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正常和肝硬化大鼠肝脏的肝动脉和门静脉血管形成

Hepatic artery and portal vein vascularization of normal and cirrhotic rat liver.

作者信息

Kassissia I, Brault A, Huet P M

机构信息

Centre de Recherche Clinique André-Viallet, Hôpital Saint-Luc, Montreal, Quebec, Canada.

出版信息

Hepatology. 1994 May;19(5):1189-97.

PMID:8175141
Abstract

The hepatic artery and portal vein vascularization of seven normal and seven cirrhotic rats was evaluated by means of the multiple-indicator dilution technique using the flow-limited model analysis. Injected 15-micron microspheres were all trapped by the liver in normal and cirrhotic rats after portal vein and hepatic artery injections, ruling out the presence of intrahepatic shunts larger than 15 microns. The albumin curve was linearly displaced relative to the red blood cell curve in both groups of rats, indicating that albumin distribution remained compatible with the flow-limited distribution model. Albumin extravascular space was similar when measured following both routes of injection. Sucrose outflow profile was also compatible with the flow-limited model after portal vein injection in normal rats, but not in severely cirrhotic rats. In contrast, after hepatic artery injection in both normal and cirrhotic rats the sucrose curve was not linearly displaced compared with that of red blood cells; its curve peak was less delayed than its downslope. This finding indicates that, after hepatic artery injection, sucrose distribution was not compatible with the flow-limited model; moreover, its extravascular space was much larger than that after portal vein injection, particularly in cirrhotic rats. This phenomenon is best explained by the peribiliary capillary plexus, lying between terminal arteries and sinusoids, a plexus enlarged in cirrhotic livers. Finally, sinusoidal volume was apparently much larger after hepatic arterial injection compared with that after portal venous injection. This occurrence may well result from an unshared arterial sinusoidal bed or the peribiliary capillary plexus.

摘要

采用多指标稀释技术并运用流量限制模型分析,对7只正常大鼠和7只肝硬化大鼠的肝动脉和门静脉血管化情况进行了评估。在正常大鼠和肝硬化大鼠中,经门静脉和肝动脉注射后,注入的15微米微球均被肝脏捕获,排除了存在大于15微米的肝内分流。两组大鼠中白蛋白曲线相对于红细胞曲线呈线性位移,表明白蛋白分布仍符合流量限制分布模型。经两种注射途径测量时,白蛋白血管外间隙相似。正常大鼠经门静脉注射后,蔗糖流出曲线也符合流量限制模型,但严重肝硬化大鼠不符合。相反,在正常大鼠和肝硬化大鼠经肝动脉注射后,蔗糖曲线与红细胞曲线相比未呈线性位移;其曲线峰值的延迟程度小于下降斜率。这一发现表明,经肝动脉注射后,蔗糖分布不符合流量限制模型;此外,其血管外间隙比经门静脉注射后大得多,尤其是在肝硬化大鼠中。这种现象最好用位于终末动脉和肝血窦之间的胆小管周围毛细血管丛来解释,该丛在肝硬化肝脏中会扩大。最后,与经门静脉注射后相比,经肝动脉注射后肝血窦容积明显大得多。这种情况很可能是由未共享的动脉肝血窦床或胆小管周围毛细血管丛导致的。

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