Journal
CARDIOVASCULAR THERAPEUTICS
Volume 36, Issue 6, Pages -Publisher
WILEY-HINDAWI
DOI: 10.1111/1755-5922.12481
Keywords
hydromorphine postconditioning; myocardial ischemia/reperfusion injury; P13K/Akt/eNOS signaling
Funding
- Scientific and Technological Research Project of the Department of Health and Family Planning Commission in Sichuan Province in China [17PJ220]
- Cooperation Project Fund of Department of Sichuan Provincial Science and Technology-Luzhou City Government-Luzhou Medical College [14JC0173]
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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 hydromorphine on myocardial I/R injury, we illuminate the underlying mechanism of the protective effect. Results Hydromorphine 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 hydromorphine. 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 hydromorphine. Conversely, the activated effects of hydromorphine on the phosphorylation of Akt and eNOS, and NO release were totally reversed by LY294002, which, used individually, show the same influence on reperfusion injury. Conclusions These findings suggest that hydromorphine postconditioning may protect isolated rat heart against reperfusion injury via activating P13K/Akt/eNOS signaling.
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