Cardioprotective Effects of a C1 Esterase Inhibitor in Myocardial Ischemia and Reperfusion

• DOI: 10.1161/01.cir.91.2.393
• Publication Date: 2012-06-12T00:34:42Z
• Authors: Michael Buerke; Toyoaki Murohara; Allan M. Lefer
• Keywords: Contractility; Creatine kinase

Background Myocardial injury after ischemia and reperfusion can be attributed largely to the effects of polymorphonuclear leukocytes (PMN). The complement system plays an important role as a chemotactic agent, affecting adhesion molecule expression neutrophil accumulation. Methods Results In present study, cardioprotective C1 esterase inhibitor (C1 INH) were examined in feline model myocardial (90 minutes followed by 270 reperfusion). INH (15 mg/kg) administered 10 before significantly attenuated necrosis compared with vehicle (10±2% 29±2% proportion area at risk, respectively; P <.01). preservation was also related reduced plasma accumulation creatine kinase activity. treatment resulted improved recovery cardiac contractility coronary vascular endothelial function, assessed relaxation response acetylcholine, function vehicle-treated animals (69±6% 20±4% relaxation, addition, myeloperoxidase activity (an index PMN accumulation) ischemic treatment. Furthermore, immunohistochemical analysis ischemic-reperfused tissue demonstrated deposition first component classic pathway, C1q, on myocytes vessels. Conclusions Blocking pathway appears effective means preserving myocardium from injury. mechanism this effect inhibition PMN-endothelium interaction; leads normal which results necrosis.