actually involves an ongoing inflammatory response. Recent advances in basic science have established a fundamental role for inflammation in mediating all stages of this disease from initiation through progression and ultimately, the thrombotic complications of atherosclerosis. Oxidised levels of LDL, increased level of VLDL are the initiation or triggering factor of atherogenesis.
Sanchaya is the early initiation of marker C-reactive Protein which prospectively defines risk of atherosclerotic complications, thus adding to prognostic information provided by traditional risk factors.
Thus new insights into inflammation in atherosclerosis not only increase understanding of disease but also have practical clinical application in risk stratification and targeting of therapy for this scourge of growing worldwide importance rightly said by Dalhan as prathama kriyakala aadya karmavasara.
PRAKOPA: In this stage dosha gets vitiated or aggravated or the dosha previously accumulated/ stagnated get swollen and excited. Vilayan rupa vridhi prakopa (Dalhan). Vilayana here means bonding (samhata) is loss and dosha gets released.
In case of acute inflammation release of inflammatory mediators responsible for the clinical signs of inflammation takes place.
In case of fever Exogenous factors contain immunological protein called lipo-polysaccharide binding protein (LBP) which binds to LPS. The LBP-LPS complex then binds to the CD14 receptors of a nearby macrophage. It causes synthesis and release of various endogenous cytokines factors such as IL-1, IL-6, Tumour Necrosing Factor alpha (TNFα).
In atherosclerosis C- Reactive Protein is elevated and noted in the blood test. Increased level of LDL, VLDL and intermediate lipoproteins activate inflammatory functions of vascular endothelial cells. During atherogenesis, inflammatory cells (eg, monocyte-derived macrophages) accumulate in arteries, releasing growth factors/cytokines (eg, platelet-derived growth factor [PDGF], transforming growth factor-beta [TGF-β], granulocyte-macrophage colony-stimulating factor). Whereas PDGF may stimulate cholesteryl ester (CE) hydrolysis in cells, TGF-β appears to cause a decrease in lysosomal CE hydrolysis. The latter could lead to a transient reduction in intracellular free cholesterol.
In case of Allergens pre-sensitized mast cells respond by degranulating, releasing vasoactive chemicals such as histamine.
Clinical knowledge of Acharyas is saluted by significant and pertinent observation made by Sushruta to rakta as the medium (or substrate) for the spread or dissemination of the morbific factors of the disease. The aggravation of the dosha goes together with the disturbed or agitated state of rakta.
Yasmad rakta……..
Dalhan says alone dosha are unable to get prakopita whereas they are always dependent (paratantra) on rakta. Therefore Acharya have mentioned vata, pitta and kapha dushita rakta. Modern Science too explains release of inflammatory mediators in blood. Vasodilation and its resulting blood flow cause the redness (rubor) and increased heat (calor), (paridaha).
Acute inflammation is an immune-vascular response to an inflammatory stimulus. Vascular response is compared with rakta prakopa and cellular/ immune response to vata, pitta and kapha.
Similarly upon contact with PAMPs, tissue macrophages and mastocytes release vasoactive amines such as histamine and serotonin, as well as eicosanoids such as prostaglandin E2 and leukotriene B4 to remodel the local vasculature. Macrophages and endothelial cells release nitric oxide. These mediators vasodilate and permeabilize the blood vessels, which results in the net distribution of blood plasma from the vessel into the tissue space.
PRASARA: The third phase signifies to spread which generally takes place with help of vata and rakta. Dosha are stated to spread over and extend to other parts of the body.
TESHAM VAYUGATIMATVAT PRASARAN HETU SATYA API ACHAITANYA I
RAJASCA PRAVARTANA SARVABHAVANAM II
The biomotor or motive force which keeps the rakta moving all over the body, through its own channels-srotas- is vata.
The doshas which have become prakupita expand and overflow the limits of their respective locations. This is explained with two analogues viz the overflow which occurs during the process of fermentation in which ferments rises acquiring new and unseen qualities and the later analogy refers to the overflowing in water dam due to an increased accumulation of water in it, resulting in the two sides of the dam being connected into one vast and continuous sheet of water. It explains the various pressure gradients which enable the vimargagaman of inflammatory mediators from vascular tract into another tissue space, organ system or tract. Pressure gradient cause permeability of srotas/ channels and due to unknown reason dosha do the dusti of rakta and prasar of dushit rakta takes place through 15 different ways as mentioned by Acharya Sushruta.
In case of fever the cytokine factors are released into general circulation, where they migrate to the circumventricular organs of the brain due to easier absorption caused by the blood–brain barrier's reduced filtration action there. The cytokine factors then bind with endothelial receptors on vessel walls, or interact with local microglial cells. When these cytokine factors bind, the arachidonic acid pathway is then activated. Prostaglandin E2 (PGE2) is released which is mediated by the enzymes phospholipase A2 (PLA2), cyclooxygenase-2 (COX-2), and prostaglandin E2 synthase.
In acute inflammation the inflammatory mediators molecules alter the blood vessels to permit the migration of leukocytes, mainly neutrophils and macrophages, outside of the blood vessels (extravasation) into the tissue. Vimargagaman as explained by Sushruta. The neutrophils migrate along a chemotactic gradient created by the local cells.
Increased permeability of blood vessels results in the net distribution of blood plasma from the vessel into the tissue space.
Vasodilation occurs first at the arteriole level (prakopa) progressing to the capillary level, and brings about and increase in the amount of blood present causing the redness and heat of inflammation. Thus paridaha symptom is present in Prakopa and prasar stage of shatkriyakala.
In allergy vasoactive chemicals like histamine propagate an excessive inflammatory response characterized by blood vessel dilation and cytokine release into the blood which move alongwith blood.
Acharya Sushruta analogues that the manner in which rain loaded clouds downpour in specific area where they are taken with help of wind similarly dosha whether permeating the entire body or a part of it- ardha sharira or become confined to a particular part or a member of the body, may give rise to disease in the site of their transportation.
Further Sushruta has also explained how sometime simple cause trigger exacerbarated symptoms of disease. Sushruta says prakupita doshas when not sufficiently excited may remain quiescent, coating (lina dosha) the internal pathways- margas- of the body and exacerbate to cause disease, when they are subsequently excited by appropriate exciting factors.
The above quiescence can be easily understood when patient says previous night he had egg and from next day he started with bloody stools with increased frequency which was later on diagnosed as Ulcerative Colitis, an inflammatory bowel disease. Here egg is exciting factor whereas in patient body the dosha/ inflammatory mediators were already prakopita and waiting for exciting causes.
Allergic rhinitis, urticarial etc are example of lina dosha wherein vascular response secrete histamine which excitingly stimulates cellular immunity to show up sudden (achaya purvak) symptoms.
STHANASANSRAYA: It is prodromal phase or the phase of purvarupa wherein disease is yet to be manifested fully. The excited dosha having extended to other parts of the body become localized and it marks the beginning of specific diseases pertaining to those sthan/ structures. It is also known as the stage of disease augmentation. Sthana samshraya means taking shelter in a place.
In case of fever PGE2 is the ultimate mediator of the febrile response. PGE2 acts on neurons in the preoptic area (POA) through the prostaglandin E receptor 3 (EP3). EP3-expressing neurons in the POA innervate the dorsomedial hypothalamus (DMH), the rostral raphe pallidus nucleus in the medulla oblongata (rRPa), and the paraventricular nucleus (PVN) of the hypothalamus. Fever signals sent to the DMH and rRPa lead to stimulation of the sympathetic output system, which evokes non-shivering thermo-genesis to produce body heat and skin vasoconstriction to decrease heat loss from the body surface. It is presumed that the innervations from the POA to the PVN mediates the neuroendocrine effects of fever through the pathway involving pituitary gland and various endocrine organs.
In case of atherosclerosis sthansansraya takes place in myocardial vessel leads to angina/ myocardial ischaemia/ infarct. If it takes place in brain it leads to Cerebro Vascular Event and if it takes place in peripheral vessel it leads to peripheral vessel disease.
If the inflammatory mediators attack the component of muscle it leads to myopathy whereas if intestine are involved it leads to Inflammatory Bowel Disease.
