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大鼠饮酒会增强革兰氏阴性脓毒症对肝脏透明质酸摄取的有害影响。

Alcohol consumption in rats potentiates the deleterious effect of gram-negative sepsis on hepatic hyaluronan uptake.

作者信息

Deaciuc I V, McDonough K H, Bagby G J, Spitzer J J

机构信息

Department of Physiology, Louisana State University Medical Center, New Orleans 70112-1393.

出版信息

Alcohol Clin Exp Res. 1993 Oct;17(5):1002-8. doi: 10.1111/j.1530-0277.1993.tb05655.x.

DOI:10.1111/j.1530-0277.1993.tb05655.x
PMID:8279658
Abstract

The role of hepatic sinusoidal endothelial cells (SECs) in the pathologic changes of the liver associated with alcohol consumption is not fully understood. The measurement of hyaluronan (HA) uptake by the SECs provides a useful means for assessing the functional state of these cells. In this study, we determined the effect of acute and chronic exposure to alcohol in rats in the absence and presence of subcutaneous Escherichia coli-induced sepsis on plasma HA concentration and HA uptake by the isolated, perfused liver. Rats were administered ethanol (two doses of 0.2 g/100 g body weight, intraperitoneally, 24 and 15 hr before killing) or fed a liquid diet for 8-10 weeks, containing alcohol (36% of the total calories) or dextrin (in isocaloric amounts). Twenty-one hr before euthanizing for liver perfusion, animals were injected subcutaneously with live E. coli (sepsis) or sterile saline (control). Neither acute nor chronic alcohol exposure by themselves altered plasma HA levels. However, both treatments exacerbated the hyperhyaluronanemic effect of sepsis. Thus, in acutely alcohol-treated rats, sepsis induced a 187% (p < 0.05) increase in plasma levels of HA, whereas in nonalcohol septic rats, the increase was only 54% (p < 0.05). Likewise, sepsis resulted in a greater increase in the plasma levels of HA (871%) in alcohol-fed rats than it did in liquid diet, control-fed rats (323%, p < 0.05). The rate of HA uptake by the isolated, perfused liver was not altered by either acute or chronic alcohol exposure. However, alcohol exposure markedly potentiated the inhibitory effect of sepsis on the capacity of the liver to take up HA.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

肝窦内皮细胞(SECs)在与酒精摄入相关的肝脏病理变化中的作用尚未完全明确。测量SECs对透明质酸(HA)的摄取为评估这些细胞的功能状态提供了一种有用的方法。在本研究中,我们确定了在不存在和存在皮下大肠杆菌诱导的脓毒症的情况下,急性和慢性酒精暴露对大鼠血浆HA浓度以及分离灌注肝脏对HA摄取的影响。给大鼠腹腔注射乙醇(两剂,每100克体重0.2克,在处死前24小时和15小时),或给予含酒精(占总热量的36%)或糊精(等热量)的液体饮食8 - 10周。在对肝脏进行灌注处死前21小时,给动物皮下注射活的大肠杆菌(脓毒症组)或无菌生理盐水(对照组)。单独的急性或慢性酒精暴露均未改变血浆HA水平。然而,两种处理都加剧了脓毒症的高透明质酸血症效应。因此,在急性酒精处理的大鼠中,脓毒症导致血浆HA水平升高187%(p < 0.05),而在非酒精脓毒症大鼠中,升高仅为54%(p < 0.05)。同样,脓毒症导致酒精喂养大鼠血浆HA水平的升高幅度(871%)大于液体饮食对照组大鼠(323%,p < 0.05)。分离灌注肝脏对HA的摄取速率不受急性或慢性酒精暴露的影响。然而,酒精暴露显著增强了脓毒症对肝脏摄取HA能力的抑制作用。(摘要截断于250字)

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