[Effect of exogenous amino acids on myocardial contraction and metabolism of nitro-compounds in the myocardium during anoxia].

Anoxic perfusion of an isolated rat heart resulted in contractility disorder, increased production of ammonia, alanine, glutamine and lowered levels of glutaminic and asparaginic acids, while the total pool of free amino acids and taurine remained unchanged. Subsequent reoxygenation partly recovered cardiac contractility. When 3.5 mM glutaminic acid or 5 mM arginine was added to the perfusate, the anoxic contracture was less pronounced, and the heart maintained a higher pressure than would be common for anoxia, while reoxygenation resulted in virtually complete recovery of contractility. Both amino acids did not basically affect ammonia synthesis, but enhanced its binding in heart tissue, i. e. glutamine and urea synthesis, the reactions requiring increased ATP spending. The findings suggest that the mechanism of exogenous amino acids' action in anoxic conditions is based on substrate phosphorylation rather than their ability to bind ammonia.