Ethanol-induced increase in portal blood flow: role of adenosine.
Ethanol-induced increase in portal blood flow: role of adenosine.
复制标题
乙醇引起的门静脉血流量增加：腺苷的作用。
DOI：
10.1152/ajpgi.1988.254.4.g495
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Israel,Y
中科院分区：
文献类型：
--
作者：
Orrego,H;Carmichael,FJ;Saldivia,V;Giles,HG;Sandrin,S;Israel,Y
用放射性标记微球研究了乙醇诱导大鼠门静脉血流增加的机制。灌胃乙醇（2 g/kg）可使大鼠门静脉血流增加50 ~ 70%。腺苷受体阻滞剂8-苯基茶碱[乙醇，61.8 +/- 4.1 ml.kg-1.min-1]可抑制乙醇引起的门静脉血流增加；乙醇+ 8-苯基茶碱（0.2 mg.kg-1）。Min-1), 44.2 +/- 2.0 ml.kg-1 Min-1；P < 0.05]。8-苯基茶碱（0.2 mg.kg-1）。Min-1)对心输出量和门静脉血流无影响。腺苷输注导致门静脉血流呈剂量依赖性增加，在0.17 mg.kg-1剂量时效果最大。min-1（对照组41.3 +/- 2.3，腺苷81.7 +/- 8.0 ml.kg-1 min-1, P < 0.05）。这种腺苷诱导的门静脉血流增加被8-苯基茶碱以剂量依赖性的方式抑制[腺苷，81.7 +/- 8.0 ml.kg-1.min-1；腺苷+ 8-苯基茶碱（0.2 mg.kg-1）Min-1), 49.8±6.6 ml.kg-1 min；P < 0.05]。酒精和腺苷分别显著降低门静脉前血管阻力40% （P < 0.02）和60% （P < 0.01）。这些作用被8-苯基茶碱完全抑制。因此，腺苷可能是介导乙醇诱导的门静脉血流增加的候选物质。提示循环乙酸增加和肝脏缺氧可能通过增加组织和间质腺苷水平介导酒精的作用。
The mechanism by which ethanol induces an increase in portal vein blood flow was studied in rats using radiolabeled microspheres. Ethanol (2 g/kg) by gavage resulted in an increase of 50-70% in portal vein blood flow. The ethanol-induced increase in portal blood flow was suppressed by the adenosine receptor blocker 8-phenyltheophylline [ethanol, 61.8 +/- 4.1 ml.kg-1.min-1; ethanol + 8-phenyltheophylline (0.2 mg.kg-1.min-1), 44.2 +/- 2.0 ml.kg-1.min-1; P less than 0.05]. By itself, 8-phenyltheophylline (0.2 mg.kg-1.min-1) was without effect on cardiac output or portal blood flow. Adenosine infusion resulted in a dose-dependent increase in portal blood flow with a maximal effect at a dose of 0.17 mg.kg-1.min-1 (control, 41.3 +/- 2.3; adenosine, 81.7 +/- 8.0 ml.kg-1.min-1; P less than 0.05). This adenosine-induced increase in portal blood flow was inhibited by 8-phenyltheophylline in a dose-dependent manner [adenosine, 81.7 +/- 8.0 ml.kg-1.min-1; adenosine + 8-phenyltheophylline (0.2 mg.kg-1.min-1), 49.8 +/- 6.6 ml.kg-1.min; P less than 0.05]. Both alcohol and adenosine significantly reduced preportal vascular resistance by 40% (P less than 0.02) and 60% (P less than 0.01), respectively. These effects were fully suppressed by 8-phenyltheophylline. It is concluded that adenosine is a likely candidate to mediate the ethanol-induced increase in portal vein blood flow. It is suggested that an increase in circulating acetate and liver hypoxia may mediate the effects of alcohol by increasing tissue and interstitial adenosine levels.