Pannen B H, Bauer M, Nöldge-Schomburg G F, Zhang J X, Robotham J L, Clemens M G, Geiger K K
Department of Anesthesiology and Critical Care Medicine, University of Freiburg, Germany.
Am J Physiol. 1997 Jun;272(6 Pt 2):H2736-45. doi: 10.1152/ajpheart.1997.272.6.H2736.
We determined the role of nitric oxide (NO) and endothelins (ETs) in the regulation of hepatic blood flow during resuscitation from hemorrhagic shock (HS) in anesthetized rats. Volume resuscitation restored systemic hemodynamics and increased hepatic arterial and portal venous flow above baseline in the vehicle group. Presence of N omega-nitro-L-arginine methyl ester (L-NAME, 1 mg/kg) during resuscitation increased systemic vascular resistance (SVR) above baseline, prevented the restoration of hepatic arterial flow, and abolished portal hyperemia. Although the ETA+B-receptor antagonist bosentan (10 mg/kg) did not alter the systemic hemodynamic response, it abolished the hepatic arterial and portal hyperemia. The ETA-receptor antagonist BQ-610 (150 micrograms/kg) reduced SVR below baseline, allowed hepatic arterial hyperemia to occur, and further enhanced the portal venous hyperemia. This indicates that 1) NO reduces SVR and acts to preserve hepatic blood flow during resuscitation from HS; 2) ETA-receptor-mediated vasoconstriction counteracts the systemic and portal hemodynamic effects of NO; and 3) simultaneous ETB-receptor stimulation enhances blood flow to the liver and may serve to modulate the ETA-receptor-mediated vasoconstrictive effects of ETs.
我们确定了一氧化氮（NO）和内皮素（ETs）在麻醉大鼠失血性休克（HS）复苏过程中对肝血流调节的作用。容量复苏恢复了全身血流动力学，并使载体组的肝动脉和门静脉血流高于基线水平。复苏期间存在Nω-硝基-L-精氨酸甲酯（L-NAME，1mg/kg）使全身血管阻力（SVR）高于基线水平，阻止了肝动脉血流的恢复，并消除了门静脉充血。尽管ETA+B受体拮抗剂波生坦（10mg/kg）未改变全身血流动力学反应，但它消除了肝动脉和门静脉充血。ETA受体拮抗剂BQ-610（150μg/kg）使SVR低于基线水平，使肝动脉充血发生，并进一步增强了门静脉充血。这表明：1）NO降低SVR，并在HS复苏过程中起到维持肝血流的作用；2）ETA受体介导的血管收缩抵消了NO对全身和门静脉血流动力学的影响；3）ETB受体的同时刺激增强了肝脏血流，并可能起到调节ETs的ETA受体介导的血管收缩作用。
