Modulation of the inflammatory response in experimental myocardial infarction.

Abstract

The role of inflammation in reperfused, ischaemic myocardium was assessed morphologically in 39 porcine hearts after 24 h (n = 23) and 72 h (n = 16) of reperfusion and after different antiphlogistic treatments. The left anterior descending coronary artery (LAD) was occluded distally for 45 min. Seven pigs received BW755C (10 mg kg-1) i.v. prior to ischaemia (A), eight pigs were given the same dose before 24 h of reperfusion (B), and eight pigs were treated with iloprost (25 ng kg-1 min-1) i.v. before occlusion and continuously for 72 h (C). Two groups of eight pigs each served as controls for 24 h (D) and 72 h (E) of reperfusion. Infarct sizes were determined, myocardium was investigated by light microscopy, and polymorphonuclear leucocytes (PMNs) and macrophages were quantitated after histo- and immunohistochemical staining. Jeopardized myocardium contained 129 neutrophils mm-2 and 120 macrophages mm-2 (D) vs 10 neutrophils mm-2 and 290 macrophages mm-2 (E). Neutrophils and infarct sizes were only significantly decreased in group A (68 neutrophils mm-2, 30% reduction of infarct size). Macrophages infiltration was not significantly affected for all treatment groups (A, B, C). It is concluded that myocardial infarct sizes are neutrophil-mediated postischaemic tissue injury can be reduced by BW755C applied prior to ischaemia. Neutrophil-mediated myocardial injury is unlikely to occur beyond 3 days of reperfusion.