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Prof. A.S. Paintal joined VPCI in 1954 and started
the neurophysiological investigations relating to Chest Diseases. Within
a few months after joining Dr. Paintal put the name of the Institute on
the physiology map of the world by announcing his discoveries on the deflation
receptors' (now known as the type J receptors). After a short stint in AIIMS,
New Delhi, and Albert Einstein Medical College, New York as visiting scientist,
Professor Paintal returned to VPCI as Director in 1964 to establish a full
fledged Physiology Department. In conformity with the Institute objectives,
the aims of the Department were to establish the infrastructure for studying
the visceral mechanisms of the body, in particular the chest; and to train
postgraduate students to pursue a career in physiology.
Neurophysiology laboratories were set up and outstanding Indian scientists from all over the world were appointed as staff members. The sensory receptors of the heart and lungs, and their afferent and efferent pathways became the main focus of research. Several noteworthy discoveries were made under the dynamic leadership of Professor Paintal. During the last three decades, major research contribution have been made in the area of sensory neurophysiology notably from the cardiopulmonary region by Prof. A.S. Paintal, Prof. P.D. Gupta, Dr. M.S. Devanadan, Dr. K.S.K. Murthy, Dr. S,R. Gupta, Dr. P. Gill Kumar, Prof, M. Fahim, Dr. A. Anand, Dr. K. Ravi. and several students and technical staff of the Department. Major Activities and Achievements 1. The type B atrial receptors (identified by Prof Paintal) were reported as volume receptors responding to atrial filling. These receptors were considered as the major receptors involved in the regulation of body fluid volume. 2. Recordings were obtained from the ventricular receptors. These receptors were thought to be responsible for the Bezold Jarisch effect. 3. The mucosal mechanoreceptors of the intestine were discovered. 4. The existence of the presser pain receptors in the muscles was reported. These receptors increased ventilation during exercise. 5. Experimental evidence was provided that pulmonary congestion was the natural stimulus for the type J receptors. Thus, their significance in pulmonary oedema was highlighted. 6. An increase in pulmonary blood flow stimulated the type J receptors. Hence, it was proposed that the J receptors could be stimulated in exercise. 7. Following the stimulation of the type J receptors, there was an inhibition of the monosynaptic reflexes of the body. This response was termed as the' J reflex'. 8. Electrolytic lesions of the brain showed that the afferent pathway for the J reflex projected to the basal ganglion and the efferent pathway descended ipsilaterally in the midline region of the spinal cord. 9. The possible existence of the type J receptors in man was reported. Evidences of the 'sensations' arising from these receptors had been sought in man. The role of J receptors in high altitude pulmonary edema was brought to focus. 10. The arterial chemoreceptors were considered as mechano-receptors and a mechanical theory was advocated to explain the transducer mechanisms. 11. It was hypothesized that drugs acted upon the regenerator region
of the sensory receptor complex. Thus, the greater susceptibility of the
non-myelinated fibers to drugs when compared with the myelinated ones,
was explained on the basis of structural differences in the regenerator
region. 13. Tachycardia was reported as the primary cardiovascular response following the stimulation of the carotid chemo-receptors in a preparation in which the heart rate was low. 14. Pulse synchronized contractions were recorded in the aorta, inferior venacava, and pulmonary artery in viva. These contractions were regulated by the cardiac pacemaker. 15. The cardiovascular effects of the carboxylic ionophore monensin were investigated in detail in dog and rabbit. 16. Pulmonary congestion occurring as a sequel to acute left ventricular dysfunction stimulated the rapidly adapting receptors of the airways. This response was enhanced after plasmapheresis. Pulmonary lymphathic obstruction stimulated these receptors also. Thus, it was hypothesized that the natural stimulus for these receptors might be the fluid flux in the pulmonary extravascular space. 17. Reporting of the existence of airway rapidly adapting receptors and pulmonary C-fiber (type J) receptors in the non human primate. 18. Demonstration of the neuronal circuit involved in the cigarette smoke induced respiratory responses. 19. Mechanism of stimulation of airway rapidly adapting receptors by neuropeptides. 20. Stimulation of rapidly adapting receptors by bradykiain and ACE inhibitor enalapril. 21. Demonstration of a new reflex resulting in an increase in urine flow
following pulmonary lymphatic obstruction. |
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