Germano I M, Bartkowski H M, Cassel M E, Pitts L H
J Neurosurg. 1987 Jul;67(1):81-7. doi: 10.3171/jns.1987.67.1.0081.
Recent studies suggest that nimodipine, a potent calcium-channel antagonist that causes significant cerebrovascular dilatation, may improve neurological outcome after acute experimental permanent focal cerebral ischemia when given before or immediately after occlusion of the middle cerebral artery (MCA) in various animals. The authors describe the effect of nimodipine on cerebral ischemia in a rat model. At 1, 4, or 6 hours after occlusion of the MCA, rats were treated in a double-blind technique with either nimodipine, placebo, or saline. Neurological and neuropathological evaluation was performed at 24 hours. Neurological outcome was better in rats treated with nimodipine 1, 4, or 6 hours after occlusion (p less than 0.001, p less than 0.01, p less than 0.05 respectively), and the size of areas of infarction was statistically smaller in nimodipine-treated groups (p less than 0.01, p less than 0.01, p less than 0.05, respectively) when compared with control rats treated with saline or placebo. The best neurological outcome and the smallest area of infarction were found in nimodipine-treated rats 1 hour after occlusion. Compared with controls, the size of the periphery of the infarcted area was smaller in nimodipine-treated rats. The results show that nimodipine improves neurological outcome and decreases the size of infarction when administered up to 6 hours after ischemic insult. These results suggest a possible mechanism of action of nimodipine on the "penumbra" of the ischemic area.
近期研究表明，尼莫地平作为一种强效钙通道拮抗剂，可引起显著的脑血管扩张，在各种动物大脑中动脉（MCA）闭塞前或闭塞后立即给药时，可能改善急性实验性永久性局灶性脑缺血后的神经功能结局。作者描述了尼莫地平在大鼠模型中对脑缺血的影响。在MCA闭塞后1、4或6小时，采用双盲技术对大鼠分别给予尼莫地平、安慰剂或生理盐水治疗。在24小时时进行神经学和神经病理学评估。在闭塞后1、4或6小时接受尼莫地平治疗的大鼠神经功能结局更好（分别为p<0.001、p<0.01、p<0.05），与接受生理盐水或安慰剂治疗的对照大鼠相比，尼莫地平治疗组的梗死面积在统计学上更小（分别为p<0.01、p<0.01、p<0.05）。在闭塞后1小时接受尼莫地平治疗的大鼠中发现了最佳的神经功能结局和最小的梗死面积。与对照组相比，尼莫地平治疗的大鼠梗死区域周边的面积更小。结果表明，在缺血性损伤后6小时内给予尼莫地平可改善神经功能结局并减小梗死面积。这些结果提示了尼莫地平对缺血区域“半暗带”的一种可能作用机制。
