Endotheli-1 Mediates the Alcohol-Induced Reduction of Pancreatic Capillary Blood Flow

被引：18

作者：

Foitzik T. ^{[1
,3
]}

Hotz H.G. ^{[1
]}

Hotz B. ^{[1
]}

Kirchengast M. ^{[1
,2
]}

Buhr H.J. ^{[1
]}

机构：

[1] Department of Surgery, Benjamin Franklin Medical Center, Freie Universität Berlin, Berlin

[2] Knoll AG, Ludwigshafen

[3] Abt. Allgemein, Gefaß T., Klinikum Benjamin Franklin, Freie Universität Berlin, D-12 200 Berlin

来源：

Journal of Gastrointestinal Surgery | 1998年 / 2卷 / 4期

关键词：

Acute Pancreatitis; Gastric Mucosal Injury; Chronic Alcoholic Pancreatitis; Pancreatic Blood Flow; Blood Ethanol Level;

D O I：

10.1016/S1091-255X(98)80078-4

中图分类号：

学科分类号：

摘要：

Increased plasma endothelin-1 (ET-1) levels in rats after alcohol administration and increased endothelin receptor expression in the pancreas in chronic alcoholic pancreatitis have led to the hypothesis that ET-1 may play a critical role in the pathogenesis of ethanol-induced pancreatic injury through impairment of perfusion. To further test the hypothesis that ET-1 mediates an alcohol-induced reduction of pancreatic perfusion, the present study compares the effect of intravenous alcohol and ET-1 on pancreatic capillary blood flow (PCBF) and investigates whether endothelin receptor blockade prevents the alcohol-induced reduction in PCBF. Anesthetized rats were randomly assigned to receive one of the following: a 1-hour infusion of 2 g/kg alcohol or the volume equivalent of saline solution plus ET-1 (1.25 μg/kg), a specific endothelin-A receptor antagonist (50 mg/kg), or saline solution (volume equivalent). The pancreas was exposed for intravital microscopy; PCBF was determined at the same location before the test solutions were given, after the infusion, and 1 hour thereafter. Alcohol and ET-1 significantly decreased PCBF from 2.0 nl/min/cap to 1.7 nl/min/cap. The reduction in PCBF was even more pronounced when alcohol and ET-1 were combined (1.5 nl/min/cap), whereas the ET receptor antagonist increased PCBF in saline-treated rats to 2.2 nl/min cap and maintained stable PCBF in alcohol-treated animals. The observation that PCBF is reduced by both alcohol and ET-1 and that the alcohol-induced reduction of PCBF can be aggravated by ET-1 and prevented by a specific endothelin-1 antagonist supports the hypothesis that ET-1 is the mediator of the alcohol-associated reduction of pancreatic perfusion.

引用

页码：379 / 384

页数：5

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