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自发性高血压大鼠脑缺血期间小脑血流自动调节功能受损。

Impairment of cerebellar blood flow autoregulation during cerebral ischemia in spontaneously hypertensive rats.

作者信息

Shiokawa O, Sadoshima S, Fujii K, Yao H, Fujishima M

机构信息

Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.

出版信息

Stroke. 1988 May;19(5):615-22. doi: 10.1161/01.str.19.5.615.

Abstract

Participation of the autonomic nervous system in cerebellar autoregulation during supratentorial cerebral ischemia induced by bilateral carotid ligation was studied using 23 spontaneously hypertensive rats. Cerebral and cerebellar blood flows measured by a hydrogen clearance method were evaluated under stepwise hemorrhagic hypotension before and 30 minutes after ligation and after a 30-minute recirculation period following 1 hour of ligation. alpha-Adrenergic blockade with phenoxybenzamine, beta-adrenergic blockade with propranolol, and muscarinic cholinergic blockade with atropine were selectively administered before ligation for inhibition of sympathetic and parasympathetic tone. Cerebral blood flow autoregulation was severely impaired during and after cerebral ischemia in each treatment group. During cerebral ischemia, cerebellar blood flow autoregulation was also significantly impaired in both the propranolol and atropine groups although it was better preserved in the phenoxybenzamine group. After recirculation, cerebellar blood flow autoregulation recovered almost to the normal range in the phenoxybenzamine and atropine groups but remained impaired in the propranolol group. Our results suggest that impaired cerebellar blood flow autoregulation in supratentorial cerebral ischemia is partly modulated by the alpha-adrenoceptor system, which is activated by hypertensive stimuli and cerebral ischemia, leading to vasoconstriction in the cerebellum.

摘要

使用23只自发性高血压大鼠,研究了自主神经系统在双侧颈动脉结扎诱导幕上脑缺血期间小脑自动调节中的作用。在结扎前和结扎后30分钟以及结扎1小时后的30分钟再循环期,通过氢清除法测量的脑和小脑血流量在逐步出血性低血压下进行评估。在结扎前选择性给予苯氧苄胺进行α-肾上腺素能阻断、普萘洛尔进行β-肾上腺素能阻断以及阿托品进行毒蕈碱胆碱能阻断,以抑制交感和副交感神经张力。在每个治疗组中,脑缺血期间及之后脑血流量自动调节严重受损。在脑缺血期间,普萘洛尔组和阿托品组的小脑血流量自动调节也显著受损,尽管苯氧苄胺组中其保存较好。再循环后,苯氧苄胺组和阿托品组的小脑血流量自动调节几乎恢复到正常范围,但普萘洛尔组仍受损。我们的结果表明,幕上脑缺血时小脑血流量自动调节受损部分受α-肾上腺素能受体系统调节,该系统由高血压刺激和脑缺血激活,导致小脑血管收缩。

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