With respect of atherosclerosis when plasma LDL concentrations become elevated, the vessel wall eventually becomes lipid-engorged because it is unable to traffic the large amounts of endocytosed LDL-CE. In addition, lipoprotein entrapment by the extracellular matrix can lead to the progressive oxidation of LDL because of the action of lipoxygenases, reactive oxygen species, peroxynitrite, and/or myeloperoxidase found in oxidized LDL particles. A range of oxidized LDL species is thus generated, ultimately resulting in their delivery to vascular cells through several families of scavenger receptors. These “molecular Trojan horses” and “cellular saboteurs,” once formed or deposited in the cell, can contribute to, and participate in, formation of macrophage- and smooth muscle–derived foam cells.
The accumulation of the WBCs is termed "fatty streaks" early on because of the appearance being similar to that of marbled steak. These accumulations contain living, active WBCs (producing inflammation) and remnants of dead cells, including cholesterol and triglycerides. The remnants eventually include calcium and other crystallized materials within the outermost and oldest plaque. The "fatty streaks" reduce the elasticity of the artery walls. However, they do not affect blood flow for decades, because the artery muscular wall enlarges at the locations of plaque. The wall stiffening may eventually increase pulse pressure; widened pulse pressure is one possible result of advanced disease within the major arteries.
Atherosclerosis is therefore a syndrome affecting arterial blood vessels due to a chronic inflammatory response of WBCs in the walls of arteries. This is promoted by low-density lipoproteins (LDL, plasma proteins that carry cholesterol and triglycerides) without adequate removal of fats and cholesterol from the macrophages by functional high-density lipoproteins (HDL). It is commonly referred to as a "hardening" or furring of the arteries. It is caused by the formation of multiple atheromatous plaques within the arteries
Thus depending on srotovaigunya or khavaigunya or depending on organ/ system disease is caused.
In acute inflammation, after resultant movement of plasma into the tissue which lead to resultant stasis due to increase in the concentration of the cells within blood. Stasis allows leukocytes to marginate (move) along the endothelium, a process critical to their recruitment into the tissues.
VYAKTI: This stage may be stated to be that of manifestation of the fully developed disease- the resultant dosha dushya samurchana.
In case of fever the brain ultimately orchestrates heat effector mechanisms via the autonomic nervous system. It causes increased heat production by increased muscle tone, shivering and hormones like epinephrine (adrenaline) and also prevents heat loss by way of vasoconstriction.
In acute inflammation the increased collection of fluid into the tissue causes it to swell (edema). The main symptoms of the inflammatory response are as follows.
The tissues in the area are red and warm, as a result of the large amount of blood reaching the site.
The tissues in the area are swollen, again due to the increased amount of blood and proteins that are present.
The area is painful, due the expansion of tissues, causing mechanical pressure on nerve cells, and also due to the presence of pain mediators.
Specific patterns of acute and chronic inflammation are seen during particular situations that arise in the body, such as when inflammation occurs on an epithelial surface, or pyogenic bacteria are involved.
Granulomatous inflammation: Characterized by the formation of granulomas, they are the result of a limited but diverse number of diseases, which include among others tuberculosis, leprosy, sarcoidosis, and syphilis.
Fibrinous inflammation: Inflammation resulting in a large increase in vascular permeability allows fibrin to pass through the blood vessels. If an appropriate procoagulative stimulus is present, such as cancer cells, a fibrinous exudate is deposited. This is commonly seen in serous cavities, where the conversion of fibrinous exudate into a scar can occur between serous membranes, limiting their function. The deposit sometimes forms a pseudo-membrane sheet. During inflammation of the intestine (Pseudo-membranous colitis), pseudo-membranous tubes can be formed.
Purulent inflammation: Inflammation resulting in large amount of pus, which consists of neutrophils, dead cells, and fluid. Infection by pyogenic bacteria such as staphylococci is characteristic of this kind of inflammation. Large, localized collections of pus enclosed by surrounding tissues are called abscesses.
Serous inflammation: Characterized by the copious effusion of non-viscous serous fluid, commonly produced by mesothelial cells of serous membranes, but may be derived from blood plasma. Skin blisters exemplify this pattern of inflammation.
Ulcerative inflammation: Inflammation occurring near an epithelium can result in the necrotic loss of tissue from the surface, exposing lower layers. The subsequent excavation in the epithelium is known as an ulcer.
Atherosclerotic lesions, or atherosclerotic plaques, are separated into two broad categories: Stable and unstable (also called vulnerable). The pathobiology of atherosclerotic lesions is very complicated but generally, stable atherosclerotic plaques, which tend to be asymptomatic, are rich in extracellular matrix and smooth muscle cells, while, unstable plaques are rich in macrophages and foam cells and the extracellular matrix separating the lesion from the arterial lumen (also known as the fibrous cap) is usually weak and prone to rupture. Ruptures of the fibrous cap expose thrombogenic material, such as collagen, to the circulation and eventually induce thrombus formation in the lumen. Upon formation, intraluminal thrombi can occlude arteries outright (e.g. coronary occlusion), but more often they detach, move into the circulation and eventually occluding smaller downstream branches causing thromboembolism. Apart from thromboembolism, chronically expanding atherosclerotic lesions can cause complete closure of the lumen. Chronically expanding lesions are often asymptomatic until lumen stenosis is so severe (usually over 80%) that blood supply to downstream tissue(s) is insufficient, resulting in ischemia.
BHEDA: It is the stage in which the disease may become sub-acute and chronic or incurable. Different types or variant of disease gets manifested.
In case of fever signs like increased blood pressure, neck stiffness, headache, giddiness, unconsciousness etc are seen in this phase.
In case of inflammation the outcome is manifested as:
Fibrosis: Large amounts of tissue destruction, or damage in tissues unable to regenerate, cannot be regenerated completely by the body. Fibrous scarring occurs in these areas of damage, forming a scar composed primarily of collagen. The scar will not contain any specialized structures, such as parenchymal cells, hence functional impairment may occur.
Abscess Formation: A cavity is formed containing pus, an opaque liquid containing dead white blood cells and bacteria with general debris from destroyed cells.
Chronic inflammation: In acute inflammation, if the injurious agent persists then chronic inflammation will ensue. This process marked by inflammation lasting many days, months or even years, may lead to the formation of a chronic wound. Chronic inflammation is characterized by the dominating presence of macrophages in the injured tissue. These cells are powerful defensive agents of the body, but the toxins they release (including reactive oxygen species) are injurious to the organism's own tissues as well as invading agents. As a consequence, chronic inflammation is almost always accompanied by tissue destruction.
The importance of the scheme of kriyakala in early diagnosis and for adopting preventive and curative measures can be appreciated better by taking into consideration some of the recent trends in the modern medicine relating to the pathogenesis of disease.
Avoid hetu which are caused of dosha vridhi. Natural antioxidants (i.e. β-carotene, vitamin C, and vitamin E) have been used as a potential strategy to reduce damage caused by oxidized LDL in patients with or at high risk for CHD, but the majority of clinical trials have not shown reductions in CHD events with this approach. More clinically reliable markers of oxidative stress or the development of more effective antioxidant therapies might make this strategy more useful.
Rakta should always be given importance in all diseases. The mode of prasar should be assessed and managed at the same level.
Elevated values of circulating inflammatory markers such as CRP, serum amyloid A, IL-6, and IL-1 receptor antagonist commonly accompany ACS. Such elevations correlate with in-hospital and short-term adverse prognosis and may reflect not only a high prevalence of myocardial necrosis, ischemia-reperfusion damage, or severe coronary atherosclerosis but also a primary inflammatory instigator of coronary instability.
Non communicable disease are the main concerned in the 21st century, Metabolic Syndrome is among the main factor thus early diagnosis and prevention taken by changing the lifestyle can improve the health of society.
Study can be made by using specific antibiotics or specific medicine for each stage of evolution of disease. It will surely reduce the chances of drug resistancy and also control the vigorous use of drugs.
Study of shatkriyakala specifically sthanasansraya will help to understand kha vaigunyakar causes and help prevention of such hetus from causing the disease.
Conclusion: The utility of this shatkriyakala is to enable the treating physician to recognize the disturbances in its early formative stages and to enable to take necessary steps in time, to correct and eliminate the offending factors before they have caused sufficient damage.

