一种新型钙拮抗剂SM-6586对实验性脑缺血的影响。

F Kashiwagi, Y Katayama, H Igarashi, S Iida, H Muramatsu, A Terashi
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引用次数: 3

摘要

SM-6586 (SM)是一种新型的二氢吡啶衍生物,具有较强的钙阻断活性和抑制Na+/H+和Na+/Ca++交换转运的活性。采用两种不同的模型评价SM对自发性高血压大鼠(SHR)存活率、脑水肿及代谢物的影响。双侧颈总动脉结扎术(BLCL)诱导全脑缺血,大脑中动脉闭塞术诱导局灶性缺血。sm治疗组BLCL术后生存率较高。sm治疗组脑含水量较对照组低,ATP水平较高,乳酸水平较对照组低。在局灶性缺血模型中,sm治疗组T1松弛时间缩短。sm治疗组脑含水量明显降低。上述结果表明,SM可有效改善全脑和局灶性脑缺血模型的缺血性损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of a new calcium antagonist (SM-6586) on experimental cerebral ischemia.

SM-6586 (SM) is a new derivative of dihydropyridine with potent calcium blocking activity and inhibitory activity of the Na+/H+ and Na+/Ca++ exchange transport. The effect of SM on survival rate, brain edema and metabolites was evaluated using two different models in spontaneously hypertensive rat (SHR). Global ischemia was induced by bilateral common carotid artery ligation (BLCL) and focal ischemia was induced by middle cerebral artery occlusion. The survival rate after BLCL was higher in the SM-treated group. The brain water content was lower, the ATP level was higher and lactate level was lower in the SM-treated group compared to the control group. In focal ischemia models, the SM-treated group showed a reduction of T1 relaxation time. The brain water content was significantly decreased in the SM-treated group. These results indicate that SM was effective in ameliorating the ischemic insult in global and focal cerebral ischemia models.

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