THE CONCEPT THAT XANTHINE OXIDASE (X0)-derived oxidants mediate the microvascular injury associated with reperfusion of the ischemic intestine was first proposed in 1981 (9). Since its inception, most of the assumptions inherent in this concept have been tested, and the concept has been extended to a number of other organ systems (19). The information derived from several studies performed in our laboratory and by others has led us to revise the biochemical scheme originally proposed to explain oxygen-dependent reperfusion injury. The revised scheme (Fig. 1) assumes that X0-derived oxidants produced after reoxygenation of ischemic intestine play an important role in recruiting and activating granulocytes, which ultimately mediate reperfusion-induced microvascular injury. The objective of this is to summarize supportive evidence and identify areas of controversy and uncertainty regarding each component of the scheme presented in Fig. 1. Although the proposed mechanism may be applicable to a number of organ systems, the foregoing discussion is largely confined to the small intestine, an organ that is unusually well endowed with the biochemical machinery necessary for the formation of cytotoxic oxidants. Relative Contributions of Ischemia and Reperfusion to Microvascular Injury An important assumption in the oxygen radical hYpothesis of ischemia-reperfusion (I/R) injury
AJP - Heart and Circulatory Physiology – The American Physiological Society
Published: Dec 1, 1988
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