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缺血/再灌注后门静脉血中内皮素-1水平与肝组织微循环障碍及肝细胞损伤的关系

Endothelin-1 levels in portal venous blood in relation to hepatic tissue microcirculation disturbance and hepatic cell injury after ischemia/reperfusion.

作者信息

Ota T, Hirai R, Urakami A, Soga H, Nawa S, Shimizu N

机构信息

Second Department of Surgery, Okayama University Medical School, Japan.

出版信息

Surg Today. 1997;27(4):313-20. doi: 10.1007/BF00941805.

DOI:10.1007/BF00941805
PMID:9086547
Abstract

This study was conducted to clarify the role of endothelin-1 in the portal vein after hepatic ischemia/ reperfusion and to ascertain whether it is related to hepatic microcirculation disturbance. Using a canine ischemic liver model, the portal and systemic endothelin-1 levels were measured before ischemia, then after 1 h and 2 h of reperfusion, and comparatively evaluated with the serum levels of GOT and lactic dehydrogenase (LDH). As an indicator of liver tissue microcirculation, tissue blood flow volume (TBF) was also measured in the site subjected to ischemia. The animals were divided into: group 1, which received ischemia for 30 min; group 2, which received ischemia for 60 min; and group 3, which received a sequence repeated four times of 15 min ischemia and 10 min reperfusion. The portal endothelin-1 level became significantly elevated after reperfusion compared to that before ischemia in all groups, being significantly higher in group 2 than in the other groups. The systemic endothelin-1 level also increased after reperfusion; significantly in group 2. The portal endothelin-1 level was generally higher than the systemic level, which again was statistically significant in group 2. After 2 h of reperfusion, a significant positive correlation was found between the portal endothelin-I level and serum LDH, whereas a significant negative correlation was found between the portal endothelin-1 level and TBF. The finding that the portal endothelin-1 level became elevated after hepatic ischemia/reperfusion suggests that it probably plays an essential role in hepatic ischemia/ reperfusion injury by adversely influencing tissue microcirculation.

摘要

本研究旨在阐明内皮素 -1 在肝脏缺血/再灌注后门静脉中的作用,并确定其是否与肝脏微循环障碍有关。使用犬缺血肝脏模型,在缺血前、再灌注1小时和2小时后测量门静脉和全身的内皮素 -1 水平,并与谷草转氨酶(GOT)和乳酸脱氢酶(LDH)的血清水平进行比较评估。作为肝组织微循环的指标,还测量了缺血部位的组织血流量(TBF)。动物被分为:第1组,缺血30分钟;第2组,缺血60分钟;第3组,接受15分钟缺血和10分钟再灌注重复四次的序列。与缺血前相比,所有组再灌注后门静脉内皮素 -1 水平均显著升高,第2组显著高于其他组。再灌注后全身内皮素 -1 水平也升高;第2组显著升高。门静脉内皮素 -1 水平通常高于全身水平,第2组再次具有统计学意义。再灌注2小时后,门静脉内皮素 -I 水平与血清LDH之间存在显著正相关,而门静脉内皮素 -1 水平与TBF之间存在显著负相关。肝脏缺血/再灌注后门静脉内皮素 -1 水平升高的发现表明,它可能通过对组织微循环产生不利影响而在肝脏缺血/再灌注损伤中起重要作用。

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本文引用的文献

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Endothelin A receptor blockade reduces hepatic ischemia/reperfusion injury after warm ischemia in a pig model.内皮素A受体阻断可减轻猪模型热缺血后肝脏缺血/再灌注损伤。
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Plasma endothelin-1 concentrations are elevated in acute hepatitis and liver cirrhosis but not in chronic hepatitis.血浆内皮素-1浓度在急性肝炎和肝硬化中升高,但在慢性肝炎中不升高。
Gastroenterol Jpn. 1993 Oct;28(5):666-72. doi: 10.1007/BF02806347.
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Endothelin-1 induces direct constriction of hepatic sinusoids.内皮素-1可直接引起肝血窦收缩。
Am J Physiol. 1994 Apr;266(4 Pt 1):G624-32. doi: 10.1152/ajpgi.1994.266.4.G624.
7
Endothelin-1 is involved in the pathogenesis of ischemia/reperfusion liver injury by hepatic microcirculatory disturbances.内皮素-1通过肝脏微循环紊乱参与缺血/再灌注肝损伤的发病机制。
Hepatology. 1994 Mar;19(3):675-81. doi: 10.1002/hep.1840190319.
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Hepatology. 1995 Apr;21(4):1138-43.
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Hepatic microcirculatory failure after ischemia and reperfusion: improvement with ATP-MgCl2 treatment.缺血再灌注后肝微循环衰竭:ATP-MgCl2治疗可改善
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