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.
D000138:Acidosis / Q000378:metabolism; D000818:Animals; D050260:Carbohydrate Metabolism; D005591:Chemical Fractionation; D003864:Depression, Chemical; D004589:Electrophoresis, Disc; D005947:Glucose / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000378:metabolism*; D007328:Insulin / Q000494:pharmacology; D009124:Muscle Proteins / Q000096:biosynthesis*; D009206:Myocardium / Q000378:metabolism*; D010100:Oxygen / Q000494:pharmacology; D010649:Phenylalanine / Q000378:metabolism; D010695:Phlorhizin / Q000494:pharmacology; D011817:Rabbits
D007328:Insulin; D009124:Muscle Proteins; D010649:Phenylalanine; D010695:Phlorhizin; D005947:Glucose; D010100:Oxygen