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Biomedical subjects

M Kessler

Publications and source records attributed to M Kessler.

At least 523 records · Page 29Linked to original sources

Disturbances of extracellular pK, pNa and pH during no-flow anoxia.

The initial period of no-flow anoxia can be divided in at least two parts. During the first period lasting approximately 1 min., the O2 available in tissue gives rise to CO2 which increases hydrogen ion activity and may lead to Na+ influx2 (presumably due to increased membrane permeability to Na+). In the second period, starting after the first minute, the increase in lactate content leads to further decrease in pH and is accompanied by extensive sodium influx and a distinct potassium efflux. However, it is striking that the isolated perfused rat liver is able to tolerate 1 hour of norm-flow anoxia without severe cellular damage, whereas two minutes of no-flow anoxia lead to a decrease in cellular ATP content by 28%.

Adenosine Triphosphate↗

Oxygen supply to the cirrhotic liver following various portacaval shunt procedures.

Direct measurements of local oxygen pressure by means of a platinum multiwire electrode were performed to investigate the effect of five different portacaval shunt procedures on hepatic oxygen content in the cirrhotic rat liver. End-to-side shunt, side-to-side shunt, mesenterico caval shunt, splenocaval shunt, and portacaval transposition were performed and surface PO2 was determined immediately after operation, 24 hours following operation and after one week. Portacaval transposition and end-to-side shunt led to a striking oxygen deficit of the liver tissue with no incidence of compensation by the hepatic artery; Oxygen supply was improved considerably by a side-to-side shunt and tissue hypoxia could be prevented by a mesenterico-caval shunt and splenocaval shunt. This improving effect is thought to be due to the pancreatico-duodenal venous blood supply which should be carefully preserved for the liver circulation when a shunt needs to be performed.

Animals↗

Fatty acyl CoA synthetase activity in normal and atherosclerotic rabbit aortic tissue.

The activity of fatty acyl CoA synthetase and fatty acyl CoA:cholesterol acyltransferase was determined in microsomal fractions from normal and atherosclerotic rabbit aortic tissue. No change in fatty acyl CoA synthetase activity was observed as a result of cholesterol feeding in contrast to the several-fold increase in the activity of fatty acyl CoA:cholesterol acyltransferase seen in atherosclerotic tissue. Inhibition of both enzymes was observed when clofibrate, or the tetrahydronapthyl analog of this drug were added in vitro. The inhibitory effects were most pronounced on the fatty acyl CoA:cholesterol acyltransferase.

Acetyl Coenzyme A↗