Prof. Dr. Satyendra Narayan Ojha ,
MD (KC), Ph.D.
Director , Yashawant ayurveda college , Post graduate teaching and research center ,
Kodoli ,Panhala , Kolhapur..
 drsnojha@rediffmail. com   - See more at: http://infoayushdarpan.blogspot.in/2016/02/ginger.html#sthash.p9onK67z.dpuf

Acharya charak, Acharya Chakrapani , and modern review : Annāvr̥ta Vāta

Acharya charak, Acharya Chakrapani , and modern review : Annāvr̥ta Vāta: 
Āhar when taken in excess the prokinetic movement is reduced and the āhar is not propelled forward leading to strech reflex. The pain of obstruction of hollow abdominal viscera is classically described as intermittent food related abdominal pain followed by remission.
Mūtra-āvr̥ta vāta: These symptoms are seen in mūtravega dharan. Normal urine formation takes place but the patient does not evacuate it timely leads to the avarodha of vāta gati. Vāta is unable to contract the detrusor muscle thus there is mūtra apravriti and inturn bladder distension. This condition may also arise in neurogenic bladder.
Atonic bladder – Micturition reflex contraction cannot occur if the sensory nerve fibres from the bladder to the spinal cord are destroyed, thereby preventing transmission of strech signals from the bladder. When this happens, a person loses bladder control, despite intact efferent fibers from the cord to the bladder and despite intact neurogenic connections within the brain. Instead of emptying periodically the bladder fills to capacity and overflows a few drops at a time through the urethra. This is called overflow incontinence. Crush injury is the common cause.
Purishāvr̥ta Vāta: Dietary fibres adsorb water and this increases the bulk of stools and helps reducing the tendency to constipation by encouraging bowel propulsive movements. Diet low in fibres content reduces the healthy bowel movements. Stools are formed but due to slow transit there is hard and pelty stool formation which finds it difficult to pass out.
Malavega dharan may also cause the above symptoms. In Diabetes mellitus whenever there is neurogenic involvement, peristalsis are reduced creating the above symptom. Spastic colon may also be considered.


Prof. Dr. Satyendra Narayan Ojha ,
MD (KC), Ph.D.
Director , Yashawant ayurveda college , Post graduate teaching and research center ,
Kodoli ,Panhala , Kolhapur..
 drsnojha@rediffmail. com   –

