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钙通道阻滞剂硝苯地平对犬肝脏缺血的影响。

The effect of nifedipine, a calcium channel blocker, on liver ischemia in dogs.

作者信息

Yoshimi F, Ishimaru M, Sodeyama M, Nagao T, Kawano N, Morioka Y

机构信息

Surgical Department, Faculty of Medicine, University of Tokyo, Japan.

出版信息

Jpn J Surg. 1988 Jan;18(1):84-92. doi: 10.1007/BF02470851.

Abstract

This study was undertaken in order to determine whether the administration of nifedipine, a calcium channel blocker, could protect the liver from ischemic damage and to investigate its effect on the hepatic cellular energy status and cardio-vascular system after 60 minutes of hepatic ischemia in dogs. The ischemia was induced by temporarily clamping the portal vein and hepatic artery. One group of animals (n = 17) received nifedipine (5 micrograms/kg body weight) intravenously 15 minutes before the induction of liver ischemia, which was continued at a dose of 0.2 microgram/kg body weight/min throughout the ischemic period, and for an additional 30 minutes afterwards. Control dogs (n = 16) were not given nifedipine and survival was observed over seven days. The survival rate was 83 per cent in the nifedipine treated animals and 0 per cent in the control animals. Serum glutamic oxaloacetic transaminase levels were greatly increased following ischemia, and they were significantly lowered with the nifedipine treatment. The hepatic energy charge decreased remarkably during the hepatic ischemia, however it increased gradually after declamping but did not returned to its preoperative value in either group until one hour later and then it was higher in the nifedipine treated animals than in the control animals. Cardiac index and portal venous blood flow ratio remained higher in the nifedipine treated animals than in the control animals, after the ischemic period. These results suggest that nifedipine may have a powerful cytoprotective effect and that the period of warm hepatic ischemia could be prolonged with its use.

摘要

本研究旨在确定钙通道阻滞剂硝苯地平的给药是否能保护肝脏免受缺血损伤,并研究其对犬肝脏缺血60分钟后肝细胞能量状态和心血管系统的影响。缺血是通过暂时夹闭门静脉和肝动脉诱导的。一组动物(n = 17)在肝脏缺血诱导前15分钟静脉注射硝苯地平(5微克/千克体重),在整个缺血期以0.2微克/千克体重/分钟的剂量持续给药,并在缺血后额外给药30分钟。对照犬(n = 16)未给予硝苯地平,并观察7天的存活率。硝苯地平治疗组动物的存活率为83%,对照组动物的存活率为0%。缺血后血清谷草转氨酶水平大幅升高,而硝苯地平治疗可使其显著降低。肝脏缺血期间肝脏能量电荷显著下降,然而夹闭解除后逐渐升高,但两组直到1小时后才恢复到术前值,且硝苯地平治疗组动物的能量电荷高于对照组动物。缺血期后,硝苯地平治疗组动物的心脏指数和门静脉血流比仍高于对照组动物。这些结果表明,硝苯地平可能具有强大的细胞保护作用,使用它可以延长肝脏热缺血时间。

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