Kenneth S Kilgore, Gregory S Friedrichs, Jonathon W Homeister, and Benedict R Lucchesi n an effort to determine the pathogenic mechanisms involved in myocardial damage, the concept of reperfusion I injury has received increased attention. These efforts have yielded a number of possibilities likely to be associated with reperfusion injury. Reperfusion injury may be defined as the conversion of reversible cell injury to irreversible cell injury upon perfusion of a previously ischaemic area. Molecular oxygen, while essential for maintaining cell viability, is believed to be one of the primary contributors to tissue damage. One of the early indications that molecular oxygen is involved in the development of reperfusion injury is the observation that reperfusion of the anoxic heart with an oxygenated solution enhanced myocardial injury, while a solution devoid of oxygen (hypoxic reperfusion) did not.’Since that time, it has become apparent that tissue damage incurred during reoxygenation or reperfusion is due to the formation of oxygen derived free radicals.’These observations are supported by the use of electron resonance spectroscopy and spin trapping agents to detect free radicals in the ischaemic zone? Superoxide anion (O;-), hydrogen peroxide (H2 O,), and the highly reactive hydroxyl radical (HO’) are the most notable free radicals in the pathogenesis of reperfusion injury.

It is evident that the inflammatory response plays a critical role in ischaemidreperfusion injury. However, it is a double edged sword. Administration of prednisone, an agent with anti-inflammatory properties, has been shown to increase the incidence of aneurysm and rupture of the ventricular wall after acute myocardial infarction, underscoring the need for proper healing after infar~ tion.~ While essential for healing, the inflammatory response also plays a pivotal role in the pathogenesis of reperfusion injury. Two components of the inflammatory reaction have been implicated following reperfusion:(1) infiltration of neutrophils into the ischaemic zone, and (2) activation of the complement system. Histological observations have shown a direct relationship between the duration of ischaemia and infarct size and the extent of neutrophil infiltrati~ n.~-~ More substantial evidence is derived from a number of studies utilising experimental animals that have been neutrophil depleted. 6 Use of filters,’cytotoxic agents: and neutrophil antisera, 16 in addition to inhibiting neutrophil adhesion,” decreases ultimate infarct size, an effect correlated with decreased neutrophil accumulation.