Search PubMed⌕ Search

Biomedical subjects

H Aune

Publications and source records attributed to H Aune.

25 records · Page 2Linked to original sources
PubMed1981

Ether inhibition of ethanol metabolism in isolated rat liver parenchymal cells.

The effect of diethyl ether on ethanol metabolism was studied in isolated rat hepatocytes and ether was found to inhibit ethanol oxidation in a dose-dependent manner. At ethanol concentrations of approximately 30 mM, diethyl ether inhibited ethanol oxidation by approximately 58%, 40%, and 20% at ether concentrations of 30, 20, and 10 mM, respectively. This inhibition was also seen at a low ethanol concentration (5.4 mM) and in pyruvate (5 mM)-stimulated hepatocytes which exhibited increased rates of ethanol metabolism closer to in vivo rates. Accumulation of acetaldehyde from ethanol in cyanamide (400 micron M)-treated hepatocyte suspensions was also reduced by approximately 16% by 30 mM ether. It was concluded that inhibition of ethanol metabolism by diethyl ether might be of practical importance in studies of ethanol metabolism in ether anesthetized animals.

Acetaldehyde↗
PubMed1980

Formation of acetaldehyde from diethyl ether in man.

Diethyl ether anaesthesia caused detectable blood acetaldehyde levels in 15 patients. The average acetaldehyde concentration was 21 micro M which approximates the level found after intake of ethanol. No acetaldehyde could be found in patients anaesthetised without ether.

Acetaldehyde↗
PubMed1977

The adhesiveness of blood platelets before, during and after cardiopulmonary bypass.

The influence of cardiopulmonary bypass on the adhesiveness of blood platelets, using both bubble (Bentley and Rygg-Kyvsgaard) and membrane (Landé-Edwards) oxygenators, was investigated. With both types of oxygenators, there was a considerable fall in platelet adhesiveness during cardiopulmonary bypass, particularly with the Rygg-Kyvsgaard apparatus. The adhesiveness increased 30 minutes after bypass, but it was still not restored to the initial value.

Cardiopulmonary Bypass↗
PubMed1975

Ketamine-pancuronium induction in patients with aortic stenosis.

In 15 patients with severe aortic stenosis who were to undergo aortic valve replacement, the induction sequence ketamine followed by pancuronium caused a 25% rise in systolic blood pressure. In a similar series, the induction sequence diazepam + morphine followed by pancuronium caused a 22% fall in systolic blood pressure. This shows that the blood pressure rise caused by ketamine is not blocked by pancuronium, although pancuronium may possibly modify the cardiovascular responses to this drug.

Aged↗
PubMedDate not supplied

A reinvestigation of the usefulness of breath analysis in the determination of blood acetaldehyde concentrations.

Human volunteers were given ethanol (0.4 g/kg) either intravenous or per os. They were also given ethanol (0.2 g/kg) intravenous 4 hr after receiving a dose of 50 mg citrated calcium carbimide, an aldehyde dehydrogenase inhibitor. During the first hour after starting the administration of ethanol, ethanol and acetaldehyde concentrations were determined in expired air, blood from the right atrium, arterial blood, and venous blood. In the absence of calcium carbimide treatment, the respective maximal blood acetaldehyde concentrations were (range): 6-30 microM (calculated from breath analysis using a blood:breath partition ratio of 190 for acetaldehyde); 0-3.5 microM (right atrium blood); and 0 microM (arterial and venous blood). After calcium carbimide treatment, the maximal blood acetaldehyde concentrations were 10-220 microM (calculated from concentrations in expired air), 38-280 microM (right atrium), 31-250 microM (arterial blood), and 7-186 microM (venous blood). With aldehyde dehydrogenase inhibition, a clear correlation existed between breath concentrations and blood concentrations. Without this inhibition, no such correlation was found. A clear arterio-venous difference was seen for acetaldehyde concentrations while they were artificially elevated by calcium carbimide. Our study suggests that factors other than the equilibration of acetaldehyde between alveolar air and pulmonary blood are of great importance in determining the concentration of acetaldehyde in expired air.

Acetaldehyde↗