GINGER

 GINGER

Ginger (Zingiber officinale) is a member of the Zingiberaceae family and is consumed widely not only as a spice but also as a medicinal agent (see also Chapter 7 on ginger). Other members of the family include turmeric and cardamom. Ginger’s cultivation appears to have begun in South Asia and has now spread to various parts of the world. It is sometimes called “root ginger” to distinguish it from other products that share the name. The principal constituents of ginger include [6]-gingerol, [6]-paradol, [6]-shogaol (dehydration gingerols), and zingerone. Several studies have investigated ginger’s antioxidant properties (Chrubasik, Pittler, and Roufogalis 2005). Gingerol has also been shown to decrease intracellular ROS formation in human keratinocyte cells (Kim et al. 2007), inhibit angiogenesis in human ECs, and limit nitrogen oxide synthase expression and epidermal growth factor-induced cell transformation and AP-1 transcriptional complexes in JB6 cells (Bode et al. 2001; Ippoushi et al. 2003; Davies et al. 2005; Kim et al. 2005).
Feeding NIN/Wistar rats a diet containing up to 0.5-5% ginger for 1 month significantly increased (p < .05) several liver antioxidant enzymes, including superoxide dismutase (76–141%), catalase (37–94%), and GPx (11–30%; Kota, Krishna, and Polasa 2008). Lipid and protein oxidation was inhibited in rats consuming ginger, as evidenced by significant decreases (p < .05) in liver and kidney levels of MDA (35-59% and 27-59%, respectively) and carbonyl levels (23-36%), compared to controls (Kota, Krishna, and Polasa 2008). Ippoushi et al. (2007) found that AIN-76 basal diets with 2% ginger decreased TBARS by 29% (p < .05) and suppressed 8-hydroxy-2′-deoxyguanosine (8-OHdG, a product of oxidative DNA damage) levels in Wistar rats. TBARS was also significantly decreased (p < .001) in Wistar rats fed with diets supplemented with 1% ginger following exposure to lindane, a pesticide that is a global pollutant, (Ahmed et al. 2008).
Various animal models have been used to examine the role of ginger in cancer prevention. For example, Ihlaseh et al. (2006) exposed male Wistar rats to N-butyl-N-(4-hydroxybutyl)-nitrosamine (BNN) and uracil salt to induce tumors resembling human low-grade papillary urothelial neoplasia. Rats fed with a basal diet supplemented with 1% ginger extract for 26 weeks had significantly fewer urothelial lesions compared to the controls or those fed with the diet with 0.5% ginger (p = .013; Ihlaseh et al. 2006). However, ginger does not appear effective in all cases, as evidenced by the lack of protection against proliferative lesions in the bladders of Swiss mice fed with a 1% or 2% extract and exposed to BNN/N-methyl-N-nitrosourea (Bidinotto et al. 2006).
Induction of phase I and II activities may partially account for ginger’s anticarcinogenic actions. Banerjee et al. (1994)found that providing 10-μL ginger oil daily for 2 weeks to Swiss mice increased aryl hydrocarbon hydroxylase activity about 25% (p < .05) and increased GST by 60% (p < .01). No significant increase in GST induction was observed in Swiss mice fed with 160 mg ginger/gram diet (Aruna and Sivaramakrishnan 1990).
Inflammation is a significant risk factor for cancer, including prostate cancer. Mitogen-activated protein kinase phosphatase-5 (MKP5) is implicated as a proinflammatory inhibitor in innate and adaptive immune response in vivo (Zhang et al. 2004). Providing [6]-gingerol upregulated MKP5 expression in normal prostate epithelial cells treated with 50 μM gingerol; likewise, it upregulated MKP5 expression in human prostate cancer cell lines (DU145, PC-3, LNCaP and LAPC-4; Nonn, Duong, and Peehl 2007). Ginger extracts, more so than their individual components, have been shown to inhibit lipopolysaccharide-induced prostaglandin E2 (PGE2) production to an extent similar to that of indomethacin, a nonsteroidal anti-inflammatory drug. Subfractions of ginger extract decreased LPS-induced COX-2 mRNA expression levels, although apparently not through the nuclear factor κB (NF-κβ) or activating protein 1 (AP-1) transcription factor pathways, because the ginger extracts did not inhibit TNF-α production (Lantz et al. 2007). [6]-paradol, another active compound in ginger, is reported to induce apoptosis in human promyelocytic leukemia cells, JB6 cells, an oral squamous carcinoma cell line, and Jurkat human T-cell leukemia cells in a dosedependent manner (Huang, Ma, and Dong 1996; Lee and Surh 1998; Keum et al. 2002; Miyoshi et al. 2003). It is unclear whether [6]-paradol has molecular targets similar to [6]-gingerol.
Ginger also appears to have antitumorigenic properties. Several cell lines have been examined for their sensitivity to ginger. For example, alcoholic extracts of ginger inhibited tumor cell growth for Dalton’s lymphocytic ascites tumor cells and human lymphocytes at concentrations of 0.2-1 mg/mL in vitro (Unnikrishnan and Kuttan 1988). In a study of cytotoxic activities of several compounds in ginger against four tumor cell lines (A549, human lung cancer; SK-OV-3, human ovarian cancer; SK-MEL-2, human skin cancer; and HCT-15, human colon cancer), [6]-shogaol was the most potent (ED50: 1.05–1.76 μg/mL), and [4]-, [6]-, [8]-, and [10]-gingerol displayed moderate cytotoxicity (ED50: 4.92-30.05; Kim et al. 2008). Adding [6]-gingerol (25 μM) has been reported to inhibit proliferation in rat ascites hepatoma cells AH109A and increase apoptosis at higher concentrations (50 μM; Yagihashi, Miura, and Yagasaki 2008). Likewise, adding [6]-shogoal (60 μM) to COLO295 cells has been reported to increase the expression of GADD153, a gene that promotes apoptosis (Chen et al. 2007). [6]-shogaol (>50 μM) also provokes DNA damage and apoptosis through an oxidative stressmediated caspase-dependent pathway (Chen et al. 2007). Similarly, incubation of HEp-2 cells with ginger (250 μg/mL, 500 μg/mL, or 1000 μg/mL) resulted in a dose-dependent decrease in nitrite generation, increased production of superoxide, and decreased GSH levels compared to untreated cells, indicating ginger-induced apoptosis through the generation of ROS (Chen et al. 2007).
Ginger is also recognized for its potential usefulness to reduce nausea. To determine whether ginger had antiemetic effects in cisplatin-induced emesis, Manusirivithaya et al. (2004) conducted a randomized, double-blinded, crossover study in 48 gynecologic cancer patients. The addition of ginger (1 g/day) to a standard antiemetic regimen has no advantage in reducing nausea or vomiting in the acute phase of cisplatin-induced emesis. In the delayed phase, ginger and metoclopramide have no statistically significant difference in efficacy (Manusirivithaya et al. 2004). In another study, 1000 mg of ginger was compared to 20-mg intravenous (IV) metoclopramide, and to 4-mg IV ondansetron in controlling nausea in patients receiving cyclophosphamide chemotherapy. Ginger was determined to be as effective as metoclopramide, but neither was as effective as ondansetron (Sontakke, Thawani, and Naik 2003).
Overall, while the anticancer findings of ginger are intriguing and several processes may be associated with the observed responses, additional studies are needed to clarify the underlying mechanisms and to determine overall benefits to humans (Pan et al. 2008).


Prof. Dr. Satyendra Narayan Ojha ,
MD (KC), Ph.D.
Director , Yashawant ayurveda college , Post graduate teaching and research center ,
Kodoli ,Panhala , Kolhapur..
 drsnojha@rediffmail. com  - See more at: http://infoayushdarpan.blogspot.in/2016/02/salient-features-of-amlapitta.html#sthash.AP6bCKCS.dpuf

शुक्रवार, 19 फ़रवरी 2016

Salient features of Amlapitta

Salient features of amlapitta ; The acid environment within the stomach leads to cleavage of the inactive precursor to pepsin and provides the low pH (<2) required for pepsin activity. Pepsin activity is significantly diminished at a pH of 4 and irreversibly inactivated and denatured at a pH of >7. Achlorhydria leads to hypergastrinaemia. Enterochromaffin- like (ECL) cell hyperplasia with frank development of gastric carcinoid tumors may result from gastrin trophic effects. Hypergastrinaemia and achlorhydria may also be seen in non pernicious anaemia- associated type A gastritis. Drugs containing katu rasa maintain required pH to activate pepsin for its action on protein digestion..therefore its known as deepaniya .. Proton pump inhibitors can develop mild to moderate hypergastrinaemia and in turn carcinoid tumors in some experimental animals.. ayurveda drugs effective in amlapitta never develop such side effects , only because of katu and tikta rasa.. katu rasa produces achchha pitta not vidagdha pitta... Heart burn and regurgitation are common symptoms of GERD (urdhvaga amlapitta). Inherent in pathophysiologic model of GERD is that gastric juice is harmful to esophageal epithelium. However , gastric acid hypersecretion is usually not a dominant factor in development of esophagitis. One caveat is with chronic H.pylori gastritis, which may have a protective effect by inducing atrophic gastritis with concomitant hypoacidity. Pepsin, bile and pancreatic enzymes within gastric secretion can also injure esophageal epithelium. Bile warrants attention because it persists in refluxate despite acid suppressing medications. Bile can transverse cell membrane , imparting severe cellular injury in a weakly acidic environment, and has also been invoked as a cofactor in pathogenesis of Barrett's metaplasia and adenocarcinoma. Hence, the causticity of gastric refluxate extends beyond hydrochloric acid.. kutaki , amrita , kiraatatikta , shataavari , aamalaki ,avipattikara churna , bhoonimbaadi kvaatha, daadimaadi ghrita , kushmaanda avaleha ,etc drugs are best options in urdhvaga amlapitta and to prevent metaplasia...

