Search PubMed⌕ Search

Biomedical subjects

M J Schmidt

Publications and source records attributed to M J Schmidt.

At least 73 records · Page 4Linked to original sources
PubMed1971

Cyclic adenosine monophosphate in brain areas: microwave irradiation as a means of tissue fixation.

Amounts of cyclic adenosine monophosphate in discrete regions of the brain were estimated after exposure of rats to microwave irradiation. Amounts were highest in the cerebellum and brainstem, intermediate in the hypothalamus and midbrain, and lowest in the hippocampus and cortex. Decapitation increased the concentration of cyclic adenosine monophosphate in all brain areas, although the increase in the cerebellum was three to four times greater than that in other areas. Microwave irradiation may provide a means of rapidly fixing brain tissue in situ while permitting easy dissection of the brain. In this way artifacts produced by decapitation can be eliminated, and concentrations of heat-stable compounds in the brain can be estimated under conditions which more closely approximate those in vivo.

Animals↗
PubMedDate not supplied

Metabolic and physiological differences between zero-flow and low-flow myocardial ischemia: effects of L-acetylcarnitine.

The metabolic and physiologic differences between low-flow and zero-flow ischemia of varying duration were compared in the isolated perfused rat heart. Hearts subjected to 60 and 90 minutes of zero-flow ischemia recovered less cardiac work than hearts subjected to low-flow ischemia. Low-flow ischemia caused a build-up of both myocardial long-chain acyl coenzyme A and acyl carnitine esters, while zero-flow ischemia produced no change in long-chain acyl carnitine and only a transient increase in long-chain acyl coenzyme A. High energy phosphate depletion was greater in zero-flow ischemia. Perfusion with excess free fatty acids decreased the recovery of cardiac work after low-flow ischemia but had no effect after repeated episodes of zero-flow ischemia. L-Acetylcarnitine improved the recovery of cardiac work after low-flow ischemia in hearts perfused with 0.4 and 1.2 mM palmitate. With zero-flow ischemia, L-acetylcarnitine had no effect on the recovery of cardiac work in hearts perfused with 0.4 mM palmitate and a slight but statistically significant effect with 1.2 mM palmitate. Possible protective mechanisms of L-acetylcarnitine against ischemic damage are discussed.

Acetyl Coenzyme A↗