The Effects of Nimodipine on Neurological and Pathological Findings Following Experimental Focal Cerebral Ischemia.
- Author:
Se Hyuck PARK
1
;
Kyu Ho LEE
;
Kyu Chang LEE
Author Information
1. Department of Neurosurgery, Hallym University College of Medicine, Korea.
- Publication Type:Original Article
- Keywords:
Nimodipine;
Focal cerebral ischemia;
Hypoperfusion;
Membrane failure
- MeSH:
Animals;
Brain Ischemia*;
Calcium;
Calcium Channel Blockers;
Calcium Channels;
Infarction;
Ions;
Logic;
Membranes;
Neurons;
Nimodipine*;
Rats
- From:Journal of Korean Neurosurgical Society
1990;19(1):5-13
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Two major factors, delayed hypoperfusion and membrane failure influence the sequelae of cerebral ischemic injury. Calcium ions play a major role in both pathophysiological mechanisms. Calcium channel blockers are a logical choice for investigation as possible therapeutic agents for the treatment of cerebral ischemia. Nimodipine, a dihydropyridine derivative, is one of the most potent calcium channel blocking agent with a selective action on the intracranial vessels. The present study was designed to test the effects of nimodipine on focal cerebral ischemia in rats. At 1,2 or 6 hours after occlusion of the middle cerebral artery(MCA), rats were treated with either nimodipine or saline. Neurological and pathological evaluation was performed at 24 hours after occlusion. Neurological outcome was better in nimodipine-treated rats and the size of the infarcted area was statistically smaller in rats treated with nimodipine 1,2 or 6 hours after occlusion(P<0.001, P<0.001, P<0.001, respectively) when compared with control rats(MCA occlusion only) or saline-treated rats. The results show that nimodipine improves neurological outcome and decreases the size of infarction after ischemic insult. The mechanism of action of nimodipine is not fully understood but nimodipine could influence cerebral postischemic changes by improving blood flow and/or by a direct action on neurons.
