Richardson P D, Withrington P G
Pflugers Arch. 1978 Dec 28;378(2):135-40. doi: 10.1007/BF00584446.
The sympathetically-innervated hepatic arterial and portal venous vascular beds of the dog were perfused simultaneously in situ. Glucagon was infused into the hepatic portal vein (1--10 microgram/min); it caused increases in hepatic portal vascular resistance and tended to reduce the hepatic arterial vascular resistance. Extrahepatic effects of intraportal infusions of glucagon included increases in superior mesenteric blood flow and heart rate and falls in systemic arterial pressure. A test dose of noradrenaline (10 microgram) injected into either the hepatic artery or the portal vein caused both hepatic arterial and portal venous vasoconstriction. The hepatic arterial constrictor responses to noradrenaline were antagonized by intraportal infusions of glucagon. In contrast, intraportal glucagon did not antagonize the portal constrictor responses to intraarterial or intraportal noradrenaline. Elevated portal blood glucagon concentrations may "protect" the hepatic arterial blood flow from vasoconstriction due to elevated systemic levels of vasoactive substances including catecholamines.
在原位同时灌注狗的受交感神经支配的肝动脉和门静脉血管床。将胰高血糖素注入肝门静脉(1 - 10微克/分钟);它导致肝门静脉血管阻力增加,并倾向于降低肝动脉血管阻力。门静脉内注入胰高血糖素的肝外效应包括肠系膜上血流量增加、心率加快和体循环动脉压下降。向肝动脉或门静脉注射一剂测试剂量的去甲肾上腺素(10微克)会导致肝动脉和门静脉血管收缩。门静脉内注入胰高血糖素可拮抗肝动脉对去甲肾上腺素的收缩反应。相比之下,门静脉内的胰高血糖素并不拮抗门静脉对动脉内或门静脉内去甲肾上腺素的收缩反应。门静脉血中胰高血糖素浓度升高可能会“保护”肝动脉血流量免受包括儿茶酚胺在内的血管活性物质全身水平升高所致的血管收缩影响。