Aulakh Amritpal Singh, Randhawa Puneet Kaur, Singh Nirmal, Jaggi Amteshwar Singh
Department of Pharmaceutical Sciences and Drug Research, Punjabi University Patiala, Patiala 147002, India.
Korean J Physiol Pharmacol. 2017 Mar;21(2):145-152. doi: 10.4196/kjpp.2017.21.2.145. Epub 2017 Feb 21.
Remote ischemic preconditioning (RIPC) is an intrinsic phenomenon whereby 3~4 consecutive ischemia-reperfusion cycles to a remote tissue (noncardiac) increases the tolerance of the myocardium to sustained ischemiareperfusion induced injury. Remote ischemic preconditioning induces the local release of chemical mediators which activate the sensory nerve endings to convey signals to the brain. The latter consequently stimulates the efferent nerve endings innervating the myocardium to induce cardioprotection. Indeed, RIPC-induced cardioprotective effects are reliant on the presence of intact neuronal pathways, which has been confirmed using nerve resection of nerves including femoral nerve, vagus nerve, and sciatic nerve. The involvement of neurogenic signaling has been further substantiated using various pharmacological modulators including hexamethonium and trimetaphan. The present review focuses on the potential involvement of neurogenic pathways in mediating remote ischemic preconditioning-induced cardioprotection.
远程缺血预处理(RIPC)是一种内在现象,即对远处组织(非心脏组织)进行3至4个连续的缺血-再灌注循环可增加心肌对持续性缺血-再灌注诱导损伤的耐受性。远程缺血预处理诱导化学介质的局部释放,这些化学介质激活感觉神经末梢,将信号传递至大脑。大脑随后刺激支配心肌的传出神经末梢,从而诱导心脏保护作用。事实上,RIPC诱导的心脏保护作用依赖于完整神经通路的存在,这已通过对包括股神经、迷走神经和坐骨神经在内的神经进行切除得以证实。使用包括六甲铵和阿方那特在内的各种药理学调节剂进一步证实了神经源性信号传导的参与。本综述重点关注神经源性通路在介导远程缺血预处理诱导的心脏保护作用中的潜在作用。