“肝脏反馈机制”并非门脉高压症高动力循环的发生机制

Liver feedback mechanism is not the pathogenesis of hyperdynamic circulatory state in portal hypertension

观察“肝脏反馈机制”在门脉高压症（PHT）内脏高动力循环发生过程中的作用，检测了门静脉分支结扎（PBL）大鼠和门静脉缩窄肝前型PHT（PVL）大鼠不同时期的血流动力学变化，结果显示：PBL术后7天由于门静脉阻力增加，门静脉压力出现一过性增高；第5、7天出现类似于PVL大鼠的短暂的全身高动力循环状态；整个实验过程中，尽管PBL大鼠部分肝脏失去了门静脉血供，但未发现象PVL大鼠所表现的内脏血管阻力下降和门静脉引流区域内脏血流量增加这一内脏高动力循环状态。因此我们认为，PHT时内脏高动力循环状态并非缺血的肝脏组织发挥其局部反馈机制的结果，PBL大鼠短暂的全身高动力循环状态可能与肝脏尚未完全增生肝功能受损有关。

To investigate the role of a feedback mechanism from liver in the development of splanchnic hyperdynamic circulation in portal hypertension (PHT), chronological changes in hemodynamics in rats after ligation of a major branch of the portal vein (PBL)and rats with PHT induced by partial ligation of the protal vein(PVL)were examined. The results showed that 7 days after PBL, the portal pressure elevated transiently because of an increased portal resistance. On the fifth and seventh days, transient hyperdynamic changes similar to that of PVL rats in the systemic circulation occured in PBL rats; the splanchnic hypenlynamic circulation in PVL rats characteriaed by reduced splanchnic vasistance and markedly increased portal venous inflow was never found in PBL rats in the experiment, despite the fact that a lop portion of the liver was lacking portal blood. From these results it was concluded that the splanchnic hyperemia found in PHT is unlikely to be caused by a feedback mechanism from the ischemic hepatic parenchyma. The transient development of systemic hyperdynamic circulation in PBL rats may be related to impaired hepatic function because of incomplete hypertrophy of the perfused lobes.