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乙醇对人脐静脉中前列环素、血栓素和前列腺素E生成的影响。

Effect of ethanol on prostacyclin, thromboxane, and prostaglandin E production in human umbilical veins.

作者信息

Randall C L, Saulnier J L

机构信息

Department of Psychiatry, Medical University of South Carolina, Charleston 29425, USA.

出版信息

Alcohol Clin Exp Res. 1995 Jun;19(3):741-6. doi: 10.1111/j.1530-0277.1995.tb01576.x.

DOI:10.1111/j.1530-0277.1995.tb01576.x
PMID:7573802
Abstract

The purpose of this study was to determine the effects of ethanol on prostacyclin (PGI2), prostaglandin E (PGE), and thromboxane (TXA2) production in perfused human umbilical veins. PGI2, PGE, and TXA2 levels were measured from human umbilical veins perfused with either 25, 50, or 100 mM ethanol by radioimmunoassay of their stable metabolites. Alcohol content was measured by an enzymatic spectrophotometric assay. Data were analyzed by ANOVA and Fisher's Protected Least Significant Difference Test. Ethanol decreased PGI2 production in a concentration-dependent manner (p < 0.05). In a concentration of 25 mM, ethanol did not affect PGI2 production, whereas 50 mM decreased levels after 60 min of perfusion (p < 0.01). With 100 mM ethanol, PGI2 production was decreased after 15, 30, and 60 min of perfusion (ps < 0.05), and the TXA2/PGI2 ratio was significantly elevated at all time points (p < 0.01). Ethanol (100 mM) did not affect TXA2 or PGE production. Reduction of PGI2 levels and the increase in the TXA2/PGI2 ratio seen after ethanol perfusion in umbilical veins may cause vascular disruption in the umbilical-placental circulation. This may, in part, be a contributing mechanism to the teratogenic effects of ethanol.

摘要

本研究的目的是确定乙醇对灌注人脐静脉中前列环素(PGI2)、前列腺素E(PGE)和血栓素(TXA2)生成的影响。通过对其稳定代谢产物进行放射免疫测定,测量用25、50或100 mM乙醇灌注的人脐静脉中的PGI2、PGE和TXA2水平。通过酶促分光光度法测定酒精含量。数据采用方差分析和Fisher保护最小显著差异检验进行分析。乙醇以浓度依赖性方式降低PGI2生成(p < 0.05)。在25 mM浓度下,乙醇不影响PGI2生成,而在50 mM浓度下,灌注60分钟后水平降低(p < 0.01)。使用100 mM乙醇时,灌注15、30和60分钟后PGI2生成降低(ps < 0.05),并且在所有时间点TXA2/PGI2比值均显著升高(p < 0.01)。乙醇(100 mM)不影响TXA2或PGE生成。乙醇灌注脐静脉后PGI2水平降低以及TXA2/PGI2比值升高可能导致脐 - 胎盘循环中的血管破坏。这可能部分是乙醇致畸作用的一个促成机制。

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Alcohol Clin Exp Res. 1995 Jun;19(3):741-6. doi: 10.1111/j.1530-0277.1995.tb01576.x.
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