Oldhafer K J, Schüttler W, Lang H, Spiegel H U, Hauss J, Pichlmayr R
Klinik für Abdominal- und Transplantationschirurgie, Medizinischen Hochschule, Hannover.
Zentralbl Chir. 1994;119(5):317-21.
The pathogenesis of the ischemia-/reperfusion injury after liver transplantation is not fully understood. The purpose of this study was to analyse blood flow and vascular resistance of the hepatic artery and the portal vein after long ischemic time.
A model of orthotopic liver transplantation in pigs was used. Two groups with different cold ischemic times (CIT) were formed: group A: short ischemic time (4-6 hrs CIT), 7 transplantations/group B: long ischemic time (20-24 hrs CIT), 7 transplantations. The blood flow was measured by means of electromagnetic technique. The intravascular pressure was determined in the aorta, portal vein and hepatic vein after direct punction or by inserted catheters.
After short ischemic time and 1 hour of reperfusion a decrease of the arterial and portal venous resistance was observed, while the total hepatic blood flow remained constant. Six hours after reperfusion the arterial and portal venous vascular resistance increased and reached almost values of the donor animal. However, marked changes of hemodynamic parameters were found after long ischemic time, especially in the portal venous vascular system. The vascular resistance of the portal vein was significantly elevated and reached values ten-times higher than during the donor operation.
The decrease of the vascular resistance during the early reperfusion period was surprising because of the well-known results of histological studies and analysis of the microcirculation. The cause remained unknown, but an increased perfusion via intrahepatic shunts or denervation of the transplant may be responsible for this observation. The elevated portal venous resistance after severe ischemic damage most likely reflected the increase of interstitial pressure. In the clinic monitoring of the portal venous vascular system by means of doppler-sonography may be an useful adjunct in the diagnosis of early postoperative transplant-dysfunction.
肝移植后缺血/再灌注损伤的发病机制尚未完全明了。本研究的目的是分析长时间缺血后肝动脉和门静脉的血流及血管阻力。
采用猪原位肝移植模型。形成两组不同冷缺血时间（CIT）的组别：A组：短缺血时间（CIT为4 - 6小时），每组7例移植；B组：长缺血时间（CIT为20 - 24小时），每组7例移植。通过电磁技术测量血流。直接穿刺或通过插入导管测定主动脉、门静脉和肝静脉内的压力。
短缺血时间再灌注1小时后，观察到动脉和门静脉阻力降低，而肝总血流量保持恒定。再灌注6小时后，动脉和门静脉血管阻力增加，几乎达到供体动物的水平。然而，长时间缺血后发现血流动力学参数有明显变化，尤其是在门静脉血管系统。门静脉的血管阻力显著升高，达到比供体手术时高10倍的值。
早期再灌注期间血管阻力降低令人惊讶，因为组织学研究和微循环分析的结果是众所周知的。原因尚不清楚，但通过肝内分流增加灌注或移植去神经可能是导致这一观察结果的原因。严重缺血损伤后门静脉阻力升高很可能反映了间质压力的增加。在临床上，通过多普勒超声监测门静脉血管系统可能是诊断术后早期移植功能障碍的有用辅助手段。
