Lee J W, Filkins J P
Department of Physiology, Stritch School of Medicine, Loyola University of Chicago, Maywood, Illinois.
Circ Shock. 1988 Feb;24(2):99-110.
The actions of exogenous adenosine triphosphate (ATP) on hepatic hemodynamics were analyzed in the isolated perfused rat liver. The effects of ATP (10, 40, and 160 microM) on hepatic circulatory resistances were determined from changes in portal vein flow, portal vein perfusion pressure, hepatic arterial perfusion pressure, and hepatic capacitance. ATP decreased portal vein flow under conditions of constant perfusion pressure, but it increased portal vein perfusion pressure under constant flow perfusion. ATP increased the resistance of the presinusoidal regions and reduced hepatic capacitance. Adenine derivatives including adenosine, adenosine monophosphate (AMP), adenosine diphosphate (ADP), and ATP also decreased portal vein flow; the order of vascular activity of the adenine compounds was ATP greater than ADP greater than AMP = adenosine. The shock-protective actions of ATP may reflect hepatic hemodynamic adjustments.
在离体灌注大鼠肝脏中分析了外源性三磷酸腺苷(ATP)对肝脏血流动力学的作用。根据门静脉血流量、门静脉灌注压、肝动脉灌注压和肝脏容量的变化,测定了ATP(10、40和160微摩尔)对肝脏循环阻力的影响。在恒定灌注压条件下,ATP可降低门静脉血流量,但在恒定流量灌注时可增加门静脉灌注压。ATP增加了窦前区域的阻力并降低了肝脏容量。包括腺苷、一磷酸腺苷(AMP)、二磷酸腺苷(ADP)和ATP在内的腺嘌呤衍生物也可降低门静脉血流量;腺嘌呤化合物的血管活性顺序为ATP>ADP>AMP = 腺苷。ATP的抗休克作用可能反映了肝脏血流动力学的调节。