.Prof. Dr. Satyendra Narayan Ojha ,
MD (KC), Ph.D.
Director , Yashawant ayurveda college , Post graduate teaching and research center ,
Kodoli ,Panhala , Kolhapur..
 drsnojha@rediffmail. com - See more at: http://infoayushdarpan.blogspot.in/#sthash.6O6eCEsw.dpuf

Acharya charak and modern hypothesis of Bronchial asthma and COPD ( Shvaasa roga )

 Acharya charak and modern hypothesis of Bronchial asthma and COPD ( Shvaasa roga )

the considerable overlap between persons with asthma and those with COPD on airway responsiveness ,airflow obstruction , and pulmonary symptoms led to the formulation of Dutch hypothesis. This suggests that asthma , chronic bronchitis and emphysema are variations of the same basic disease, which is modulated by environmental and genetic factors to produce these pathologicaly distinct entities. The alternative British hypothesis contends the asthma and COPD are fundamentally different diseases ; Asthma is viewed as largely an allergic phenomenon, while COPD results from smoking-related inflammation and damage. Acharya Charak mentioned Rajasa (pollen grains/allergens) Dhooma ( smoking ) vaataabhyam.... etc as hetu of shvaasa roga.. as per acharya chakrapani ; rajasa ityaadinaa prayo vaata prakopakagano vichchhidyoktah gadaavimaavityantena , nishpaava ityaadinaa kaphakaaranatayaa hikka shvaasayoh kaphaprakopa hetu gano abhihitah ; tadanena vaatajanaka kaphajanaka hetu varga dvaya vichchhet paathena vaatakaphayoh atra svahetukupitatvena svaatantryam darshayati , na anubandhamaroopatvam.. it means two different groups of etiological factors induce shvaasa roga separately ; vaata and kapha are vitiated by their hetu separately to initiate disease process.. Both extrinsic and intrinsic factors are mentioned as hetu of shvaasa roga. In samprapti of shvaasa roga acharya charak mentions vishvagvrajati ( sarvato gachchhati ) , means nonuniform ventillation , discarded ventillation and mismatching between ventillation and perfusion , a cardinal pathophysiology of shvaasa roga.. in an other reference ( ch.chi 18/131) acharya refered Tamakah kaphakaase tu syaachchet pittaanubandhajah... when there is secondary infection occurs in patient with chronic bronchitis , airway obstruction develops and in turn manifests severe dyspnea similar to episode of bronchial asthma (earlier known as infective bronchial asthma ). Since centuries the concept about shvaasa roga is very clear in ayurveda.. Determination of the validity of Dutch hypothesis Vs. British hypothesis awiats identification of the genetic predisposing factors for asthma and /or COPD ,as well as the interactions between these postulated genetic factors and environmental risk factors.. acharya charak mentioned very clearly the role of vaata and kapha in shvaasa roga ; Yadaa srotaansi sanroodhya maarootah kaphapoorvakah. Vishvagvrajati sanroodhah tadaa shvaasaat karoti sah..maaroota , kapha  Hyperresponsiveness of bronchial smooth muscles and inflammation of airways  airway obstruction  shvaasa roga ( bronchial asthma and COPD)..Acharya charak mentions tila taila as hetu of hikkashvaasa ( ch.chi 17).. Nishpaava maasha pinyaaka tila tail nishevanaat are observed as hetu of pandu roga and shvaasa hikka.. Acharya charak mentioned the same hetu in vidhi shonatiya adhyaaya.. means these are causes of raktaja roga. I think these all nishpaavaadi are hetu of kapha prakopa and rakta dushti..its kaphaprakopaka hetu , very clearly told by acharya chakrapani..Tila may lead to histamine liberation by mast cells after allergen - IgE binding on surface of mast cells.. Hyperresponsiveness may be caused by tila or tila tail or any hetu mentioned in shvaasa roga.. Ie srotaansi sanroodhya/airway obstruction.. references ; Charak sanhita and Harrison 's principles of internal medicine...

.Prof. Dr. Satyendra Narayan Ojha ,
MD (KC), Ph.D.
Director , Yashawant ayurveda college , Post graduate teaching and research center ,
Kodoli ,Panhala , Kolhapur..
 drsnojha@rediffmail. com

The conceptual study of connective tissue diseases as one of causative factors in Interstitial lung diseases (ILDs)

The conceptual study of connective tissue diseases as one of causative factors in Interstitial lung diseases (ILDs) : both modern and ayurveda perspective ;patients with ILDs come with the onset of progressive exertional dyspnea or a persistent nonproductive cough. Hemoptysis , wheezing and chest pain may be present. Often , the identification of interstitial opacities on chest X-ray focuses the diagnostic approach on one of the ILDs. Rheumatoid arthritis is one of connective and autoimmune diseases which cause ILDs.. inflammation in the air space and alveolar walls and interstitial fibrosis are present due to autoimmunity.. the presence of jts pain , stiffness and deformity like swan neck etc with +ve antinuclear antibodies and anti- immunoglobulin antibodies ( RA factors ) confirm the diagnosis , however these tests are +ve even in absence of defined connective tissue diseases. ILDs are characterized as a significant part of a multiorgan process , as may occur in the connective tissue diseases ( SLE, RA , Ankylosing Spondylitis, systemic sclerosis , sjogren's syndrome , polymyositis-dermatomyositis. Aamavaata mentioned in madhav nidan is classical example of autoimmune diseases , otherwise in relation to grahani chikitsa acharya charak mentions yakshma peenas mehaadeen kaphajaan kaphasangatam; aamavisha along with kapha when reaches into urahsthaana , can induce yakshmaa peenasa like diseases. I consider the role of aamavisha yukta kapha as part of autoimmunity , since vaata is major initiator of immune phenomenon , so vaata and kapha as predominant dosh can be considered in ILDs. The presence of inflammation and fibrosis is due to autoimmune reaction , ie aamaavisha yukta kapha reactions with vaata on surface of epithelium.. shirisha tulasi gorakhamundi darvi haridra amrita karkatashringi shunthi pippali aamalaki dashamoola pushkaramoola kantakaari bharangimoola kushtha ashwagandha like drugs are found somewhat effective in ILDs...Salient features in pathogenesis of ILDs ; the lung is naturally exposed to repetitive injury from a variety of exogenous and endogenous stimuli . Several local and systemic factors e.g. fibroblasts , circulating fibrocytes, chemokines , growth factors , and clotting factors contribute to tissue healing and functional recovery. Dysregulation of this intricate network through genetic predisposition and autoimmune conditions ,or superimposed diseases can lead to aberrant wound healing , with the result of pulmonary fibrosis. Alternatively , excessive injury to the lung may overwhelm even intact reparative mechanisms and lead to pulmonary fibrosis..For inhibition of dysregulation , or promotion of reparative mechanisms , rasaayana chikitsa may be helpful.. Tulasi saarivaa kushtha haridraa daruharidra ashwagandhaa gokshuru shati lashuna jivanti musta bhumyamalaki pippali dashamoola kutaki haritaki aamalaki tejapatra shirisha bilva pushkaramoola chitraka pravaala tamra lauha rajata bhasma abhraka etc can be tried in different form..



