Abstract

Mechanisms of attenuation of membrane injury and metabolic disturbances in postischemic cardiomyocytes have been studied on a model of ischemic and reperfusion stress of rat heart using a modified early reperfusion. Optimization of reperfusion infusate composition augmented cardiac pump and contractile function recovery. This was accompanied by a reduced release of lactate dehydrogenase activity and systems generating short-lived reactive oxygen species into myocardial effluent and was associated with more efficient oxidative metabolism recovery and decreased losses of intracellular total creatine and amino acids pools. The results indicate availability of postischemic functional and metabolic myocardial injury correction by means of a controlled reperfusion.

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