In isolated perfused rat liver, adenosine infusion (50 microM) led to increases in glucose output and portal pressure and a net K+ release of 3.7 +/- 0.21 mumol/g, which was followed by an equivalent net K+ uptake after cessation of the nucleoside infusion. These effects were accompanied by a transient stimulation of hepatic prostaglandin D2 and thromboxane B2 release. The Ca2+ release observed upon adenosine infusion (50 microM) was 23.5 +/- 5.2 nmol/g, i.e. 10-20% of the Ca2+ release observed with extracellular ATP (50 microM). Indomethacin (10 microM) prevented the adenosine-induced stimulation of glucose output and the increase in portal pressure by 79 and 63% respectively, and completely abolished the stimulation of prostaglandin D2 release. The thromboxane A2 receptor antagonist BM 13.177 (20 microM), the phospholipase A2 inhibitor 4-bromophenacyl bromide (20 microM) and the cyclo-oxygenase inhibitor ibuprofen (50 microM) also decreased the glycogenolytic and vasoconstrictive responses of the perfused rat liver upon adenosine infusion by 50-80%. When the indomethacin inhibition of adenosine-induced prostaglandin D2 release was titrated, a close correlation between prostaglandin D2 release and the metabolic and vascular responses to adenosine was observed. These findings suggest an important role for eicosanoids in mediating the nucleoside responses in the perfused rat liver. Since eicosanoids are known to be formed by non-parenchymal cells in rat liver [Decker (1985) Semin. Liver Dis. 5, 175-190], the present study gives further evidence for an important role of eicosanoids as signal molecules between the different liver cell populations.

译文

:在离体灌流的大鼠肝脏中,腺苷输注(50 microM)导致葡萄糖输出和门脉压力增加,净K释放量为3.7 /-0.21 mumol / g,随后在终止核苷后有相等的净K吸收量输液。这些作用伴随着肝脏前列腺素D2和血栓烷B2释放的短暂刺激。腺苷输注(50 microM)时观察到的Ca2释放为23.5 /-5.2 nmol / g,即细胞外ATP(50 microM)观察到的Ca2释放的10-20%。消炎痛(10 microM)分别阻止了腺苷诱导的葡萄糖输出刺激和门脉压力增加79%和63%,并完全取消了对前列腺素D2释放的刺激。血栓烷A2受体拮抗剂BM 13.177(20 microM),磷脂酶A2抑制剂4-溴苯甲酰溴(20 microM)和环加氧酶抑制剂布洛芬(50 microM)也降低了腺苷输注后灌注肝脏的糖原分解和血管收缩反应。减少了50-80%滴定吲哚美辛对腺苷诱导的前列腺素D2释放的抑制作用时,观察到前列腺素D2释放与对腺苷的代谢和血管反应之间存在密切的相关性。这些发现表明类花生酸在介导灌注大鼠肝脏中的核苷反应中起着重要作用。由于已知类花生酸是由大鼠肝脏中的非实质细胞形成的[Decker(1985)Semin。肝病[5,175-190],本研究为类花生酸作为不同肝细胞群之间的信号分子的重要作用提供了进一步的证据。

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