Control of hepatic carbohydrate metabolism and haemodynamics in perfused rat liver by arterial and portal angiotensin II
Control of hepatic carbohydrate metabolism and haemodynamics in perfused rat liver by arterial and portal angiotensin II
复制标题
动脉和门静脉血管紧张素 II 对灌注大鼠肝脏中肝脏碳水化合物代谢和血流动力学的控制
DOI：
10.1097/00042737-199603000-00017
复制
发表时间：
1996
影响因子：
2.1
通讯作者：
A. Gardemann
中科院分区：
文献类型：
--
作者：
Frank Reisenleiter;N. Katz;A. Gardemann
设计：血管紧张素II （All； 0.2、5和25 nM）通过肝动脉和门静脉（门脉或动脉All）单次灌注大鼠肝脏。输注发生在at1受体拮抗剂氯沙坦（1 μ m和10μM）不存在和存在的情况下。代谢：动脉和门脉均增加葡萄糖输出和转移乳酸吸收释放。门脉All在增加肝脏葡萄糖释放方面的效果是动脉All的3倍（0.2 nM）和1.5倍（5和25 nM）。然而，0.2,5和25 nM的动脉和门户应用All在转换乳酸摄取到释放方面具有相似的效率水平。然而，添加1 μM氯沙坦（一种at1受体拮抗剂）可强烈抑制动脉和门脉的代谢改变，并被10μM氯沙坦完全阻断。血流动力学：动脉和门静脉均在相同程度上减少了同侧血管的流量，两者均表现出相似的动力学。中高水平的动脉和门静脉均引起对侧血管明显的血流改变。1 μM氯沙坦的存在强烈抑制了动脉和门静脉血流的全依赖性减少，并被10μM氯沙坦阻断。结果：结果表明，动脉和门脉均引起肝脏代谢的改变，表现出明显（葡萄糖平衡）或无（乳酸平衡）差异，产生类似的同侧血流减少，以及对侧血流明显而复杂的调节。
Design: Angiotensin II (All; 0.2, 5 and 25 nM) was infused during a single-pass perfusion of a rat liver via both the hepatic artery and the portal vein (portal or arterial All). Infusion occurred both in the absence and in the presence of the AT1-receptor-antagonist losartan (1 and 10μM). Metabolism: Arterial and portal All increased glucose output and shifted lactate uptake to release. Portal All was 3 (0.2 nM) and 1.5 times (5 and 25 nM) more effective in increasing hepatic glucose release than similar levels of arterial All. However, 0.2, 5 and 25 nM of arterially and portally applied All had a similar level of efficiency in switching lactate uptake to release. The metabolic alterations by arterial and portal All were, however, strongly inhibited by the addition of 1 μM losartan (an AT1-receptor-antagonist) and completely blocked by the presence of 10μM losartan. Haemodynamics: Arterial and portal All decreased the flow in the ipsilateral vessels to a similar extent, both demonstrating similar kinetics. Medium and high levels of arterial and portal All caused pronounced flow alterations of the contralateral vessels. The All-dependent reductions of arterial and portal flow were strongly inhibited by the presence of 1 μM losartan and were stopped by 10μM of this blocker. Results: The results demonstrate that arterial and portal All caused alterations in the hepatic metabolism, demonstrating either clear (glucose balance) or no (lactate balance) differences, produced similar reductions of the ipsilateral flow, and pronounced and complex modulations of the contralateral flow.