J Korean Neurosurg Soc.
1991 Aug;20(8):664-677.
The Effects of Nicardipine on Regional Cerebral Electrolytes and Water Shifts after Permanent Occlusion of the Middle Cerebral Artery in Rabbits
- Affiliations
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- 1Departments of Neurosurgery, Pusan National University, School of Medicine, Busan, Korea.
Abstract
- Dihydropyrdine-type calcium channel blockers, such as nicardipine have been used for the treatment of cerebral ischemic diseases, including cerebral occlusive disease and cerebral vasospasm after subarachniod hemorrhage. Although experimental studies demonstrated that various types of calcium channel blocker have an inhigitory effect on vasoconstriction induced by vasoactive agents, it is still controversial as to whether the therapeutic benefit of the calcium channel blockers is caused by their preventive action or by other meechanisms of the cerebral ischemia. It is of very clinical imprtance to understand the effect of calcium channel blockers in the brain. And then the effects of the calcium channel blockers, incardipine on regional tissue CA2+, NA+, K+ and water shifts after permanent occlusion of the middle cerebral artery in the brain of rabbits were studied. The result were as follows : 1) Ca2+ and Na+ concentrations and water content were increased, and K+ concentraion was decreased in focal cerebral ischemia induced by permanent occlusion of the middle cerebral artery. 2) Nicardipine treatment significantly reduced Ca2+ accumulation in the middle cerebral artery territory by 32.5% compared with untreated rabbits 6 hours after arterial occlusion. 3) Nicardipine treatment also significantly reduced the Na+, K+ and water shifts in the middle cerebral artery territory by 18.3%, 24.9% and 21.2% respectively, 6 hours after arterial occlusion. 4) Nicardipine appeared to reduce Ca2+ accumulation more than in reduced of Na+ and water accumulation and loss of K+ loss. It might be suggested that calcium channel blocker can protect brain tissue in early stage in a model of focal cerebral infarction by directly reducing Ca2+ entry into ischemic brain cells.