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Biomedical subjects

J S Sarma

Publications and source records attributed to J S Sarma.

42 records · Page 3Linked to original sources
PubMedDate not supplied

Comparative effects of chronic ethanol and acetaldehyde exposure on myocardial function in rats.

This study was conducted to compare separately the chronic effects of high blood levels of ethanol and acetaldehyde on the metabolism of the heart. Levels of ethanol and acetaldehyde were altered by administration of either 4-methylpyrazole (4-MP), a potent alcohol dehydrogenase inhibitor, or pargyline (PAR), a monoamine oxidase inhibitor that markedly increases acetaldehyde levels in the blood following ethanol administration. Measurements were made in rats consuming ethanol for three to four weeks. Mitochondrial respiration, in vitro contractility of glycerinated heart muscle fibers, and myocardial protein synthesis were determined. As compared to animals receiving only ethanol, administration of either-4-methyl-pyrazole or pargyline plus ethanol resulted in more severe damage to mitochondrial respiration and myocardial protein synthesis. The data illustrate that both acetaldehyde and ethanol in high concentrations can cause severe damage to myocardial metabolism.

Acetaldehyde↗
PubMedDate not supplied

Biochemical and histological effects of intermittent carbon monoxide exposure in cynomolgus monkeys (Macaca fascicularis) in relation to atherosclerosis.

The data in this report do not suggest any association between periodic carbon monoxide exposure and the development of atherosclerosis in cynomolgus monkeys. Animals were exposed to 200 to 400 ppm CO in the inspired air for 10 alternate half hours daily for approximately 12 months. These conclusions are reached from both histological and biochemical studies (aortic cholesterol content, arterial cholesterol influx, aortic oxygen consumption, as well as plasma triglyceride concentrations and HDL cholesterol to total cholesterol ratios). A rise in plasma and tissue free fatty acids (FFA) was observed in the experimental group exposed to carbon monoxide. However, the increase in FFA tissue levels was not believed to be due to any inhibitory effect of CO on the electron transfer system since mitochondrial respiratory function was not depressed.

Animals↗
PubMedDate not supplied

The effect of carbon monoxide on lipid metabolism of human coronary arteries.

Human coronary arteries were perfused under sterile conditions in vitro with blood containing high or low concentrations of carbon monoxide. Lipid synthesis in the arterial wall was investigated by incorporating [14C]acetate; synthesis of the following lipids was measured: cholesterol, cholesterol ester, di- and triglycerides and phospholipids. Cholesterol uptake by the arterial wall was studied by using [3H]cholesterol as a tracer. No influence of CO on lipid synthesis in the arterial wall could be demonstrated. In contrast, arteries which were exposed to CO showed a higher uptake of cholesterol as compared to their corresponding control. The concentration of CO in the perfusate did not alter the degree of cholesterol uptake. These results are in general agreement with those of others, who found that CO significantly increases the permeability of endothelial membranes.

Arteriosclerosis↗