Li X, Benjamin I S, Naftalin R, Alexander B
Liver Sciences Unit, Academic Department of Surgery, St Thomas's Hospital, Guy's, King's, and St Thomas's School of Medicine, London, UK.
Gut. 2003 Sep;52(9):1339-46. doi: 10.1136/gut.52.9.1339.
In the present study we determined the proportion of shunt flow due to patent intrahepatic portal systemic shunts in the normal rat liver and its relationship with microsphere induced portal hypertension.
Systemic and hepatic haemodynamics were measured continuously before, during, and after intraportal injection of 15 micro m diameter microspheres in anaesthetised male Wistar rats. Functional hepatic blood flow and intrahepatic shunt flow were determined by the use of constant intraportal infusion of sorbitol and simultaneous measurements in the portal vein, hepatic vein, and carotid artery. The percentage of large shunts of diameter >15 micro m were estimated by intraportal injection of (51)Cr labelled 15 micro m diameter microspheres.
Hepatic sorbitol uptake was 97.9 (0.5)% in normal control rats, with functional hepatic blood flow equalling total hepatic blood flow (2.52 (0.23) ml/min/100 g body weight). Microsphere injection decreased sorbitol uptake to 12.8 (4.3)% and further to 4.1 (0.7)% when followed by hepatic arterial ligation. In the latter two groups, intrahepatic shunt flow (1.46 (0.15) and 1.16 (0.19) ml/min/100 g body weight, respectively) was not significantly different from portal venous flow (1.36 (0.20) and 1.20 (0.20) ml/min/100 g body weight, respectively). Portal venous flow remained at 70% of basal values and portal venous pressure only increased by 50% from baseline. (51)Cr labelled microsphere shunt fraction through large shunts (>15 micro m) was less than 1.0%.
The site of confluence between the hepatic artery and portal vein is in zone II. Intrahepatic shunts originate in presinusoidal regions in zone I in the normal liver and, when activated by intraportal injection of microspheres, divert 70% of the total portal blood flow away from zone III and thereby reduce acute increases in portal venous pressure.
在本研究中，我们测定了正常大鼠肝脏中因肝内门体分流开放导致的分流量及其与微球诱导的门静脉高压的关系。
在麻醉的雄性Wistar大鼠门静脉内注射直径15μm的微球之前、期间和之后，连续测量全身和肝脏血流动力学。通过持续门静脉输注山梨醇并同时测量门静脉、肝静脉和颈动脉来测定功能性肝血流量和肝内分流量。通过门静脉内注射（51）Cr标记的直径15μm的微球来估计直径>15μm的大分流的百分比。
正常对照大鼠肝脏山梨醇摄取率为97.9（0.5）%，功能性肝血流量等于肝脏总血流量（2.52（0.23）ml/min/100g体重）。微球注射后，山梨醇摄取率降至12.8（4.3）%，肝动脉结扎后进一步降至4.1（0.7）%。在后两组中，肝内分流量（分别为1.46（0.15）和1.16（0.19）ml/min/100g体重）与门静脉血流量（分别为1.36（0.20）和1.20（0.20）ml/min/100g体重）无显著差异。门静脉血流量维持在基础值的70%，门静脉压力仅比基线升高50%。通过大分流（>15μm）的（51）Cr标记微球分流分数小于1.0%。
肝动脉和门静脉的汇合部位在Ⅱ区。正常肝脏中肝内分流起源于Ⅰ区的窦前区域，当通过门静脉内注射微球激活时，将70%的门静脉总血流量从Ⅲ区转移，从而减少门静脉压力的急性升高。
