Tósaki A, Szerdahelyi P, Joó F
Laboratory of Molecular Neurobiology, Institute of Biophysics, Biological Research Centre, Szeged, Hungary.
Eur J Pharmacol. 1994 Nov 3;264(3):455-8. doi: 10.1016/0014-2999(94)00546-x.
Cerebral ischemia was produced by bilateral common carotid artery occlusion in female Sprague-Dawley rats. Ranitidine, a histamine H2 receptor blocking agent, given intraperitoneally 30 min prior to ischemia, exerted a dose-dependent protective effect on water accumulation and ion shifts in the brain (Na+, K+ and Ca2+). To decide whether ranitidine can prevent ischemia-induced brain edema when given in the postischemic period, ranitidine (10 mg/kg i.p.) was administered 1, 2, and 3 h respectively after the onset of cerebral ischemia. Early (1 h) postocclusion treatment was still able to attenuate the ischemia-induced water accumulation and maldistribution of ions in the brain tissue.
通过双侧颈总动脉闭塞在雌性斯普拉格-道利大鼠中诱导脑缺血。雷尼替丁是一种组胺H2受体阻断剂,在缺血前30分钟腹腔注射,对脑内水蓄积和离子转移(Na+、K+和Ca2+)具有剂量依赖性保护作用。为了确定雷尼替丁在缺血后给药时是否能预防缺血性脑水肿,在脑缺血发作后分别于1、2和3小时给予雷尼替丁(10mg/kg腹腔注射)。闭塞后早期(1小时)治疗仍能减轻缺血诱导的脑组织水蓄积和离子分布异常。