.Prof. Dr. Satyendra Narayan Ojha ,
MD (KC), Ph.D.
Director , Yashawant ayurveda college , Post graduate teaching and research center ,
Kodoli ,Panhala , Kolhapur..
 drsnojha@rediffmail. com

HCM and HOCM with Ayurveda perspective

HCM and HOCM with Ayurveda perspective ; 

Hypertrophic cardiomyopathy is characterized by non dilated left ventricular hypertrophy. Later there may be hypertrophic obstructive cardiomyopathy due to left ventricular outflow tract pressure gradient. Three basic mechanisms are involved ; (1) increased left ventricular contractility ( effect of prakupita kapha ), (2)- decreased ventricular volume (preload),( aadaana karma of praana vaayu is impaired ), (3)- decreased aortic impedance and pressure (afterload) -( vyaana vaata karma haani ) 2&3 are because of hridaya gata vaata ( angina pectoris , fatigue and syncope are present with dyspnea , a common symptom due to diastolic dysfunction/ impaired left ventricular filling indicate predominance of vaata Kaphaja hridroga with hridaya gat vaata can be considered in HCM and HOCM.. Hridayarnava rasa , chandraprabha vati , gokshuraadi guggula , kvaatha of combination of dashamoola arjuna punarnava gokshuru varuna haritaki devadaru pushkaramoola kamal shatavari ashwagandha chitraka vacha shunthi . Shaalaparni with milk. Kamadudha , arjunaarishta , hrida basti by dashamoolaadi tail or prepared as per ch.chi 26 vaatika hridroga..Advice for salt restriction , no physical and mental stress , no alcohal, no smoking , small bolus of food at a time 4-5 times per day. Pomegranate grape orange fig are good fruits .. Gandharva haritaki can be added at night for proper bowel motion to avoid straining during defaecation...Food intake increases blood suply to splanchnic circulation so demand is increased which in turn develops overload on failing ( compromised ) heart and manifests dyspnea fatigue giddiness chest pain... Its due to vaata prakopa in hridayashtha sthaan ie hridaya gata vaata. Anshumati sapayasaa is indicated by acharya charak...
I have elaborated 3 specific underlying pathology in HCM and HOCM with vaata predominace , but initial factor is kapha prakopa leading to non dilated cardiomyopathy , increased mass of myocardium , mass represents sthoola bhaava so its due to kapha , later contractility preload and afterloads are impaired . due to diastolic dysfunction dyspnea manifests , due to increased mass demand for O2 is increased and that is not supplied adequately so there is imbalance between demand and supply leading to ischaemia and chest pain ie due to apatarpana vaata prakopa in hridaya so hridaya gata vaata can be considered.. decreased cardiac output (due to left ventricular outflow obstruction - sanga ) causes decreased effective arteriolar volume and renal hypoperfusion resulting in activated renin angiotensin aldosterone system to manifest salt and water retention vasoconstriction and remodelling of ventricle. These are consequences of disease process and can be considered as vitiated vaata to bring ambu dhatu to retain beneath tvaka and maansa ie edema.. treatment plan includes to work on 3 basics ; arjuna shatavari kakamachi ashwagandha for srength of contractility to maintain diastolic function. Punarnava gokshuru varuna to reduce preload and pushkaramoola dashamoola to maintain normal after load.. chitraka vacha trikatu to decrease sanga or obstruction.. hridayarnava rasa contains tamra and kaakamaachi so better option in this condition.. chandraprabhavati gokshuradi guggula to decrease congestion , gokshuru is hridya too. Kamadudha acts on action potential to provide normal ionic changes across cell membrane . Angiotensin 2 is potent vasoconstrictor( increases peripheral resistance) , increases sympathetic activity (increased cardiac output), secretion of arginine vassopressin so increase renal reabsorption of water , increase aldosterone secretion so promote salt and water retention( increase venous return so increased cardiac output )  hypertension.. salt is major cause of activated RAAS - pitta prakopaand rakta vriddhi. Kapha prakopa and dhamanipratichaya...HTN. Aamaashaya gata vaata manifests shvaasa , as pranavaha sroto dushti since pitta sthaana samudbhava is mentioned in shvaasa roga.. here shvaasa is one of symptom of HCM.
Hridaya as a whole organ is moola sthaana of prana vaha rasa vaha and rakta vaha.In dhamanipratichaya sakapha meda and maansa interplay to develop uplepana on dhamani .. it leads to avarodha of vaata gati.. it should not be considered as dhamanipoorana: In Aortic stenosis pathogenesis occurs similar to as that of atherosclerosis so modern dr advice statins in AS . CAD, AS and HCM are different disease entities .. but in AS and HCM angina pectoris is present without CAD , only due to increased demand caused by hypertrophy..


.Prof. Dr. Satyendra Narayan Ojha ,
MD (KC), Ph.D.
Director , Yashawant ayurveda college , Post graduate teaching and research center ,
Kodoli ,Panhala , Kolhapur..
 drsnojha@rediffmail. com

Acute pancreatitis

Acute pancreatitis ;

