[Mechanisms of organ failure following cardiopulmonary bypass--preventive effects of Ca2+ blocker (nicardipine)].

The causes of organ failure following cardiopulmonary bypass (CPB) were multi-factorial. Damage was initiated by elastase which was released from activated granulocytes under conditions of significant reduction in the protease inhibitor level (p < 0.01). The increase in endothelin excretion observed during and after the CPB induced a further vasoconstrictive response in the microvasculature and accelerated ischemic cellular damage. Upon completion of the CPB, the elevation of the lysosomal enzyme beta-glucuronidase was influenced by the elastase and endothelin concentrations (r = 0.8 and r = 0.67 respectively). Renal damage, which was detected by an increase in renal tubular enzymes (N-acetyl-beta-D-glucosaminidase and gamma-glutamyltranspeptidase), was affected by endothelin (r = 0.61, 0.75) and elastase concentrations (r = 0.74, 0.75) respectively. In the group treated with nicardipine during the CPB, an increase in beta-glucuronidase was significantly low (p < 0.01) and renal tubular damage was significantly reduced. Moreover, lesser elevation of the elastase level on arrival in the ICU was evidenced (p < 0.05). Thus we concluded that nicardipine inhibited the release of elastase from the activated neutrophils and prevented the vasoconstriction caused by the endothelin secretion.