Ultrastructural and metabolic features of stress-adaptive rearrangements of myocardium in infants after surgery-induced up-regulation of lipoperoxidation processes.

Surgical correction of complicated congenital heart disease in infants is terminated by postischemic reperfusion of myocardium accompanied with closure of more than 20% microvessels in the coronary bed by edematous endothelial cells, their bleb-like fragments, and aggregates of the blood formed elements. Degradation of the transmission capacity of the coronary microvessels developed in parallel with moderation of activity of the antiradical protection enzymes and positively correlated with the level of LPO secondary products, whose elevation during the surgery stages was not reduced by catalase activation.