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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Modulation of the inflammatory response in experimental myocardial infarction.

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.[1]


  1. Modulation of the inflammatory response in experimental myocardial infarction. Bohle, R.M., Pich, S., Klein, H.H. Eur. Heart J. (1991) [Pubmed]
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