Myocardial injury caused by
ischemia and reperfusion comes from multiple pathogenic events, including endothelial damage, neutrophil extravasation into tissue, platelet and mast cell activation, and peroxidation of
cell membrane lipids, which are followed by myocardial cell alterations resulting eventually in cell
necrosis. The current study was designed to test the possible cardioprotective effect of the
hormone relaxin, which has been found to cause coronary vessel dilation and to inhibit platelet and mast cell activation.
Ischemia (for 30 minutes) was induced in rat hearts in vivo by
ligature of the left anterior descending coronary artery; reperfusion (for 60 minutes or less if the rats died before this predetermined time) was induced by removal of the
ligature.
Relaxin (100 ng) was given intravenously 30 minutes before
ischemia. The results obtained showed that
relaxin strongly reduces 1) the extension of the myocardial areas affected by
ischemia-reperfusion-induced damage, 2) ventricular arrhythmias, 3) mortality, 4) myocardial neutrophil number, 5)
myeloperoxidase activity, a marker of neutrophil 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 shows that
relaxin can be regarded as an agent with a marked cardioprotective action against
ischemia-reperfusion-induced myocardial injury.