Effects of sufentanil postconditioning and sevoflurane postconditioning on myocardial ischemia/reperfusion injury in isolated rat hearts / 中华麻醉学杂志

ABSTRACT

Objective To investigate the effects of sufentanil postconditioning and sevoflurane postconditioning on myocardial ischemia/reperfusion (I/R) injury in isolated rat hearts. Methods Healthy male SD rats weighing 230-250 g were anesthetized with intraperitoneal 5% chloral hydrate 8 ml/kg. Their hearts were excised and perfused in a Langendorff apparatus with modified K-H solution saturated with 95% O2-5% CO2 at 37℃. Forty isolated rat hearts with I/R injury were randomly assigned into 4 groups ( n = 10 each) Ⅰ I/R group, Ⅱ sevoflurane postconditioning group, Ⅲ sulfentanil postconditioning group and Ⅳ postconditioning with sevoflurane and sulfentanil group. After 30 min of stablization, the hearts were subjected to 40 min of global ischemia followed by 120 min of reperfusion. Fifteen minutes of drug postconditioning were performed in group Ⅱ , Ⅲ and Ⅳ3.0% sevoflurane was introduced into K-H solution in group Ⅱ , 100 nmol/L sulfentanil was added to K-H solution in group Ⅲ , sevoflurane postconditioning and sulfentanil postconditioning were performed simultaneously in group Ⅳ . Left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure ( LVEDP), left ventricular developed pressure (LVDP), maximum increase in rate of LVDP ( + dp/dtmax), maximum decrease in rate of LVDP ( - dp/dtmax), HR and coronary flow (CF) were measured at the end of 30 min stablization (baseline), and at 15, 30, 60, 90 and 120 min of reperfusion. Coronary effluent was collected at 5 min of reperfusion for determination of activities of creatine kinase (CK) and lactate dehydrogenase (LDH). Myocardial tissues were obtained at the end of reperfusion for determination of infarct size (by triphenyltetrazolium chloride staining) and expression of Bcl-2 and Bax (by Western blot). The ratio of Bcl-2/Bax was calculated. Results LVSP, LVDP, ± dp/dtmax,CF, Bcl-2 expression and ratio of Bcl-2/Bax were significantly higher, LVEDP, activities of CK and LDH and Bax expression were significantly lower, and the infarct size was smaller in group Ⅱ , Ⅲ and Ⅳ than in group Ⅰ (P ＜ 0.05 or 0.01 ). There were no differences in the indices mentioned above between Ⅱ , Ⅲ and Ⅳ groups.Conclusion Sufentanil postconditioning can attenuate myocardial I/R injury, and there is no enhancement of myocardial protection when combined with sevoflurane postconditioning. The mechanism of myocardial protection is related to the inhibition of cell apoptosis via up-regulation of Bcl-2 expression and down-regulation Bax expression.