Cerebral ischemia was produced by bilateral common carotid artery occl
usion in female Sprague-Dawley rats. Ranitidine, a histamine H-2 recep
tor blocking agent, given intraperitoneally 30 min prior to ischemia,
exerted a dose-dependent protective effect on water accumulation and i
on shifts in the brain (Na+, K+ and Ca2+). To decide whether ranitidin
e can prevent ischemia-induced brain edema when given in the postische
mic period, ranitidine (10 mg/kg i.p.) was administered 1, 2, and 3 h
respectively after the onset of cerebral ischemia. Early (1 h) postocc
lusion treatment was still able to attenuate the ischemia-induced wate
r accumulation and maldistribution of ions in the brain tissue.