Mechanism of protection against "reperfusion injury" by aprotinin. Roles of polymorphonuclear leucocytes and oxygen radicals.

We have proposed that reperfusion injury results from the overproduction of reactive oxygen metabolites by PMN as a result of increased sensitivity to oxygen during the low oxygen phase. Aprotinin was demonstrated to inhibit this overproduction and also radical production evoked by chemotactic peptide, 50% inhibitions occurring in the range 5-20 microM. Over this range, no effect on cell viability was observed. This inhibitory effect may provide a scientific basis for the protective effect of aprotinin in reperfusion induced injury.