Li Y, Kawamura S, Yasui N, Shirasawa M, Fukasawa H
Department of Surgical Neurology, Research Institute for Brain and Blood Vessels-Akita, Japan.
Exp Brain Res. 1994;99(1):1-6. doi: 10.1007/BF00241406.
The present study was conducted to investigate the therapeutic effects of nilvadipine, a Ca2+ entry blocker, on rat focal cerebral ischemia. Under halothane anesthesia, a 3-0 nylon thread was introduced into the neck internal carotid artery to occlude the left middle cerebral artery. Either nilvadipine (3.2 mg/kg) or vehicle was administered subcutaneously 1, 2, 3, 4, 5 and 6 h following the occlusion (groups 1-6, respectively). Twenty-four hours after the occlusion, the percentage infarct volumes in nilvadipine-treated animals in groups 1-3 (21 +/- 11%, 24 +/- 11%, and 26 +/- 7%, respectively) were smaller than those in the respective control groups (36 +/- 5%, 35 +/- 3%, and 35 +/- 3%; P < 0.05). Compared with controls, the infarct size of the periphery of the fronto-parietal cortex decreased in nilvadipine-treated animals. The results indicate that nilvadipine decreases the size of infarction when administered up to 3 h after an ischemic insult. Thus, nilvadipine can be considered a potential therapeutic agent for acute focal cerebral ischemia, and may be clinically useful in stroke patients.
