Tomimoto H, Wakita H, Akiguchi I, Kimura J
Department of Neurology, Kyoto University Hospital, Japan.
No To Shinkei. 1994 Mar;46(3):251-6.
Alteration of evolution of delayed neuronal death in the gerbil after intraperitoneal injection of nicardipine was investigated by using immunohistochemistry for microtubule associated protein (MAP) which enables early detection of ischemic injuries. Male Mongolian gerbils were subjected to intraperitoneal injection of nicardipine at concentrations of 0.01-10 mg/kg and subsequent occlusion of bilateral carotid arteries for 5 min. Extent of the lesions estimated by immunohistochemistry for MAP was reduced at the dosages of 0.2 mg/kg nicardipine as compared with control, while lesser or larger amounts have failed to protect the brain tissue from ischemic insults. Furthermore, pre- and postoperative treatment of 0.2 mg/kg of nicardipine two times daily succeeded to partially attenuate the development of delayed neuronal death in gerbils which underwent ischemia for 5 min and subsequent reperfusion for 4 days. These results indicate that optimal concentration of nicardipine ameliorates delayed neuronal death, presumably because of the increase of cerebral blood flow and intervention of intracellular influx of calcium ions.
通过使用针对微管相关蛋白(MAP)的免疫组织化学方法,研究了腹腔注射尼卡地平后沙鼠延迟性神经元死亡演变的改变,该方法能够早期检测缺血性损伤。雄性蒙古沙鼠腹腔注射浓度为0.01 - 10 mg/kg的尼卡地平,随后双侧颈动脉闭塞5分钟。与对照组相比,在0.2 mg/kg尼卡地平剂量下,通过MAP免疫组织化学估计的损伤程度降低,而较小或较大剂量未能保护脑组织免受缺血性损伤。此外,每天两次给予0.2 mg/kg尼卡地平进行术前和术后治疗,成功部分减轻了经历5分钟缺血和随后4天再灌注的沙鼠延迟性神经元死亡的发展。这些结果表明,尼卡地平的最佳浓度可改善延迟性神经元死亡,可能是由于脑血流量增加和细胞内钙离子内流的干预。