Role of mitochondrial ATP sensitive potassium channel in delayed preconditioning with sevoflurane reducing myocardial ischemia-reperfusion injury in rats
Ke Ran
Abstract
Ke Ran
Abstract
Objective To investigate the role of mitochondrial ATP sensitive potassium channel(mito-KATP)in the delayed cardioprotection produced by sevoflurane in ischemia-reperfusion(I-R)injured rats.Methods Eighty male Sprague-Dawley rats were randomly divided into five groups:a sham operation group(group A);an ischemia-reperfusion injury group(group B),occlusion of left anterior descending coronary artery for 30 min and followed by 120min of reperfusion;a sevoflurane preconditioning group(group C),breathing 2.5% sevoflurane for one hour 24 h before IR;a sevoflutane preconditioning+5-hydroxydecanoate(5-HD,a mito-KATP inhibitor)group(group D),5-HD 5mg/kg was given before sevoflurane preconditioning;and a 5-HD group(group E).After 120 min of reperfusion,myocardial area at risk in ischemia and infarcted size(IS)were measured by double stain with evans blue and TTC.Serum cTnI levels were detected with ELISA.The expression of Bcl-2 and Bax was measured with immunoblotting.Results Preconditioning with sevoflurane decreased the IS induced by I-R,reduced cTnI level,upregulated Bcl-2 protein and downregulated Bax expression(all P0.05),but this effect was inhibited by 5-HD.Conclusion Delayed preconditioning with sevoflurane protects myocardial ischemia-reperfusion injury by regulating Bcl-2 and Bax expression that may be associated with mito-KATP channel activation.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Objective To investigate the role of mitochondrial ATP sensitive potassium channel(mito-KATP)in the delayed cardioprotection produced by sevoflurane in ischemia-reperfusion(I-R)injured rats.Methods Eighty male Sprague-Dawley rats were randomly divided into five groups:a sham operation group(group A);an ischemia-reperfusion injury group(group B),occlusion of left anterior descending coronary artery for 30 min and followed by 120min of reperfusion;a sevoflurane preconditioning group(group C),breathing 2.5% sevoflurane for one hour 24 h before IR;a sevoflutane preconditioning+5-hydroxydecanoate(5-HD,a mito-KATP inhibitor)group(group D),5-HD 5mg/kg was given before sevoflurane preconditioning;and a 5-HD group(group E).After 120 min of reperfusion,myocardial area at risk in ischemia and infarcted size(IS)were measured by double stain with evans blue and TTC.Serum cTnI levels were detected with ELISA.The expression of Bcl-2 and Bax was measured with immunoblotting.Results Preconditioning with sevoflurane decreased the IS induced by I-R,reduced cTnI level,upregulated Bcl-2 protein and downregulated Bax expression(all P0.05),but this effect was inhibited by 5-HD.Conclusion Delayed preconditioning with sevoflurane protects myocardial ischemia-reperfusion injury by regulating Bcl-2 and Bax expression that may be associated with mito-KATP channel activation.
Key concepts: Sevoflurane, Medicine, Cardioprotection, Ischemic preconditioning, Reperfusion injury, Ischemia, Troponin I, Anesthesia