Abstract
It has been found that, in children with Roger’s disease corrected under conditions of two fundamentally different procedures of anesthetic management, myocardial reperfusion after cardiac arrest under artificial hypothermic circulation is accompanied with obstruction of more than 70% of coronary bed microvessels, one-third of them being blocked with hydropic endothelial cells or their cystiform fragments. It hampers or even totally prevents their functioning in the postoperative period. The content of necrotic cells increases, while the three “working” cell types demonstrate a decrease in myocropinocytotic transport. Circulatory arrest during perfusionless hypothermia and immersion reperfusion do not result in a dramatic change of general morphology of microvessels as compared to the control group maintaining the endothelial cell population unaltered. Ultrastructural organization of endothelial microvessels displayed no features of intracellular regeneration. However, a heterogenic response of the structures responsible for transendothelial transfer of macromolecules provides the basis for the recovery of endothelium structure and function, as a patient’s temperature reaches the standard value.
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