Tags

Type your tag names separated by a space and hit enter

Relaxin counteracts myocardial damage induced by ischemia-reperfusion in isolated guinea pig hearts: evidence for an involvement of nitric oxide.
Endocrinology. 1997 Nov; 138(11):4713-20.E

Abstract

Relaxin was previously shown to cause coronary vasodilation and to inhibit mast cell activation through a stimulation of endogenous nitric oxide production. This suggests that relaxin may have beneficial effects on ischemia-reperfusion-induced myocardial injury, which is triggered by endothelial damage and impaired nitric oxide generation. In this study, we tested the effect of relaxin on isolated and perfused guinea pig hearts subjected to ischemia and reperfusion. Ischemia was induced by ligature of the left anterior descending coronary artery; removal of the ligature induced reperfusion. Relaxin, at the concentration of 30 ng/ml of perfusion fluid, causes: a significant increase in coronary flow and in nitric oxide generation; a significant decrease in malonyldialdehyde production and in calcium overload, both markers of myocardial injury; an inhibition of mast cell granule exocytosis and histamine release, which are known to contribute to myocardial damage; a reduction of ultrastructural abnormalities of myocardial cells; an improvement of heart contractility. The beneficial effects of relaxin were blunted by the NO synthase inhibitor L-NMMA. The current study provides first experimental evidence that relaxin has a powerful protective effect on the heart undergoing ischemia and reperfusion acting through a nitric oxide-driven mechanism.

Authors+Show Affiliations

Department of Preclinical and Clinical Pharmacology, University of Florence, Italy.No affiliation info availableNo 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

9348198

Citation

Masini, E, et al. "Relaxin Counteracts Myocardial Damage Induced By Ischemia-reperfusion in Isolated Guinea Pig Hearts: Evidence for an Involvement of Nitric Oxide." Endocrinology, vol. 138, no. 11, 1997, pp. 4713-20.
Masini E, Bani D, Bello MG, et al. Relaxin counteracts myocardial damage induced by ischemia-reperfusion in isolated guinea pig hearts: evidence for an involvement of nitric oxide. Endocrinology. 1997;138(11):4713-20.
Masini, E., Bani, D., Bello, M. G., Bigazzi, M., Mannaioni, P. F., & Sacchi, T. B. (1997). Relaxin counteracts myocardial damage induced by ischemia-reperfusion in isolated guinea pig hearts: evidence for an involvement of nitric oxide. Endocrinology, 138(11), 4713-20.
Masini E, et al. Relaxin Counteracts Myocardial Damage Induced By Ischemia-reperfusion in Isolated Guinea Pig Hearts: Evidence for an Involvement of Nitric Oxide. Endocrinology. 1997;138(11):4713-20. PubMed PMID: 9348198.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Relaxin counteracts myocardial damage induced by ischemia-reperfusion in isolated guinea pig hearts: evidence for an involvement of nitric oxide. AU - Masini,E, AU - Bani,D, AU - Bello,M G, AU - Bigazzi,M, AU - Mannaioni,P F, AU - Sacchi,T B, PY - 1997/11/5/pubmed PY - 1997/11/5/medline PY - 1997/11/5/entrez SP - 4713 EP - 20 JF - Endocrinology JO - Endocrinology VL - 138 IS - 11 N2 - Relaxin was previously shown to cause coronary vasodilation and to inhibit mast cell activation through a stimulation of endogenous nitric oxide production. This suggests that relaxin may have beneficial effects on ischemia-reperfusion-induced myocardial injury, which is triggered by endothelial damage and impaired nitric oxide generation. In this study, we tested the effect of relaxin on isolated and perfused guinea pig hearts subjected to ischemia and reperfusion. Ischemia was induced by ligature of the left anterior descending coronary artery; removal of the ligature induced reperfusion. Relaxin, at the concentration of 30 ng/ml of perfusion fluid, causes: a significant increase in coronary flow and in nitric oxide generation; a significant decrease in malonyldialdehyde production and in calcium overload, both markers of myocardial injury; an inhibition of mast cell granule exocytosis and histamine release, which are known to contribute to myocardial damage; a reduction of ultrastructural abnormalities of myocardial cells; an improvement of heart contractility. The beneficial effects of relaxin were blunted by the NO synthase inhibitor L-NMMA. The current study provides first experimental evidence that relaxin has a powerful protective effect on the heart undergoing ischemia and reperfusion acting through a nitric oxide-driven mechanism. SN - 0013-7227 UR - https://www.unboundmedicine.com/medline/citation/9348198/Relaxin_counteracts_myocardial_damage_induced_by_ischemia_reperfusion_in_isolated_guinea_pig_hearts:_evidence_for_an_involvement_of_nitric_oxide_ L2 - https://academic.oup.com/endo/article-lookup/doi/10.1210/endo.138.11.5520 DB - PRIME DP - Unbound Medicine ER -