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Biomedical subjects

M Lesch

Publications and source records attributed to M Lesch.

At least 127 records · Page 7Linked to original sources
PubMed1975

Thermoregulation of myocardial protein synthesis.

The effect of temperature on myocardial protein synthesis was evaluated using L-[14C]phenylalanine incorporation into total protein of isolated rabbit right ventricular papillary muscles. Muscles were incubated in oxygenated Krebs-Ringer buffer containing tracer amino acid at temperatures of 25-43 degrees C or incubated without tracer at varying temperatures up to 120 min and then incubated at 37 degrees C for an additional 2 h with the tracer present for the final hour of incubation. Higher as well as lower than physiological temperatures depressed tracer amino acid incorporation. Recovery of myocardial protein synthesis from thermal injury was incomplete when the experimental temperature deviated by 6 degrees C or more from the control and exposure exceeded 60 min. In addition, tracer amino acid incorporation on reoxygenation and return to 37 degrees C in muscles exposed to anoxia at 25 degrees C did not differ from that in muscles exposed to anoxia at 37 degrees C. Specific activity of the intracellular amino acid pool was directly measured in appropriate experiments and variation of this parameter could not account for the depressed tracer amino acid incorporation. Likewise methylprednisolone (10-5 M), chloroquine phosphate (10-5 M), and glucose (15 mM), if present during hyperthemia, did not ameliorate thermal damage. It is concluded that hyperthermia as well as hypothermia can cause irreversible alterations rather than reversible inhibition of myocardial protein synthesis.

Animals↗
PubMed1975

Reversibility of thermal injury to myocardial protein synthesis.

The ability of transient temperature variations for up to 120-min duration to affect myocardial protein synthesis (MPS) with return to normal temperatures was evaluated using 14C-phenylalanine incorporation into total protein of isolated rabbit right ventricular papillary muscles as in vitro model. Muscles were incubated in oxygenated Krebs-Ringer bicarbonate buffer containing tracer amino acid at temperatures of 28-43 degrees C or incubated without tracer at the same temperatures for up to 120 min and then incubated at 37 degrees C for an additional 2 hr with the tracer amino acid present for the final hour of incubation. Higher as well as lower than physiological temperatures depressed MPS. Recovery from thermal injury to MPS was significantly incomplete when the experimental temperature deviated by 6 degrees C or more from the control (28 and 43 degrees C, respectively) and exposure exceeded 60-min duration. Specific activity of the intracellular amino acid pool was directly measured, and variations in specific activity of the tracer pool were not responsible for the observed effects on MPS. Methylprednisolone (10(-5)M), chloroquine phosphate (10(-5) M), and glucose (15 mM) if present during hyperthermia did not ameliorate thermal damage. It is concluded that hypothermia causes inhibition as well as a degree of irreversible inactivation of the protein synthetic mechanism whereas hyperthermia causes predominant denaturation and irreversibile damage to MPS.

Animals↗
PubMed1975

Studies on the anoxic inhibition of myocardial protein synthesis.

The present study demonstrates that exposure of cardiac muscle to high levels of glucose during anoxia appears to retard damage to myocardial protein synthesis. The mechanism of this "glucose" effect is glucose-specific and appears related to the intracellular metabolism of glucose by the anoxic myocardium.

Acidosis↗