Huet P M, Du Reau A, Marleau D
Gut. 1979 Sep;20(9):792-6. doi: 10.1136/gut.20.9.792.
The uptake of (125)I albumin microaggregates (U-(125)I-AMA) from portal blood, during a single passage through the hepatic reticuloendothelial system, has been found to be generally decreased in cirrhosis. To investigate if a similar phenomenon occurs for the colloid flowing through the hepatic artery, the U-(125)I-AMA was first calculated in normal dogs after injection of a mixture of (51)Cr red blood cells ((51)Cr-RBC) and (125)I-AMA into the hepatic artery by comparing hepatic indicator dilution curves (IDC) obtained with both indicators. In nine dogs, the U-(125)I-AMA from hepatic artery blood was generally over 90%, as previously reported for the same colloid flowing through the portal vein in another group of normal dogs. This approach was then applied in nine patients with alcoholic cirrhosis who underwent combined umbilicoportal vein, hepatic vein, and hepatic artery catheterisation because of severe portal hypertension. Hepatic indicator dilution curves were obtained in the nine patients after injection of a mixture of (51)Cr-RBC and (125)I-AMA into the portal vein and the hepatic artery. The U-(125)I-AMA from portal and hepatic artery blood was measured by comparing (51)Cr-RBC and (125)I-AMA hepatic IDC. U-(125)I-AMA varied between 5.2 and 90.5% after portal vein injection and between 13.7 and 90.1% after hepatic artery injection; not difference was found between paired values. In all patients the extraction of indocyanine green (E-ICG) was calculated during a continuous infusion and significant correlations were found between E-ICG and U-(125)I-AMA from portal blood (r=0.931; p <0.001) or from hepatic artery blood (r=0.861; p <0.005). The decreased uptakes can be related to intrahepatic shunts or sinusoidal changes responsible for ineffective phagocytosis and restricted access of dye to parenchymal cells. These data indicate that in cirrhosis the hepatic artery and portal vein blood is cleared of colloid and ICG in a similar fashion and suggest nearly identical blood supply to the regenerative nodules by the hepatic artery and portal vein. Thus U-(125)I-AMA from hepatic artery or portal vein blood, as well as the E-ICG, may be used to estimate the functional hepatic blood supply in cirrhosis; this may prove to be useful in the prognosis of patients before portacaval shunts.
研究发现，在单次通过肝网状内皮系统期间，肝硬化患者门静脉血中（125）I 白蛋白微聚体（U-（125）I-AMA）的摄取通常会降低。为了研究流经肝动脉的胶体是否也会出现类似现象，首先在正常犬中，通过比较用两种示踪剂获得的肝脏指示剂稀释曲线（IDC），在向肝动脉注射（51）Cr 红细胞（（51）Cr-RBC）和（125）I-AMA 的混合物后计算 U-（125）I-AMA。在9只犬中，肝动脉血中的 U-（125）I-AMA 通常超过90%，这与先前在另一组正常犬中报道的流经门静脉的相同胶体的情况一致。然后将该方法应用于9例因严重门静脉高压而接受脐门静脉、肝静脉和肝动脉联合插管的酒精性肝硬化患者。在向门静脉和肝动脉注射（51）Cr-RBC 和（125）I-AMA 的混合物后，在这9例患者中获得肝脏指示剂稀释曲线。通过比较（51）Cr-RBC 和（125）I-AMA 的肝脏 IDC 来测量门静脉和肝动脉血中的 U-（125）I-AMA。门静脉注射后 U-（125）I-AMA 在5.2%至90.5%之间，肝动脉注射后在13.7%至90.1%之间；配对值之间未发现差异。在所有患者中，在持续输注期间计算吲哚菁绿提取率（E-ICG），并且发现 E-ICG 与门静脉血中的 U-（125）I-AMA（r = 0.931；p <0.001）或肝动脉血中的 U-（125）I-AMA（r = 0.861；p <0.005）之间存在显著相关性。摄取减少可能与肝内分流或窦状隙变化有关，这些变化导致吞噬作用无效以及染料进入实质细胞受限。这些数据表明，在肝硬化中，肝动脉血和门静脉血以相似的方式清除胶体和 ICG，并提示肝动脉和门静脉对再生结节的血液供应几乎相同。因此，肝动脉血或门静脉血中的 U-（125）I-AMA 以及 E-ICG 可用于估计肝硬化患者的功能性肝血供；这可能在门腔分流术前患者的预后评估中有用。
