首页> 美国卫生研究院文献>Biochemical Journal >Differential control of glycogenolysis and flow by arterial and portal acetylcholine in perfused rat liver.
【2h】

Differential control of glycogenolysis and flow by arterial and portal acetylcholine in perfused rat liver.

机译:灌注大鼠肝脏中动脉和门静脉乙酰胆碱对糖原分解和血流的差异控制。

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

The effects of acetylcholine on glucose and lactate balance and on perfusion flow were studied in isolated rat livers perfused simultaneously via the hepatic artery (100 mmHg, 25-35% of flow) and the portal vein (10 mmHg, 75-65% of flow) with a Krebs-Henseleit bicarbonate buffer containing 5 mM-glucose, 2 mM-lactate and 0.2 mM-pyruvate. Arterial acetylcholine (10 microM sinusoidal concentration) caused an increase in glucose and lactate output and a slight decrease in arterial and portal flow. These effects were accompanied by an output of noradrenaline and adrenaline into the hepatic vein. Portal acetylcholine elicited only minor increases in glucose and lactate output, a slight decrease in portal flow and a small increase in arterial flow, and no noradrenaline and adrenaline release. The metabolic and haemodynamic effects of arterial acetylcholine and the output of noradrenaline and adrenaline were strongly inhibited by the muscarinic antagonist atropine (10 microM). The acetylcholine-dependent alterations of metabolism and the output of noradrenaline were not influenced by the alpha 1-blocker prazosin (5 microM), whereas the output of adrenaline was increased. The acetylcholine-dependent metabolic alterations were not inhibited by the beta 2-antagonist butoxamine (10 microM), although the overflow of noradrenaline was nearly completely blocked and the output of adrenaline was slightly decreased. These results allow the conclusion that arterial, but not portal, acetylcholine caused sympathomimetic metabolic effects, without noradrenaline or adrenaline being involved in signal transduction.
机译:在通过肝动脉(100 mmHg,流量的25-35%)和门静脉(10 mmHg,流量的75-65%)同时灌注的离体大鼠肝脏中,研究了乙酰胆碱对葡萄糖和乳酸平衡以及对血流的影响。 )用含有5 mM葡萄糖,2 mM乳酸盐和0.2 mM丙酮酸盐的Krebs-Henseleit碳酸氢盐缓冲液。动脉乙酰胆碱(10 microM正弦曲线浓度)引起葡萄糖和乳酸盐输出增加,动脉和门脉血流略有减少。这些作用伴随着去甲肾上腺素和肾上腺素向肝静脉输出。门静脉乙酰胆碱仅引起葡萄糖和乳酸输出的少量增加,门静脉血流的轻微降低和动脉血流的少量增加,而没有去甲肾上腺素和肾上腺素的释放。毒蕈碱拮抗剂阿托品(10 microM)强烈抑制了动脉乙酰胆碱的代谢和血液动力学作用以及去甲肾上腺素和肾上腺素的输出。乙酰胆碱依赖的新陈代谢变化和去甲肾上腺素的输出不受α1-受体阻断剂哌唑嗪(5 microM)的影响,而肾上腺素的输出却增加。尽管去甲肾上腺素的溢流几乎完全被阻断并且肾上腺素的输出略有降低,但是β2-拮抗剂丁氧胺(10 microM)并未抑制乙酰胆碱依赖性的代谢改变。这些结果得出这样的结论,即动脉而非门静脉乙酰胆碱引起拟交感神经的代谢作用,而去甲肾上腺素或肾上腺素不参与信号转导。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号