 Gall stones alcohol etc - pitta prakopa in term of ushna tikshna vriddhi - paaka karma vriddhi in agni sthaana *(pittaja gulma )- agnisaada - (pittavrita samaana). shoola jvara chhardi due to pitta prakopa , indigestion and malabsorption due to aavrita samaana . Due to pitta vridhi vaata marga avarodha leading to rakta pitta sanchiti in udara ; jalodara.. sanga pradhaan dushti so eka sthaana vriddhi (jalodar) and itar (other ) sthaana kshaya - circulatory failure.. excessive pitta prakopa - rakta dushti - paaka- septicaemia..
Pitta prakopa and vaata gati hanana result in gulma and jalodara , aavrita samaana leading to agnisaada.. apatarpana is severely present.. managament ; laghu santarpana , deepaniya yavaagu , shrita yoosha , shadanga paaniya , pitta shamana , agni vardhana , due to chhardi amalaki mashi with pravala or shankh bhasma and mayurapuchchha bhasma muhurmuhuh , especialy before intake of fluid, food and drugs
Already apatarpana so sanshodhana chikitsa is contraindicated , tiktaksheera ghrita basti /yaapana basti can be considered to work on pitta & vaata.There is exocrine insufficiency - less pancreatic enzyme secretion - indigestion & malabsorption - diarrhea and steatorrhea ( in acute phase severe abdominal pain vomiting and fever ) - agni vardhan chikitsa will decrease the load on pancrease , hence recovery from inflammation will be fast.. Electrolytes and water maintainance is crucial with nutritional support ; shrita yoosha / deepaniya yavaagu are best choice ..
Swarna makshika bh 10 grm+
Pravalapisti 10 grm+
Guduchi satwa 10 grm+
Amlaki churna 30 grms
1 grm twice daily.
On 2-3 days pain intensity gradually drops.lashunaadi vati like drugs are effective.. aamalaki mashi combination is effective in chhardi.In acute pancreatitis (pitta prakopa ) due to inflammatory degeneration of exocrine cells , enzyme secretion is very less *(aavrita samaana), so indigestion and malabsorption (agnisaada) occurs
Agniboosting drugs which provide enzymes to help in digestion so load on pancrease is decreased providing time for healing.. Lashuna ksheerapaaka is mentioned in gulma with indication in antarvidradhi...For samaana boosting chitraka lashuna like drugs are found effective , its not hypothesis , its observation.. Pulling of fluid in peritoneum indicates the role of vaata.These drugs are also helpfull in removing obstructive pathology
. Jalodar is another consequence present in pancreatitis excludes paittik shoola ..ERCP with stent placement is also indicated for pancreatic ductul disruptions that occur as part of the inflammatory process and result in peripancreatic fluid collections...In addition to nutritional support , enteral feeding helps to maintain integrity of the intestinal tract during severe acute pancreatitis..
The maintainance of intestinal integrity is possible with drugs acting on agni or samaana vaayu..
Enteral feeding with a nasojejunal tube has been demonstrated have fewer infectious complications than with TPN and is preffered method of nutritional support.. Therefore i prefer the use of shadangapaaniya , shrita yoosha and laghu santarpana through nasojejunal tube in place of IV fluids and colloid to maintain normal intravascular volume... Analgesics for pain ; shankha vati /chitrakaadi vati /lashunaadi vati/ agnitundi vati..There is future prospectus in ayurveda to treat such diseases which can cause multiple organ failure ; need to select appropriate treatment modalities.. thanks for discussion Gulma chikitsa in charak is best reference to understand the diseases related to GIT and their line of treatment ..Later in charak chikitsa 26 in reference to hridroga acharya charak mentions various shoola for differential diagnosis purpose... acharya madhav referred such shoola dominating diseases in details.. As parinaama shoola annadrava shoolaadi..
In sushruta uttaratantra after gulma hridroga chikitsa is classified and at the end of gulma description , acharya sushruta mentions hrichchhula , the purpose is differential diagnosis. Diagnosis is crucial to decide perfect line of treatment...


.Prof. Dr. Satyendra Narayan Ojha ,
MD (KC), Ph.D.
Director , Yashawant ayurveda college , Post graduate teaching and research center ,
Kodoli ,Panhala , Kolhapur..
 drsnojha@rediffmail. com

The relation of Praanaadi Vaata Bheda with Praana Vahaanaam Srotas

The relation of Praanaadi Vaata Bheda with Praana Vahaanaam Srotas ;
 iti praana sangyaka vaata vahaanaam . Etat cha *praanaakya* vishishtasya vaayoh vishishta srotah, saamaanyena tu vaayoh sarvaa eva dhamanya iti na virodhah.. it means it carries specifically praana vaayu.. Hetu ; kshayaat * ( dhaatu kshaya or yakshmaa ) sandhaaranaat roukshyaat vyaayaamaat kshudhitasya cha  vaata prakopa ( specificaly praana vaayu )  praana vaahini dushyanti  atisrishtam kupitam abhiksham sashabdam ( deep and rapid ventillation /hyperventillation/kussmaul's breathing as in metabolic acidosis ,etc ), atibaddham kupitam alpa alpam sashoolam ( shallow , slow breathing with pleuritic chest pain as in pleurisy/restricted chest diseses). These features are concerned with impairement of CNS , Airways , lungs parenchyma , and pulmonary circulation..chikitsa; shvaasiki chikitsaa ;as per shvaasa roga.. it means shvaasa roga is primary diseases of praanavaha srotas...now vaayu bheda description ; praana apaanau ; uchchhvaasa nihshvaasu..shvaasa karma is reffered as karma of praana vaata. Whether nihshwasa and uchchhvaasa both or only nihshvaasa , a debate is welcome here. Praana apaanau iti uchchhvaasa nihshwaasau , kechit tu praana apaanau yathaa uktau eva vaatau praahuh ; tatra apaano yadyapi merdh shroni aadi aashraya eva iti aahuh , tathaapi * hridayaavyatirikta anuvidhaayitvaat "hridaya aashrita " iti uchyate; referring uchchhvaasa karma by apaana since expiration helps in rid off undue CO2 ; end product of metabolism ( dhaatu mala ). After referring annam aadaana karmaa tu praanah koshtham prakarshayati , it seems as ispiration helps the entry of gases , karma of praana vaayu.. now applied approach ; vishvaga vrajati iti sarvato gachchhati ( discarded ventillation ) is due to yadaa srotaansi sanroodhya maarootah kaphapoorvakah sanroddhah tadaa and results in shvaasa roga. It shows mismatching between ventillation and perfusion , a leading pathophysiology of respiratory dyspnea.. urdhvam dhooyamaana vaatah (hyperventillation ) ,deergham shvasiti iti shvaasasya bahirnigamanam deergha kaalam karooti ( delayed forceful expiration ie FEV1sec is reduced ) , shvasiti vichchhinam iti nihshvasya punah kshana anten shvasiti ( cheyne stokes breathing & ataxic breathing) , n vaa shvasiti na shvaasam labhate ( apnea)etc; indicate impairment all components of respiratory system including cns and thoracopulmonary and pulmonary circulation.. only in aamaashaya gata vaata shvaasa roga is reffered , it shows the involvement of mahaasrotas by prakupita vaat. In praanaavrita udaana nihshvaasa uchchhvaasa sangrah ; shows interplay between praana and udaana ( both are urah sthaanashtha vaata bheda , so vulnerable to influence each other , if becomes prakupita ) chikitsa; urdhvabhaagikam karma /vamaanaadi . Udaanaa vrita apaana manifests shvaasadi roga( shvaasa hikka and kaasa ); pratilomam apaana vaayuh ( forceful expiration as in tamaka shvaasa : chikitsa- anulomanam , tamaku tu virechanam ) / udaana bhaavam aapannna iti urdhvagati *svabhaavam*aapanah ( forceful or explosive expiration is cause of kaasanaat kaasah as in kaasa ). Kaphaavrita praana manifests nihshvaasa uchchhvaasa sangrah . In kaasa udaana and apaana , in shvaasa roga praana udaana and apaana are being affected.. After studying acharya sharangadhara ' s interpretation and all these references concerned with praanavaha sroto dushti ; the role of praana in nihshvaasa and apaana in uchchhvaasa seems logic and clinicaly as well as therapeuticaly accepteble.. being sthaanashtha udaana vaata helps in respiration as a whole .After understanding the role of Cardiopulmonary circulation in perfusion it shows the role of vyaana vaata in rasa vikshepana. When vyaana vaata becomes abnormal as in pulmonary hypertension dyspnea manifests.. in metabolic acidosis and alkalosis hyper and hypo ventillation menifests respectively , the role of samaana vaata cnt be ignored.... i think the role of panchaatmaa vaata is crucial in praanavaha srotas to maintain matching between ventillation and perfusion.. abnormality of any one leads to mismatching , a cardinal pathophysioligy of shvaasa roga..There is inspiratory and expiratory center in medulla under controle of praana and apaana respectively.. eg. In hypercapnea hyperventillation is to expell (nihsarana/utsarjana ) excess CO2 , waste product *(mala ) of carbohydrate and fat metabolism.


