Recent advances in the role of reactive oxygen intermediates in ischemic injury. I. Evidence demonstrating presence of reactive oxygen intermediates; II. Role of metals in site-specific formation of radicals.

This article has attempted to bring the reader up to date on advances in selected facets of the area of reactive oxygen intermediate-induced ischemic injury. Specifically, we have discussed the more recent reports that provide evidence for the presence of these species in reperfused ischemic tissue. In addition, we have attempted to introduce the reader to the relatively new concept of "site-specific" formation of radicals and how the use of "push-pull" techniques, such as chelation by high-affinity chelators or displacement by non-redox-active metals such as zinc, may decrease postischemic reperfusion injury. Finally, we have identified a class of compounds that affect the oxidation state of redox-active metals, and have demonstrated how these compounds may also represent a new therapeutic modality. In conclusion, both academic and nonacademic surgeons should have profited from reading this article. For the academic surgeon, who may do research, several new cytoprotectants requiring further study in both in vitro and in vivo models have been identified. For the nonacademic surgeon in clinical practice the realization that there are several promising areas of research that may yield new therapies to mitigate postischemic reperfusion injury should have been gained.