Effects of Acetazolamide on Cerebral Ischemia and Infarction After Experimental Occlusion of Middle Cerebral Artery
Effects of Acetazolamide on Cerebral Ischemia and Infarction After Experimental Occlusion of Middle Cerebral Artery
复制标题
乙酰唑胺对实验性大脑中动脉闭塞后脑缺血和梗死的影响
DOI：
10.1161/01.str.2.5.456
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发表时间：
1971
期刊：
影响因子：
8.3
通讯作者：
A. G. Waltz
中科院分区：
文献类型：
--
作者：
F. Regli;Takenori Yamaguchi;A. G. Waltz
在大脑中动脉（MCA）硬膜外闭塞后，对10只猫中的5只给予乙酰唑胺48至54小时。在7 - 8天后，测量局部脑血流量（CBF）并估计脑缺血和梗死区域的大小。给予乙酰唑胺的猫神经功能缺损更严重，缺血和梗死区域更大。即使在MCA闭塞后1周，给药猫中也存在脑水肿（脑肿胀）和反应性充血。乙酰唑胺引起的高碳酸血症和非缺血性脑组织pH值降低对缺血性脑组织有害，可能是因为非缺血性脑组织血管扩张，导致颅内压升高和缺血区域CBF降低。
Acetazolamide was given to five of ten cats for 48 to 54 hours after extradural occlusion of a middle cerebral artery (MCA). At seven to eight days later, measurements of regional cerebral blood flow (CBF) and estimates of the sizes of the ischemic and infarcted areas of the brains were made. Neurological deficits were more severe and the ischemic and infarcted regions were larger in the cats given acetazolamide. Cerebral edema (brain swelling) was present and reactive hyperemia was common in the treated cats, even one week after MCA occlusion. The hypercapnia and decreases of pH of nonischemic brain tissue that are caused by acetazolamide are harmful for ischemic brain tissue, presumably because of vasodilatation in nonischemic brain tissue with resultant increases of intracranial pressure and decreases of CBF of ischemic regions.