Fujita Y, Takaori M
Department of Anesthesiology, Kawasaki Medical School, Kurashiki.
Masui. 1991 Feb;40(2):166-78.
Hepatic artery blood flow changes to buffer portal blood flow alterations, maintaining a constant total hepatic blood flow. Portal blood flow is regulated by preportal organs, such as intestine, pancreas and spleen. The liver plays an important role as a blood reservoir for cardiovascular homeostasis. Hepatic blood volume is mobilized actively to the systemic circulation by sympathetic stimulation. Sinusoid, the specialized capillary of the liver, and Disse's space are separated by endothelial cells, which have numerous fenestrations, allowing effective exchanges of solutes between hepatocytes and blood. Unidirectional blood flow in the acinus causes functional differences of hepatocytes according to the lobular zones. Although the majority of anesthetics decreases liver blood flow in a dose dependent manner, halothane inhibits hepatic arterial buffer response, while isoflurane and narcotics preserve it. Energy depletion, cellular acidosis, alteration of calcium homeostasis and superoxide-induced membrane damage, are all implicated as important factors for ischemia-induced liver injury. A better understanding of ischemia-induced derangements of cell function will lead to more rational preservation of the liver cells in the future.
肝动脉血流发生变化以缓冲门静脉血流改变，从而维持肝脏总血流量恒定。门静脉血流受门静脉前器官（如肠、胰腺和脾脏）调节。肝脏作为心血管稳态的血库发挥着重要作用。肝血容量通过交感神经刺激被积极动员至体循环。肝血窦是肝脏的特殊毛细血管，狄氏间隙与肝血窦由内皮细胞分隔，内皮细胞有许多窗孔，允许肝细胞与血液之间有效进行溶质交换。肝腺泡内的单向血流导致肝细胞根据小叶区域产生功能差异。尽管大多数麻醉剂以剂量依赖方式减少肝血流量，但氟烷会抑制肝动脉缓冲反应，而异氟烷和麻醉性镇痛药则可保留该反应。能量耗竭、细胞酸中毒、钙稳态改变以及超氧化物诱导的膜损伤，均被认为是缺血性肝损伤的重要因素。更好地理解缺血引起的细胞功能紊乱将有助于未来更合理地保护肝细胞。
