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Biomedical subjects

R Viswanathan

Publications and source records attributed to R Viswanathan.

At least 73 records · Page 4Linked to original sources
PubMed1978

Further studies on pulmonary oedema of high altitude. Abnormal responses to hypoxia of men who had developed pulmonary oedema at high altitude.

101 Indian soldiers, 57 of whom had developed pulmonary oedema of high altitude (POHA) and 44 who had not developed this condition in spite of being at high altitudes for over 2 years, were investigated for observing the differences, if any, in their reaction to acute hypoxic stress. Each subject was made to breathe a 10% hypoxic mixture for 5 min. Haemodynamic parameters like pulmonary artery pressure (systolic, diastolic and mean), brachial artery pressure, wedge pressure, cardiac output, minute ventilation, arterial oxygen saturation and oxygen uptake before and at the end of hypoxic breathing were estimated. In addition, results of the cold pressor test were recorded and the Vd/Vt ratio was estimated. The results obtained in the present study confirmed those obtained in our previous studies. In addition, it was observed that oxygen uptake was significantly higher and oxygen saturation lower after hypoxia in the POHA subjects than in the controls. Certain parameters for screening of subjects possibly susceptible to POHA have been suggested.

Adult↗
PubMed1977

Effect of acute hypobaric hypoxia on fatty acid metabolism in rat lung.

Exposure of male albino rats in the weight range of 70-200 g to 25,000 ft of simulated altitude for 6 h at 32 degrees C caused an increase in plasma free fatty acids with decreased oxidation of palmitic acid-1-14C in lung slices of hypoxic rats. The in vivo esterification of palmitic acid-1-14C to form truglycerides, phosphatidylcholine and phosphatidylethanolamine was also low indicating decreased utilization of fatty acids by hypoxic lungs. De novo lipogenesis was observed to decreased to decrease because of decreased fatty acid biosynthesis as judged from acetate---14C incorporation. The specific activities of triglycerides, phosphatidylcholine and free cholesterol were also decreased. The decreased incorporation into phosphatidylcholine affected the incorporation into phosphatidylcholine of alveolar surfactant (2,000 g sediment fraction). The results are discussed in view of possible decreased energy status of hypoxic lungs.

Animals↗
PubMed1977

Fatty acid metabolism in hypoxic rat liver.

Fatty acid metabolism was investigated in adult male albino rats exposed to hypobaric hypoxia at 25,000 ft simulated altitude for 6 h at 32 degrees C. Oxidation and esterification of palmitic acid-1-14C and de novo lipogenesis from acetate-1-14C were studied. Palmitic acid-1-14C oxidation in liver slices was normal while acetoacetate formation was increased. In vivo esterification of palmitic acid-1-14C to form triglycerides was increased while formation of phosphatidylcholine and phosphatidylethanolamine was observed to decrease. Decreased incorporation into plasma phosphatidylcholine with unaltered total activity in plasma triglycerides was observed. The incorporation of acetate-1-14C was observed to remain unaltered in triglycerides and phospholipids of liver with a similar pattern in the plasma indicating unaltered de novo lipogenesis. There appears to be increased esterification of fatty acids with probably impaired release of triglycerides into plasma while fatty acid biosynthesis remains unaffected.

Adrenal Glands↗
PubMed1976

Effect of acute hypoxia on blood serotonin in human beings and rats.

The object of this study was to see if the blood level of 5-hydroxytryptamine (5-HT) increased under acute hypoxic stress in human beings and rats. Soldiers who had been stationed at high altititudes 2-7 months prior to study were selected. 17 had suffered from pulmonary oedema and the remaining eight, who had not developed the condition, acted as controls. The technique of YUWILER [18] with suitable modifications was used for estimation of 5-HT. No significant change in 5-HT levels was observed either in subjects or controls. Rats exposed to simulated high altitude for 6 h also did not show any significant change in blood 5-HT levels.

Altitude↗
PubMed1976

Pulmonary vascular response to ventilation hypercapnia in man.

The effect of ventilation hypercapnia on pulmonary circulation in man was investigated through separate studies. In the first study on 44 patients with little or no airway obstruction and 20 normal men, 5% CO2 breathing produced (a) significant rise in pulmonary artery pressure (PAP), (b) no significant change in cardiac output, (c) rise in pulmonary vascular resistance, (d) rise in brachial artery pressure (BAP) and (e) no change in wedge pressure (WP). The rise in PAP was more pronounced after 2 min of 10% CO2 breathing in 12 bronchitics. The scond study was carried out in 39 bronchitics and 22 normals while breathing 10% CO2 for 1 min and showed that pulmonary vascular response was independent of systemic vascular response, in that BAP rose later and came back earlier to original level during CO2 breathing. In the third study on 26 severe bronchitics and 15 normals the observed rise in PAP during 10% CO2 breathing was independent of H-ion concentration in the blood since PAP continued to rise even when pH was maintained at air breathing level by intravenous injection of 130 mEq of sodium bicarbonate in 250 cm3 of 5% glucose solution. This study also confirmed the findings in the first study that there was minimal rise in cardiac output, no rise in WP, while PAP and pulmonary vascular resistance rose significantly during ventilation hypercapnia. The responses were pronounced compared with those observed in the first study with 5% CO2. It is postulated that the responses might be due to direct action of CO2 on muscular pulmonary arteries.

Bicarbonates↗
PubMed1975

Effect of acute hypobaric hypoxia on 32-P incorporation into phospholipids of alveolar surfactant, lung, liver and plasma of rat.

Exposure of adult rats to hypobaric hypoxia caused hypolipidemia, hypotriglyceridemia and hypophospholipidemia. Hypobaric hypoxia produced an increase in liver triglyceride and cholesterol levels and a decrease in lung triglyceride, total phospholipid and phosphatidyl choline. The proportion of phosphatidyl choline in the pulmonary surfactant fraction I phospholipids (responsible for reducing surface tension) decreased (55.2% as compared to 80.4% in control animals). Incorporation of 32-P into liver phosphatidyl ethanolamine was significantly increased, incorporation into lung phosphatidyl choline and phosphatidyl ethanolamine was increased whereas a decreased incorporation into plasma phosphatidyl choline was observed. The data suggest an enhanced lipid synthesis in liver with a probable impairment of mobilization into plasma.

Animals↗
PubMed1975

Glutamine synthetase, glutaminase and phosphodiesterase activities in brain under hypoxia: in vitro effect of cortisol, GABA and serotonin on glutamine synthetase.

The effect of hypobaric hypoxia on the activities of glutamine synthetase, glutaminase and cyclic 3'5' AMP phosphodiesterase in rat brain was studied after exposure to 25,000' for 6 h. Glutamine synthetase activity was increased in all the regions of brain studied, and addition of gamma amino butyric acid, serotonin and cortisol in vitro produced a differential response. Glutaminase activity decreased in the whole brain. Cyclic 3'5' AMP phosphodiesterase activity decreased in cerebellum, medulla, hypothalamus and pituitary showing an accumulation of cyclic 3'5' AMP in these regions. The results suggest that glutamine synthesis and degradation are regulated in the central nervous system by cyclic AMP and cortisol: Gamma aminoburyric acid and other compounds can modulate the activity of glutamine synthetase and glutaminase.

3',5'-Cyclic-AMP Phosphodiesterases↗