Hydromorphone Postconditioning Protects Isolated Rat Heart against Ischemia-Reperfusion Injury via Activating P13K/Akt/eNOS Signaling.
Cardiovasc Ther. 2018 Dec 29;:e12481
Authors: Liu Q, Li Z, Liu Y, Xiao Q, Peng X, Chen Q, Deng R, Gao Z, Yu F, Zhang Y
INTRODUCTION: Myocardial ischemia/reperfusion injury (myocardial I/R injury) has a high disability rate and mortality. Novel treatments for myocardial I/R injury are necessary.
AIM: In order to explore the protective effect of hydromorphone on myocardial I/R injury, we illuminate the underlying mechanism of the protective effect.
RESULTS: Hydromorphone significantly reduced myocardial infarct size (IFN/AAR), CKMB (Creatine Kinase MB) and TN-T (Troponin T) release, and improved cardiac function compared with I/R group. However, these advantageous effects were partly suppressed in the presence of hydromorphone. Myocardial I/R injury significantly decreased the phosphorylation of Akt and eNOS, and down-regulated total nitric oxide and nitrotyrosine content, while these inhibitory effects were partly abolished by hydromorphone. Conversely, the activated effects of hydromorphone on the phosphorylation of Akt and eNOS, NO release were totally reversed by LY294002, which, used individually, show the same influence on reperfusion injury.
CONCLUSIONS: These findings suggest that hydromorphone postconditioning may protect isolated rat heart against reperfusion injury via activating P13K/Akt/eNOS signaling. This article is protected by copyright. All rights reserved.
PMID: 30597772 [PubMed – as supplied by publisher]