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在体外,肝动脉灌注调节正常大鼠肝脏肝血窦与肝内分流之间的门静脉血流。

Hepatic arterial perfusion regulates portal venous flow between hepatic sinusoids and intrahepatic shunts in the normal rat liver in vitro.

作者信息

Alexander B, Cottam H, Naftalin R

机构信息

Liver Sciences Unit, Academic Department of Surgery, GKT School of Medicine and Dentistry, St Thomas' Hospital, Lambeth Palace Road, London, SE1 7EH, UK.

出版信息

Pflugers Arch. 2001 Nov;443(2):257-64. doi: 10.1007/s004240100682.

Abstract

Intrahepatic shunts regulate portal venous pressure during periods of acute portal hypertension when the transhepatic portal resistance is momentarily increased in the normal rat liver in vivo. Hepatic arterial inflow may also increase the transhepatic portal resistance and activate intrahepatic shunts. In the present study, the transhepatic portal resistance and the activity of intra-hepatic shunts were measured in vitro and the point of confluence between the hepatic artery and portal vein in the rat determined. Livers of male Sprague-Dawley rats were single-pass, dual-perfused in vitro. Total cessation or diversion of the hepatic arterial inflow to the portal venous vasculature, whilst maintaining total hepatic perfusate flow, decreased intrasinusoidal pressure, increased transhepatic portal venous resistance and opened the portal venous intrahepatic shunts in a manner similar to intraportal injection of 15-microm diameter microspheres. Injections of the microspheres into the hepatic arterial circulation increased hepatic arterial pressure dramatically, consistent with complete occlusion of the arterial vasculature. The intrahepatic shunts are located at a pre-sinusoidal level because no increases were detected in hepatic arterial pressure following intraportal injection of microspheres. The hepatic arterial vasculature, unlike the portal supply, does not possess a collateral shunt circulation and coalesces with the portal vein at an intrasinusoidal location

摘要

在正常大鼠肝脏体内,当经肝门静脉阻力瞬间增加时,肝内分流可在急性门静脉高压期间调节门静脉压力。肝动脉血流也可能增加经肝门静脉阻力并激活肝内分流。在本研究中,在体外测量了经肝门静脉阻力和肝内分流的活性,并确定了大鼠肝动脉与门静脉的汇合点。雄性Sprague-Dawley大鼠的肝脏在体外进行单通道、双灌注。在维持肝脏灌注液总流量的同时,完全停止或转移肝动脉流入门静脉系统的血流,会降低肝窦内压力,增加经肝门静脉阻力,并以类似于门静脉内注射直径15微米微球的方式开放门静脉肝内分流。向肝动脉循环中注射微球会显著增加肝动脉压力,这与动脉血管的完全阻塞一致。肝内分流位于窦前水平,因为门静脉内注射微球后未检测到肝动脉压力升高。与门静脉供应不同,肝动脉血管系统不具有侧支分流循环,而是在肝窦内位置与门静脉汇合。

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