Tweed W A, Wade J G, Davidson W J
Can J Neurol Sci. 1977 Feb;4(1):19-23.
Resuscitation of the brain following total circulatory arrest may be impeded by difficulty in establishing cerebral tissue perfusion, a postischemic "low-flow"state. We have confirmed this hypothesis in a rat model of total cerebral ischemia and have demonstrated marked imporvement in post-ischemic brain tissue perfusion following epinephrine injection. This is mainly due to the systemic vascular effects of epinephrine, resulting in improved central arotic pressure and cerebral perfusion pressure. Hyperkalemic induced vasoconstriction has also been postulated as a cause of the "low-flow/. We have, therefore, investigated the in vitro effects of increasing potassium ion concentration on cerebrovascular smooth muscle strips. Large arteries constrict, while small arteries dilate in response to hyperkalemia. The net effect on cerebral blood flow remains unsettled. Our research to date suggests that resuscitation of the totally ischemic brain, in animal models at least, is enhanced by epinephrine, mainly via its effects on central aortic pressure.
全循环骤停后脑复苏可能会因难以建立脑组织灌注（一种缺血后的“低流量”状态）而受到阻碍。我们已在全脑缺血的大鼠模型中证实了这一假设，并证明注射肾上腺素后缺血后脑组织灌注有显著改善。这主要归因于肾上腺素的全身血管效应，从而导致中心主动脉压和脑灌注压升高。高钾血症诱导的血管收缩也被认为是“低流量”的一个原因。因此，我们研究了增加钾离子浓度对脑血管平滑肌条的体外作用。大动脉会收缩，而小动脉对高钾血症的反应是扩张。对脑血流量的净效应仍未确定。我们目前的研究表明，至少在动物模型中，肾上腺素可增强完全缺血脑的复苏，主要是通过其对中心主动脉压的作用。
