Orrego H, Carmichael F J, Saldivia V, Giles H G, Sandrin S, Israel Y
Department of Anesthesia, Toronto Western Hospital, Ontario, Canada.
Am J Physiol. 1988 Apr;254(4 Pt 1):G495-501. doi: 10.1152/ajpgi.1988.254.4.G495.
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.
采用放射性微球技术在大鼠中研究了乙醇诱导门静脉血流增加的机制。经口灌胃给予乙醇（2 g/kg）可使门静脉血流增加50% - 70%。乙醇诱导的门静脉血流增加被腺苷受体阻滞剂8 - 苯基茶碱所抑制[乙醇，61.8±4.1 ml·kg⁻¹·min⁻¹；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]。单独使用时，8 - 苯基茶碱（0.2 mg·kg⁻¹·min⁻¹）对心输出量或门静脉血流无影响。输注腺苷导致门静脉血流呈剂量依赖性增加，在剂量为0.17 mg·kg⁻¹·min⁻¹时达到最大效应（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]。乙醇和腺苷分别使门静脉前血管阻力显著降低40%（P＜0.02）和60%（P＜0.01）。这些效应被8 - 苯基茶碱完全抑制。结论是腺苷可能是介导乙醇诱导的门静脉血流增加的介质。提示循环中乙酸盐增加和肝脏缺氧可能通过增加组织和间质腺苷水平来介导酒精的作用。
