Abstract
Summary; Mechanisms of organ failures following a cardiopulmonary bypass (CPB) were multi factorial although the hypoperfusion pressure was considered as a main cause. Plate-let aggregation initiated by the institution of CPB alternated eicosanoid metabolism, in which thromboxane A2 became dominant to prostaglandin I2. Reactive increase of endothelin excretion observed after the CPB also aggravated ischemic cellular damages due to induced vasoconstrictive status in the micro-vasculature. Further damages were accelerat-ed by elastase released from activated granulocytes. The damages were thought to be continued by both elastase and endothelin even after the CPB, however, thromboxane A2 related only during the CPB. The renal damage mainly concerned with endothelin and elastase, but not thromboxane A2.
