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Sevoflurane post-conditioning reduces rat myocardial ischemia reperfusion injury through an increase in NOS and a
Jianfang Cao1, Hong Xie1, Ying Sun1
1Department of Anesthesiology, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, P.R. China.
International Journal of Molecular Medicine
|October 14, 2015
Summary
Sevoflurane post-conditioning protects the heart from ischemia/reperfusion injury by reducing infarct size. This protection involves increased nitric oxide synthase and decreased NHE1 phosphorylation, mitigating apoptosis and autophagy.
Area of Science:
- Cardiology
- Anesthesiology
- Molecular Biology
Background:
- Myocardial ischemia/reperfusion (I/R) injury (MIRI) is a significant clinical challenge.
- Sevoflurane post-conditioning has shown protective effects against MIRI, but its underlying mechanisms are not fully understood.
- Investigating these mechanisms is crucial for developing targeted therapeutic strategies.
Purpose of the Study:
- To elucidate the molecular mechanisms behind the cardioprotective effects of sevoflurane post-conditioning in isolated rat hearts subjected to MIRI.
- To assess the role of nitric oxide synthase (NOS) and Na+/H+ exchanger 1 (NHE1) in sevoflurane-mediated protection.
Main Methods:
- Isolated Sprague-Dawley rat hearts were divided into six groups: sham, sevoflurane, I/R, sevoflurane post-conditioning + I/R, sevoflurane post-conditioning + L-NAME + I/R, and L-NAME + I/R.
- Infarct size was measured by 2,3,5-triphenyl tetrazolium chloride (TTC) staining.
- Levels of nitric oxide (NO), NOS, NAD+, Bcl-2, cleaved caspase-3, Beclin-1, LC3-I/II, NHE1, and phosphorylated NHE1 were determined using biochemical assays, transmission electron microscopy, western blot, and RT-qPCR.
Main Results:
- Sevoflurane post-conditioning significantly reduced myocardial infarct size, autophagic vacuole numbers, and levels of cleaved caspase-3, Beclin-1, and LC3-I/II compared to the I/R group.
- Sevoflurane post-conditioning increased myocardial NO and NOS levels and Bcl-2 protein expression.
- The protective effects of sevoflurane were partially abolished by the NOS inhibitor L-NAME, and sevoflurane decreased phosphorylated NHE1 levels.
Conclusions:
- Sevoflurane post-conditioning effectively protects the myocardium against I/R injury by reducing infarct size.
- The protective mechanisms involve inhibition of mitochondrial permeability transition pore opening, attenuation of cardiomyocyte apoptosis and excessive autophagy.
- These effects are mediated by increased NOS activity and decreased phosphorylated NHE1 levels.
