首页> 美国卫生研究院文献>Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease >Remote Limb Ischemic Preconditioning Attenuates Cerebrovascular Depression During Sinusoidal Galvanic Vestibular Stimulation via α1‐Adrenoceptor–Protein Kinase Cε–Endothelial NO Synthase Pathway in Rats
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Remote Limb Ischemic Preconditioning Attenuates Cerebrovascular Depression During Sinusoidal Galvanic Vestibular Stimulation via α1‐Adrenoceptor–Protein Kinase Cε–Endothelial NO Synthase Pathway in Rats

机译:通过α1-肾上腺素受体-蛋白激酶Cε-内皮一氧化氮合酶途径在大鼠正弦电流前庭刺激过程中远端肢体缺血预处理可减轻脑血管抑制

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摘要

BackgroundVasovagal syncope (VVS) is characterized by hypotension and bradycardia followed by lowering of cerebral blood flow. Remote limb ischemic preconditioning (RIPC) is well documented to provide cardio‐ and neuroprotection as well as to improve cerebral blood flow. We hypothesized that RIPC will provide protection against VVS‐induced hypotension, bradycardia, and cerebral hypoperfusion. Second, because endothelial nitric oxide synthase has been reported as a mediator of cerebral blood flow control, we hypothesized that the mechanism by which RIPC primes the vasculature against VVS is via the α1‐adrenoceptor–protein kinase Cε–endothelial nitric oxide synthase pathway.
机译:背景血管迷走性晕厥(VVS)的特征在于低血压和心动过缓,然后脑血流量降低。远端肢体缺血预处理(RIPC)有充分的文献记载,可提供心脏和神经保护作用,并改善脑血流量。我们假设RIPC将提供针对VVS引起的低血压,心动过缓和脑灌注不足的保护作用。第二,因为据报道内皮一氧化氮合酶是控制脑血流的介质,我们假设RIPC引发血管对抗VVS的机制是通过α1-肾上腺素受体-蛋白激酶Cε-内皮一氧化氮合酶途径。

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