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在离体灌注大鼠肝脏的缺血再灌注损伤中,肝血窦压力升高与早期肝脏重量增加有关。

Increased sinusoidal pressure is associated with early liver weight gain in ischemia-reperfusion injury in isolated perfused rat liver.

作者信息

Ling Y Q, Shibamoto T, Honda T, Kamikado C, Hironaka E, Hongo M, Koyama S

机构信息

Department of Physiology, Division 2, Shinshu University School of Medicine, Matsumoto, 390-8621, Japan.

出版信息

J Surg Res. 2000 Feb;88(2):70-7. doi: 10.1006/jsre.1999.5779.

DOI:10.1006/jsre.1999.5779
PMID:10644470
Abstract

BACKGROUND

Hepatic ischemia-reperfusion (I/R) is accompanied by liver weight gain and ascites formation. This could be caused by an increase in sinusoidal pressure, a determinant of hepatic transvascular fluid movement. We determined the role of sinusoidal pressure, assessed by triple vascular occlusion pressure (P(to)), in the I/R injury in isolated rat livers perfused with leukocyte-free diluted blood bivascularly via the portal vein and hepatic artery.

MATERIALS AND METHODS

Ischemia was induced at room temperature by occlusion of either the inflow lines of the hepatic artery and portal vein (the open outflow group, n = 10) or both the inflow and the outflow (hepatic venous) lines (the closed outflow group, n = 10) for 1 h, followed by 1-h reperfusion in a recirculating manner.

RESULTS

Liver weight in both groups increased biphasically after reperfusion; the initial peak occurred at 3 min and the second peak at 60 min. Immediately after reperfusion, P(to) peaked, followed by a gradual decline. The initial weight increase in groups combined was significantly and positively correlated with an increase in P(to) (r = 0.716, P = 0.0002), but the second peak was independent of P(to). Liver injury, assessed by perfusate levels of hepatic enzymes and reduced bile flow rate, was observed at 60 min after reperfusion in both groups.

CONCLUSIONS

These findings suggest that increased sinusoidal pressure contributes to only the early liver weight gain after reperfusion in isolated perfused rat livers. The late weight gain may be presumably due to liver injury.

摘要

背景

肝缺血再灌注(I/R)伴有肝脏重量增加和腹水形成。这可能是由窦状隙压力升高引起的,窦状隙压力是肝脏跨血管液体流动的一个决定因素。我们通过三重血管闭塞压力(P(to))评估窦状隙压力在经门静脉和肝动脉双血管灌注无白细胞稀释血液的离体大鼠肝脏I/R损伤中的作用。

材料与方法

在室温下,通过闭塞肝动脉和门静脉的流入线(开放流出组,n = 10)或流入线和流出线(肝静脉)(封闭流出组,n = 10)1小时诱导缺血,然后以循环方式再灌注1小时。

结果

两组肝脏重量在再灌注后均呈双相增加;初始峰值出现在3分钟,第二个峰值出现在60分钟。再灌注后立即P(to)达到峰值,随后逐渐下降。两组合并后的初始体重增加与P(to)升高显著正相关(r = 0.716,P = 0.0002),但第二个峰值与P(to)无关。两组在再灌注60分钟时均观察到肝损伤,通过灌注液中肝酶水平和胆汁流速降低来评估。

结论

这些发现表明,窦状隙压力升高仅导致离体灌注大鼠肝脏再灌注后早期肝脏重量增加。后期体重增加可能推测是由于肝损伤。

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