Niiya T, Murakami M, Aoki T, Murai N, Shimizu Y, Kusano M
Second Department of Surgery, School of Medicine, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8666, Japan.
J Hepatobiliary Pancreat Surg. 1999;6(3):275-80. doi: 10.1007/s005340050118.
The mechanisms whereby hepatocytes in the normal liver can be primed for replication following partial hepatectomy (PHx) are poorly understood. To determine whether "shear stress," which is induced by acute portal hypertension after PHx, is involved in liver regeneration, we studied liver regeneration in rats with splenic transposition (SPT) in which we can minimize the postoperative elevation of portal pressure. Rats underwent 70% PHx following splenic transposition or sham surgery and were killed at various time points to measure portal pressure and other factors. In the control groups, the portal pressure was significantly increased immediately after surgery, peaking at 48 h, and returning to near the preoperative levels by 168 h after PHx. In the SPT group, although portal pressure increased immediately, it decreased to the control levels 6 h after PHx and thereafter repeatedly increased. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels peaked at 24 and 6 h after PHx, respectively. Proliferative cell analysis was done using MIB-5 antibody, and there were no significant differences between the two groups. Furthermore, liver weight was restored in the same way in both groups. Taken together, the results suggest that an immediate increase in portal pressure is necessary for the initiation of liver regeneration.
正常肝脏中的肝细胞在部分肝切除术后能够被启动进行复制的机制目前仍知之甚少。为了确定部分肝切除术后急性门静脉高压所诱导的“剪切应力”是否参与肝脏再生，我们研究了脾转位（SPT）大鼠的肝脏再生情况，在这种情况下我们可以将术后门静脉压力的升高降至最低。大鼠在脾转位或假手术后接受70%的部分肝切除术，并在不同时间点处死以测量门静脉压力和其他因素。在对照组中，术后门静脉压力立即显著升高，在48小时达到峰值，并在部分肝切除术后168小时恢复到术前水平附近。在脾转位组中，尽管门静脉压力立即升高，但在部分肝切除术后6小时降至对照水平，此后反复升高。肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）水平分别在部分肝切除术后24小时和6小时达到峰值。使用MIB-5抗体进行增殖细胞分析，两组之间没有显著差异。此外，两组肝脏重量均以相同方式恢复。综上所述，结果表明门静脉压力的立即升高是肝脏再生启动所必需的。
