脳血管攣縮の平滑筋細胞障害におけるアポトーシスの関与とサイトカインの効果の研究

脑血管痉挛所致平滑肌细胞损伤中细胞凋亡及细胞因子作用的研究

基本信息

批准号：
07671501
负责人：
KIM Phyo
金额：
$ 1.54万
依托单位：
Dokkyo University School of Medicine (1996)The University of Tokyo (1995)
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1995
资助国家：
日本
起止时间：
1995 至 1996
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07671501/
关键词：
Intracellular calcium Basilar artery Dog Cerebral arterial spasm Viability Smooth muscle Subarachnoid hemorrhage Fura-2

项目摘要

The intracellular calcium level was determined in the canine basilar artery in order to investigate whether Ca2+ regulation of its smooth muscle is altered during chronic vasospasm following subarachnoid hemorrhage. A double hemorrhage model was used. The occurrence of vasospasm was confirmed angiographically seven days after initial hemorrhage. The intracellular calcium concentration ( [Ca2+] i) of smooth muscle was measured using Fura-2. Fluorescence to excitation at 340 and 356 nm was monitored and the ratio R340/356 was used as the indicator of [Ca2+] i. When the extracellular calcium concentration ( [Ca2+] e) was increased from pCa 8 to 2, [Ca2+] i also increased. In the spastic arteries, the [Ca2+] e- [Ca2+] i curve was elevated as compared to the normal rteries. Treatment with ionomycin elevated the curve in the normal group, but it had little effect in the spastic arteries. Values of [Ca2+] i, calculated in multiples of Kd, were greater in the spastic arteries. Diltiazem (10-5 mol/l) partially suppressed the augmented [Ca2+] i signal in the spastic arteries, whereas it did not affect the curve in the control group. These results indicate that calcium regulation of smooth muscle impaired after subarachnoid hemorrhage, which may contribute to the pathogenesis of chronic vasospasm.

在犬基底动脉中确定细胞内钙水平，以研究在蛛网膜下腔出血后慢性血管痉挛期间的Ca2+调节平滑肌的调节。使用了双出血模型。初始出血后七天，血管造影证实了血管痉挛的发生。使用Fura-2测量平滑肌的细胞内钙浓度（[Ca2+] I）。监测在340和356 nm处激发的荧光，并将比率R340/356用作[Ca2+] i的指标。当细胞外钙浓度（[Ca2+] E）从PCA 8增加到2时，[Ca2+]也会增加。在痉挛性动脉中，[Ca2+] E- [Ca2+] I曲线与正常术语相比升高。用离子霉素的治疗升高了正常组的曲线，但对痉挛性动脉的影响很小。在痉挛性动脉中，以KD倍数计算的[Ca2+] I的值更大。 Diltiazem（10-5 mol/L）部分抑制了痉挛性动脉中的增强[Ca2+] I信号，而它不影响对照组的曲线。这些结果表明，蛛网膜下腔出血后平滑肌的钙调节可能有助于慢性血管痉挛的发病机理。