Kurihara J, Nishimura H, Oda N, Kato H
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Teikyo University, Kanagawa, Japan.
Jpn J Pharmacol. 1989 Feb;49(2):255-65. doi: 10.1254/jjp.49.255.
Influence of transient global cerebral ischemia on baroreceptor reflex sensitivity (BRS) was investigated in anesthetized dogs. Cerebral ischemia was produced by the combined occlusions of the left subclavian (LSA) and the brachiocephalic (BCA) arteries with preceding ligations of the intercostal arteries (ICA). BRS was assessed by phenylephrine-induced reflex bradycardia. Ischemia of 5- and 10-min duration produced a significant decrease in BRS during the reperfusion period of 60-120 min. On the other hand, such a change was not observed following the ischemia of less than 2-min or occlusions of LSA and BCA without preceding ligations of ICA. Heart rate response to the electrical stimulation of the vagal afferent nerve was attenuated by 10-min ischemia, while response to the vagal efferent nerve stimulation and ECG parameters were not influenced. These results indicate that some regions vulnerable to the relatively short duration of cerebral ischemia may be involved in the central pathway of the baroreflex mechanism.
在麻醉犬中研究了短暂性全脑缺血对压力感受器反射敏感性(BRS)的影响。通过结扎肋间动脉(ICA)后联合阻断左锁骨下动脉(LSA)和头臂动脉(BCA)来制造脑缺血。通过去氧肾上腺素诱导的反射性心动过缓评估BRS。持续5分钟和10分钟的缺血在60 - 120分钟的再灌注期导致BRS显著降低。另一方面,在缺血时间少于2分钟或未预先结扎ICA而阻断LSA和BCA后未观察到这种变化。对迷走神经传入神经的电刺激的心率反应在10分钟缺血后减弱,而对迷走神经传出神经刺激的反应和心电图参数未受影响。这些结果表明,一些易受相对短时间脑缺血影响的区域可能参与压力反射机制的中枢通路。