.Prof. Dr. Satyendra Narayan Ojha ,
MD (KC), Ph.D.
Director , Yashawant ayurveda college , Post graduate teaching and research center ,
Kodoli ,Panhala , Kolhapur..
 drsnojha@rediffmail. com

Aama , autoimmune phenomennon , and Ayurveda.

Aama , autoimmune phenomennon , and Ayurveda.


.certain biomarkers like immune complexes can be considered as aama and they are measurable..Oxidized LDL - cholesterol can be correlated with saama meda..Ch.chi.15 in reference to ajeerna , acharya charak is very clear to demonstrate aama and its related disorders.. autoantibodies are best examples of circulating aama
There is autoantibody to iselet cells of langerhans causing type 1 DM , aama in samaana sthaana and manifesting madhumeha.. We should evaluate immunomodulator effect of mustaa like drugs in clinical / experimental trial..
Mustaa can grow at any place ,shows its strongest behaviour to survive..CRP is acute phase reactant , can be considered as rasa/rakta gata aama marker..triglycerides is major culprit in chronic complications of DM , biomarker for saama meda /kapha , responsible for atherogenesis...For such purpose our choice is katu and tikta dravya enriched in vaayu agni and aakaasha mahaabhoota helping in countering the saamata ..Rasaadibhihcha samsrishtam kuryaat rogaan rasaadijaan ch.chi.15/49...Antibody to gastric parietal cells  atrophic gastritis amlapitta.. paandu...Ghora anna visha / environmental factors , especialy diet components are triggering factors in genetic predisposed persons to induce auto immunity..The identification of aama , cross reaction due to molecular mimicry and self to non self reaction are very crucial in auto immunity.. Identification of aama by vaayu , molecular mimicry by kapha and self to non self reaction by pitta and eventually initiation of auto immune induced disease process is concerned with tridosha...amritaa , pippali , patola , kiraatatikta , shunthi , kumaari ,ashwagandhaa , shataavari , balaa , etc are effective in autoimmune disorders.



.Prof. Dr. Satyendra Narayan Ojha ,
MD (KC), Ph.D.
Director , Yashawant ayurveda college , Post graduate teaching and research center ,
Kodoli ,Panhala , Kolhapur..
 drsnojha@rediffmail. com

Acharya chakrapani on kloma

Acharya chakrapani on kloma ;
        Kloma hridayastha pipaasaa sthaanam ( acharya chakrapani on ch.vi.5/8), kloma pipaasaa sthaanam ( acharya chakrapani on ch.sh. 7/10) , kloma hridaya avayava visheshah ( acharya chakrapani on ch.chi. 13/45). These references show that kloma is a regulatory organ of ambuvaha srotas, to maintain fluidity in rasaraktaadi ambu dhaatu , 10 dooshya of prameha are enriched in aap mahaabhoota and need to have due amount of udaka for their transportation.Osmoreceptors in thirst center of hypothalamus regulate the amount of fluidity in blood, its activation is based on osmolality of plasma. Increased osmolality increases desire to intake of water, vice versa.. maarootah klomni samsthitah...... vardhayetam tadeva ambu svasthaanat udaraaya tau ( ch.chi 13/46) , svasthaana means peritoneal cavity which contains serous fluid similar to interstitial fluid.. there is exchange of fluid between plasma and interstitial space , dependent on hydrostatic and colloid oncotic pressure.. the imbalance can lead to accumulation of fluid in interstitial space /serous cavity and in turn edema/ascites/pleural effusion etc manifest.. this is reason why acharya charak describes udara chikitsa after shotha chikitsa.. intracellular and extracellular fluid maintainance is based on concentration gradient as well pressure gradient.. over all the maintainance of fluidity in body is well controlled by various factors, e.g. osmoreceptors, brain and atrial natriuretic peptides , Renin angiotensin aldosterone system.. osmolality of plasma is main initiator of activation of thirst center followed by others.. the balance between parthiva and aapa mahaabhoota in rasaraktaadi ambu dhaatu is essential to continue nonstop transportation.. the imbalance leads to sanga or atipravriti like sroto dushti.. the role of ambuvaha sroras is very critical to connect all cells with each other for their nutrition. Acharya chakrapani ; aahaara rasaat sarva dhaatu poshako dhaatu rasa utpadyate , sa cha * raso dehaposhako ambu bhava * iti aapya iti arthah . Tasya kshayaat iti rasa kshayat" trishyate", rasa kshayat ambu kshayo bhavati , ten cha ambu kshayena purushah "paaniya prathanaa roopa" ( desire to intake of water ) trishnayaa yukto bhavati iti yuktam iti darshayati. Uktam hi sushrute - dosha dhaatu mala ksheeno bala ksheeno api maanavah , sva yoni vardhanam yat tat annapaanam prakaamkshati ( su.soo.15).. iti : ihaapi cha uktam tasya 'kshayaat cha trishyeddhi 'iti ( on ch.chi. 22/16).all these references show the importance of ambu , pipaasaa and in turn pipaasaa sthaanam iti kloma; hridayastha pipaasaa sthaanam iti thirst center..Rasa roopo dhaatuh , kimvaam rasati iti raso drava dhaatuh uchyate , ten roodhiraadeenaamapi dravaanaam grahanam bhavati (acharya chakrapani on ch.chi 15/36)..


.Prof. Dr. Satyendra Narayan Ojha ,
MD (KC), Ph.D.
Director , Yashawant ayurveda college , Post graduate teaching and research center ,
Kodoli ,Panhala , Kolhapur..
 drsnojha@rediffmail. com