NEUTROPHILS AND MYOCARDIAL REPERFUSION INJURY

Ischaemia induces an acute inflammatory response in myocardial tissue with an early phase of neutrophil accumulation, which is accelerated b y reperfusion. In experimental models, interventions that deplete neut rophils or inhibit their function cause a significant reduction in myo cardial infarct size. These cells, therefore, may exacerbate tissue in jury through the release of free radicals and proteolytic enzymes. Neu trophil recruitment depends on the presence of inflammatory mediators. Leukotriene B-4, interleukin 8 and the complement fragment C5a have b een implicated in this process. Studies using antibodies to the select in, integrin and immunoglobulin superfamily adhesion molecules indicat e that they also have a crucial role in myocardial neutrophil recruitm ent. Copyright (C) 1996 Elsevier Science Inc.