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Relaxin protects against myocardial injury caused by ischemia and reperfusion in rat heart.
Am J Pathol. 1998 May; 152(5):1367-76.AJ

Abstract

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.

Authors+Show Affiliations

Department of Human Anatomy and Histology, University of Florence, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9588905

Citation

Bani, D, et al. "Relaxin Protects Against Myocardial Injury Caused By Ischemia and Reperfusion in Rat Heart." The American Journal of Pathology, vol. 152, no. 5, 1998, pp. 1367-76.
Bani D, Masini E, Bello MG, et al. Relaxin protects against myocardial injury caused by ischemia and reperfusion in rat heart. Am J Pathol. 1998;152(5):1367-76.
Bani, D., Masini, E., Bello, M. G., Bigazzi, M., & Sacchi, T. B. (1998). Relaxin protects against myocardial injury caused by ischemia and reperfusion in rat heart. The American Journal of Pathology, 152(5), 1367-76.
Bani D, et al. Relaxin Protects Against Myocardial Injury Caused By Ischemia and Reperfusion in Rat Heart. Am J Pathol. 1998;152(5):1367-76. PubMed PMID: 9588905.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Relaxin protects against myocardial injury caused by ischemia and reperfusion in rat heart. AU - Bani,D, AU - Masini,E, AU - Bello,M G, AU - Bigazzi,M, AU - Sacchi,T B, PY - 1998/5/20/pubmed PY - 1998/5/20/medline PY - 1998/5/20/entrez SP - 1367 EP - 76 JF - The American journal of pathology JO - Am. J. Pathol. VL - 152 IS - 5 N2 - 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. SN - 0002-9440 UR - https://www.unboundmedicine.com/medline/citation/9588905/Relaxin_protects_against_myocardial_injury_caused_by_ischemia_and_reperfusion_in_rat_heart_ L2 - https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/9588905/ DB - PRIME DP - Unbound Medicine ER -