RELAXIN PROTECTS AGAINST MYOCARDIAL INJURY CAUSED BY ISCHEMIA AND REPERFUSION IN RAT-HEART

Myocardial injury caused by ischemia and reperfusion comes from multip le pathogenic events, including endothelial damage, neutrophil extrava sation into tissue, platelet and mast cell activation, and per oxidati on of cell membrane Lipids, which are followed by myocardial cell alte rations resulting eventually in cell necrosis, The current study was d esigned to test the possible cardioprotective effect of the hormone re laxin, which has been found to cause coronary vessel dilation and to i nhibit platelet and mast cell activation. Ischemia (for 30 minutes) wa s induced in rat hearts in vivo by ligature of the left anterior desce nding coronary artery; reperfusion (for 60 minutes or less if the rats died before this predetermined time) was induced by removal of the li gature. Relaxin (100 ng) was given intravenously 30 minutes before isc hemia, The results obtained showed that relaxin strongly reduces 1) th e extension of the myocardial areas affected by ischemia-reperfusion-i nduced damage, 2) ventricular arrhythmias, 3) mortality, 4) myocardial neutrophil number, 5) myeloperoxidase activity, a marker of neutrophi l accumulation, 6) production of malonyldialdehyde, an end product of lipid peroxidation, 7) mast cell granule release, 8) calcium overload, and 9) morphological signs of myocardial cell injury. This study show s that relaxin can be regarded as an agent with a marked cardioprotect ive action against ischemia-reperfusion-induced myocardial injury.