The rat liver microcirculation in alcohol‐induced hepatomegaly
The rat liver microcirculation in alcohol‐induced hepatomegaly
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酒精性肝肿大大鼠肝脏微循环
DOI：
10.1002/hep.1840100608
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发表时间：
1989
期刊：
影响因子：
13.5
通讯作者：
J. Belgiorno
中科院分区：
文献类型：
--
作者：
Ricardo Mastaï;P. Huet;A. Brault;J. Belgiorno
肝细胞增大可导致细胞外空间（窦状隙和间质）受压，诱发门静脉高压。然而，这一假设从未通过测量完整肝脏中的血管和血管外空间来验证。本研究的目的是在离体灌注大鼠肝脏中使用Goresky多指示剂稀释技术研究慢性酒精摄入对肝脏微循环的影响。对同窝雌性大鼠配对饲喂乙醇（n = 7）或等热量碳水化合物饲料（n = 7）21天。正如预期的那样，长期酒精摄入导致肝脏/体重比（+32%，p < 0.01）和肝细胞大小（+45%，p < 0.001）显著增加，同时伴随细胞水空间显著增加（对照：3.3 ± 0.6 ml;乙醇喂养：4.9 ± 0.9 ml; p < 0.001）。当表示每个总肝脏的数据时，两组的窦状隙相似（对照：1.87 ± 0.2;乙醇喂养：1.95 ± 0.2 ml;不显著），而与对照组相比，酒精大鼠的间质隙增加（白蛋白间隙+58%，p < 0.01;蔗糖间隙+51%，p < 0.01）。在酒精性大鼠中，窦状隙可能被拉伸，总体横向直径减小，如数据以每克肝脏重量表示时发现的减小值所示。然而，尽管这一发现和酒精性大鼠中观察到的肝脏和肝细胞的扩大，两组之间的门静脉灌注压和肝内血管阻力的值相似。目前的数据表明，由于慢性酒精摄入导致的肝脏和肝细胞的扩大：（i）不会以牺牲总血管空间为代价而发展，并且意外地增加了间质空间，并且（ii）在我们的实验条件下，不会改变肝脏的整体阻力。
It has been suggested that hepatocyte enlargement can lead to compression of the extracellular space (sinusoidal and interstitial) and induce portal hypertension. However, this hypothesis has never been tested by measuring the vascular and extravascular spaces in the intact liver. The aim of the present study was to investigate the effects of chronic alcohol intake on the hepatic microcirculation using Goresky's multiple‐indicator dilution technique in the isolated perfused rat liver. Female rat littermates were pair‐fed either ethanol (n = 7) or an isocaloric carbohydrate diet (n = 7) for 21 days. As expected, chronic alcohol intake produced a significant increase in liver/body weight ratio (+32%, p < 0.01) and hepatocyte size (+45%, p < 0.001), which was accompanied by a marked increase in the cellular water space (control: 3.3 ± 0.6 ml; ethanol‐fed: 4.9 ± 0.9 ml; p < 0.001). When expressing data per total liver, the sinusoidal space was similar in the two groups (control: 1.87 ± 0.2; ethanol‐fed: 1.95 ± 0.2 ml; not significant), whereas the interstitial space was increased in alcohol rats compared to controls (albumin space +58%, p < 0.01; sucrose space +51%, p < 0.01). In alcoholic rats, the sinusoidal space was probably stretched, with an overall reduced transversal diameter, as suggested by the reduced values found when data were expressed per gm of liver weight. However, despite this finding and the enlargement of the liver and hepatocytes observed in alcoholic rats, similar values were obtained between the two groups for the portal perfusion pressure and thus the intrahepatic vascular resistance. The present data show that the enlargement of the liver and hepatocytes due to chronic alcoholic intake: (i) does not develop at the expense of the total vascular space and unexpectedly increases the interstitial space, and (ii) under our experimental conditions, does not modify the overall resistance of the liver.
酒精喂养狒狒肝硬化前门静脉高压症的发病机制。
影响因子：
29.4
作者：
Miyakawa,H;Iida,S;Leo,MA;Greenstein,RJ;Zimmon,DS;Lieber,CS
通讯作者：
Lieber,CS