Shwas-rog Series-3 Understanding the mechanism of Samprapti with 'URASTHAH KAPHAMUDDHUYA' by Prof. Satyendra Ojha

मारुतः प्रणवाहीनि स्रोतांसि आविश्य  कुप्यति !
उरस्थ: कफमुद्धूय हिक्काश्वासाङकरोति  !!
                                                 (Ch.chi.17/17)

  Explains the hyperplasia of mucus secretion as seen in COPD wherein small airways may become narrowed by cells (hyperplasia and accumulation), mucus, and fibrosis. Characteristic cellular changes include goblet cell metaplasia, with these mucus-secreting cells replacing surfactant-secreting Clara cells. Smooth-muscle hypertrophy (kupyati maruta) may also be present. 

These abnormalities may cause luminal narrowing by fibrosis, excess mucus, edema, and cellular infiltration.

Vitiated vata expels kapha from its sthana can be easily understood in case of cystic fibrosis. Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) which is an integral membrane protein that functions as an epithelial anion channel. The ~1480-amino-acid molecule encodes a passive conduit for chloride and bicarbonate transport across plasma membranes of epithelial tissues, with direction of ion flow dependent on the electrochemical driving force. 

The function resembles that of vata thus it can be said that CFTR is vatadharmi dravya. Along respiratory mucosa, CFTR is necessary to provide sufficient depth of the periciliary fluid layer (PCL), allowing normal ciliary extension and mucociliary transport (normal function of vata). But in cystic fibrosis this CFTR-deficient airway cells exhibit depleted PCL (kupita vata), causing ciliary collapse and failure to clear overlying mucus. In airway submucosal glands, CFTR is highly expressed in acini and may participate both in the formation of mucus and extrusion of glandular secretion onto the airway surface (udhuya kapham) thus obstructing, the gati of pran leading to oxygen and carbon dioxide mismatch and therefore difficulty in breathing.

In other condition this kapha (inspissated mucus) helps in further growth of bacterial infection leading to collateral tissue injury and further aggravates respiratory decline.

Sometimes inorganic and organic dust, are associated with chronic mucus hypersecretion (chronic bronchitis), with or without reduction of expiratory flow rates.

Mucus hyper secretion Increased mucus secretion contributes to the viscid mucous plugs that occlude asthmatic airways, particularly in fatal asthma. There is hyperplasia of submucosal glands that are confined to large airways and of increased numbers of epithelial goblet cells. IL-13 (kupyati maruta dharma dravya) induces mucus hypersecretion in experimental models of asthma.

Inflammatory Mediators Multiple inflammatory mediators have been implicated in asthma, and they may have a variety of effects on the airways that account for the pathologic features of asthma. Mediators such as histamine, prostaglandin D2, and cysteinyl-leukotrienes contract airway smooth muscle, increase microvascular leakage, increase airway mucus secretion (kapham udhuya), and attract other inflammatory cells. Because each mediator has many effects, the role of individual mediators in the pathophysiology of asthma is not yet clear. Although the multiplicity of mediators makes it unlikely that preventing the synthesis or action of a single mediator will have a major impact in clinical asthma, recent clinical studies with antileukotrienes suggest that cysteinyl-leukotrienes have clinically important effects. The mediators are the vata dharma dravya.

Such description can help to get more effective treatment for तमक श्वास ।

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Prof. Satyendra Narayan Ojha  

MD PhD

(Kayachikitsa)
Director,

Yashwant Ayu.College & P.G.Training&Research Center, 

Kodoli, Kolhapur, Maharashtra, India.

Mobile No.- +91 9822177155     

email: drsnojha@rediffmail.com