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硝苯地平对离体猫心脏的保护作用。

The protective effects of nifedipine in the isolated cat heart.

作者信息

Okamatsu S, Lefer A M

出版信息

J Surg Res. 1983 Jul;35(1):35-40. doi: 10.1016/0022-4804(83)90123-3.

Abstract

The calcium channel blocking agent, nifedipine, was studied during global ischemia and reperfusion in isolated cat hearts perfused with Krebs-Henseleit solution. Nifedipine was added to the reservoir and 0.1 micrograms/ml perfusate/hr of nifedipine was infused for 150 min. After 120 min of ischemia (flow at 1% of control), the heart was reperfused with nifedipine-containing perfusate for 20 min and with nifedipine-free perfusate for an additional 25 min. In control hearts, nifedipine significantly reduced the percent free activity of the lysosomal protease cathepsin D (P less than 0.01). In ischemic hearts, nifedipine protected against the increased myocardial tissue edema (P less than 0.01), the increased percent free cathepsin D activity (P less than 0.02) and the postreperfusion increased creatine kinase activity (P less than 0.01). Thus, nifedipine showed membrane stabilizing and cytoprotective activities in myocardial cells, after postischemic reperfusion. These data suggest that calcium ions contribute to the lysosome labilization and cytoplasmic enzyme leakage observed in ischemia and reperfusion, and that calcium channel blockade may protect myocardial cellular integrity during both ischemia and reperfusion.

摘要

在使用克雷布斯 - 亨泽莱特溶液灌注的离体猫心脏的全心缺血和再灌注过程中,对钙通道阻滞剂硝苯地平进行了研究。将硝苯地平加入储液器中,并以0.1微克/毫升灌注液/小时的速度输注硝苯地平150分钟。在缺血120分钟(血流量为对照的1%)后,心脏先用含硝苯地平的灌注液再灌注20分钟,然后用不含硝苯地平的灌注液再灌注25分钟。在对照心脏中,硝苯地平显著降低了溶酶体蛋白酶组织蛋白酶D的游离活性百分比(P<0.01)。在缺血心脏中,硝苯地平可防止心肌组织水肿增加(P<0.01)、组织蛋白酶D游离活性百分比增加(P<0.02)以及再灌注后肌酸激酶活性增加(P<0.01)。因此,硝苯地平在缺血后再灌注的心肌细胞中表现出膜稳定和细胞保护活性。这些数据表明,钙离子促成了在缺血和再灌注中观察到的溶酶体不稳定和细胞质酶泄漏,并且钙通道阻滞可能在缺血和再灌注期间保护心肌细胞的完整性。

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