Nitrendipine Facilitates Recovery of Cerebral Blood Flow, EEG and Metabolites Following Cerebral Ischemia in Anesthetized Rabbits

AIHARA, K. and INUI, J. Nitrendipine Facilitates Recovery of Cerebral Blood Flow, EEG and Metabolites Following Cerebral Ischemia in Anesthetized Rabbits. Tohoku J. Exp. Med., 1991, 165 (1), 13-24-The effect of nitrendipine, an antihypertensive calcium antagonist, on the impairment of cerebral blood...

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Published inThe Tohoku Journal of Experimental Medicine Vol. 165; no. 1; pp. 13 - 24
Main Authors AIHARA, KENICHI, INUI, JUN
Format Journal Article
LanguageEnglish
Published Japan Tohoku University Medical Press 1991
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Summary:AIHARA, K. and INUI, J. Nitrendipine Facilitates Recovery of Cerebral Blood Flow, EEG and Metabolites Following Cerebral Ischemia in Anesthetized Rabbits. Tohoku J. Exp. Med., 1991, 165 (1), 13-24-The effect of nitrendipine, an antihypertensive calcium antagonist, on the impairment of cerebral blood flow and EEG observed after 10-min complete cerebral ischemia in anesthetized rabbits was compared with those of nicardipine. The ischemia was produced by neck tourniquet in combination with hypotension (50-60mmHg). Blood flow was measured by hydrogen-clearance method. Transient reactive hyperemia was observed immediately after the cessation of ischemic procedure, and was followed by a decrease in blood flow in the range of 58-73% of corresponding basal values in the total brain, cortex and thalamus. The postischemic decrease in blood flow was suppressed when nitrendipine (0.3-1mg/kg) or nicardipine (3-10mg/kg) was given intraduodenally before ischemia. The postischemic decrease in total intensity and frequency index in EEG recovered rapidly when nitrendipine was pretreated, whereas the recovery of EEG parameters was not obtained by the nicardipine pretreatment. These results suggest that the effect of nitrendipine and nicardipine on the postischemic cerebral blood flow may be due to the inhibition of calcium-induced contraction in cerebral vessels, whereas the discrepancy between the effects of these agents on EEG may not be due solely to the improvement in cerebral circulation. Furthermore, the improvement in postischemic cerebral energy metabolism was confirmed by nitrendipine pretreatment (0.3mg/kg).
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ISSN:0040-8727
1349-3329
DOI:10.1620/tjem.165.13