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麻醉性异丙酚通过 TRPV1 受体削弱创伤诱导的心脏保护的远程预处理。

Anesthetic propofol blunts remote preconditioning of trauma-induced cardioprotection via the TRPV1 receptor.

机构信息

Hefei National Laboratory for Physical Sciences at the Microscale, Department of Biophysics and Neurobiology, University of Science and Technology of China, Hefei, 230027, PR China; Department of Anesthesiology, The Third Affiliated Hospital of Anhui Medical University, Hefei, 230061, PR China.

Department of Anesthesiology, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, PR China.

出版信息

Biomed Pharmacother. 2019 Oct;118:109308. doi: 10.1016/j.biopha.2019.109308. Epub 2019 Aug 8.

DOI:10.1016/j.biopha.2019.109308
PMID:31401396
Abstract

Remote preconditioning of trauma (RPCT) by surgical incision is an effective cardioprotective strategy via the transient receptor potential vanilloid 1 (TRPV1) channel as a form of remote ischemic preconditioning (RIPC). However, cardioprotection by RIPC has been shown to be completely blocked by propofol. We thus hypothesized that propofol may interfere with RPCT induced cardioprotection, and that RPCT induces cardioprotection via the cardiac TRPV1 channel. Male Sprague-Dawley rats were subjected to 30 min of myocardial ischemia followed by 2 h of reperfusion. RPCT was achieved by a transverse abdominal incision. Additionally, propofol or the TRPV1 receptor inhibitor capsazepine (CPZ) was given before RPCT. Infarct size was assessed by triphenyltetrazolium staining. Heart TRPV1 expression was detected by Western blot and immunofluorescence. RPCT significantly reduced infarct size compared to control treatment (45.6 ± 4% versus 65.4 ± 2%, P < 0.01). This protective effect of RPCT was completely abolished by propofol and CPZ. TRPV1 channels are present in the heart. Therefore, cardioprotection by RPCT is also abolished by propofol, and cardiac TRPV1 mediates this cardioprotection.

摘要

创伤性远程预处理(RPCT)通过外科切口是一种有效的心脏保护策略,通过瞬时受体电位香草素 1(TRPV1)通道作为远程缺血预处理(RIPC)的一种形式。然而,已经表明 RIPC 的心脏保护作用被异丙酚完全阻断。因此,我们假设异丙酚可能会干扰 RPCT 诱导的心脏保护作用,并且 RPCT 通过心脏 TRPV1 通道诱导心脏保护作用。雄性 Sprague-Dawley 大鼠进行 30 分钟的心肌缺血,随后进行 2 小时的再灌注。通过横切口实现 RPCT。此外,在 RPCT 之前给予异丙酚或 TRPV1 受体抑制剂辣椒素(CPZ)。通过三苯基四唑染色评估梗塞面积。通过 Western blot 和免疫荧光检测心脏 TRPV1 表达。与对照处理相比,RPCT 显著减少梗塞面积(45.6±4%对 65.4±2%,P<0.01)。RPCT 的这种保护作用被异丙酚和 CPZ 完全消除。TRPV1 通道存在于心脏中。因此,RPCT 的心脏保护作用也被异丙酚消除,而心脏 TRPV1 介导这种心脏保护作用。

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