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舒芬太尼通过保存磷酸化连接蛋白 43 来限制心肌梗死面积。

Sufentanil limits the myocardial infarct size by preservation of the phosphorylated connexin 43.

机构信息

Department of Anesthesiology, The First Affiliated Hospital of Anhui Medical University, 218 Jixi Road, Hefei, China.

出版信息

Int Immunopharmacol. 2012 Jul;13(3):341-6. doi: 10.1016/j.intimp.2012.04.009. Epub 2012 May 3.

DOI:10.1016/j.intimp.2012.04.009
PMID:22561119
Abstract

Sufentanil, with a potent analgesia effect, has been wildly used in anesthesia and analgesia, especially for the cardiovascular surgeries. The aim of the study was to evaluate whether sufentanil provides cardioprotection and the effect of connexin 43 on the cardiac infarct size reduction. Sufentanil post-conditioning (bolus injection at 0.1, 0.3, 1, 3, 10 μg/kg) or ischemic post-conditioning (3 cycles of a 10s reperfusion alternating with a 10s ischemia) was induced in an intact rat heart model of ischemia-reperfusion injury. Both ischemic and sufentanil post-conditioning reduced the myocardial infarct size compared with control group. The infarct size limitation of sufentanil was dose-dependent, 1 μg/kg has the optimal effect and increasing dosage could not afford further cardioprotection. Connexin 43 underwent dephosphorylation in response to ischemia-reperfusion measured by Western blot at the anterior myocardium tissues of left ventricle while sufentanil preserved the phosphorylation of connexin 43. The results demonstrated that sufentanil limits myocardial infarct size which is similar with ischemic post-conditioning at the dosage of 1 μg/kg. Preservation of phosphorylation of connexin 43 plays an important role in the cardioprotection of ischemic and sufentanil post-conditioning.

摘要

舒芬太尼具有较强的镇痛作用,在麻醉和镇痛中被广泛应用,尤其适用于心血管手术。本研究旨在评估舒芬太尼是否具有心肌保护作用,以及连接蛋白 43 对心肌梗死面积缩小的影响。在缺血再灌注损伤的完整大鼠心脏模型中,诱导舒芬太尼后处理(0.1、0.3、1、3、10μg/kg 推注)或缺血后处理(3 个 10s 再灌注与 10s 缺血交替的循环)。与对照组相比,缺血和舒芬太尼后处理均减少了心肌梗死面积。舒芬太尼的梗死面积限制呈剂量依赖性,1μg/kg 具有最佳效果,增加剂量不能提供进一步的心脏保护。通过左心室前心肌组织的 Western blot 测量,连接蛋白 43 在缺血再灌注时发生去磷酸化,而舒芬太尼则保留了连接蛋白 43 的磷酸化。结果表明,舒芬太尼限制心肌梗死面积的作用与 1μg/kg 剂量的缺血后处理相似。连接蛋白 43 磷酸化的保留在缺血和舒芬太尼后处理的心肌保护中起着重要作用。

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