Ezzat W R, Lautt W W
Am J Physiol. 1987 Apr;252(4 Pt 2):H836-45. doi: 10.1152/ajpheart.1987.252.4.H836.
Pressure-flow autoregulation, although weak, was seen in the hepatic artery (HA) of every cat that also showed dilation to infused adenosine. Several means of quantitating autoregulation are described and evaluated, and all indices showed that the selective adenosine antagonists, 8-phenyltheophylline and 8-(p-sulfophenyl)theophylline, inhibited autoregulation as well as the vasodilator response to exogenous adenosine and the hepatic arterial buffer response (HABR; vasodilation of HA in response to reduced portal flow). The mechanism of HABR is proposed to be dependent on washout of locally produced adenosine into portal blood; reduced portal flow causes adenosine accumulation and dilation of HA. The present data suggest that local levels of adenosine can also be washed into HA blood so that reduced arterial flow will also lead to raised adenosine levels and arterial vasodilation. Thus the mechanisms of the HABR and HA pressure-flow autoregulation are suggested to be the same, i.e., washout of locally produced adenosine, probably from the space of Mall just prior to entry of the vessels into sinusoids.
压力-流量自动调节功能虽然较弱,但在每只对注入腺苷有扩张反应的猫的肝动脉(HA)中都能观察到。文中描述并评估了几种量化自动调节的方法,所有指标均显示,选择性腺苷拮抗剂8-苯基茶碱和8-(对磺基苯基)茶碱既能抑制自动调节功能,又能抑制对外源性腺苷的血管舒张反应以及肝动脉缓冲反应(HABR;HA对门静脉血流减少的血管舒张反应)。HABR的机制被认为依赖于局部产生的腺苷被冲刷到门静脉血中;门静脉血流减少会导致腺苷积累和HA扩张。目前的数据表明,局部腺苷水平也可以被冲刷到HA血液中,因此动脉血流减少也会导致腺苷水平升高和动脉血管舒张。因此,HABR和HA压力-流量自动调节的机制被认为是相同的,即局部产生的腺苷被冲刷,可能是在血管进入窦状隙之前从Mall间隙冲刷出来的。