Takeshita K, Ishibashi H, Suzuki M, Kodama M
First Department of Surgery, Shiga University of Medical Science, Japan.
Cell Transplant. 1993 Jul-Aug;2(4):319-24. doi: 10.1177/096368979300200414.
The function of transplanted hepatocytes in acute ischemic liver failure was studied in an experimental model using rats. Ischemic liver failure was induced by occlusion of the proximal portal vein and hepatic artery immediately following extracorporeal portofemoral venous bypass. All rats were bred in a closed colony. Rats in Group 1 were untreated and served as controls (n = 10). Rats in Group 2 received an intrasplenic transplant of hepatocytes (1 x 10(7) cells) 48 h before liver ischemia (n = 10). Serum ammonia and blood glucose were measured before, and 1 h after, ischemia. Serum ammonia was significantly higher than normal (Group 1, 930 micrograms/dL vs < 110 micrograms/dL) after liver ischemia. On the other hand, serum ammonia in group 2 also was elevated (355 micrograms/dL), but significantly less so than in Group 1 (p < 0.001). Blood glucose was lower in both groups after liver ischemia, compared to normal (50-100 mg/dL), but it was higher in Group 2 (30 mg/dL) than in Group 1 (14 mg/dL, p < 0.01). Liver histology 1 h after ischemia showed similar degrees of necrosis in the two groups. Transplanted hepatocytes were viable, and clearly identified in the splenic parenchyma after ischemia. Intrasplenic transplanted hepatocytes provide temporary metabolic support of acute ischemic liver failure in rats, as reflected by enhanced ammonia removal and gluconeogenesis.
在一个使用大鼠的实验模型中，对移植肝细胞在急性缺血性肝衰竭中的功能进行了研究。通过在体外股静脉转流术后立即结扎门静脉近端和肝动脉来诱导缺血性肝衰竭。所有大鼠均饲养在一个封闭的种群中。第1组大鼠未接受治疗，作为对照组（n = 10）。第2组大鼠在肝脏缺血前48小时接受了脾内肝细胞移植（1×10⁷个细胞）（n = 10）。在缺血前和缺血后1小时测量血清氨和血糖。肝脏缺血后，血清氨显著高于正常水平（第1组，930微克/分升对<110微克/分升）。另一方面，第2组的血清氨也有所升高（355微克/分升），但显著低于第1组（p < 0.001）。与正常情况（50 - 100毫克/分升）相比，两组肝脏缺血后的血糖均较低，但第2组（30毫克/分升）高于第1组（14毫克/分升，p < 0.01）。缺血后1小时的肝脏组织学检查显示两组坏死程度相似。移植的肝细胞是存活的，并且在缺血后可在脾实质中清晰识别。脾内移植的肝细胞为大鼠急性缺血性肝衰竭提供了暂时的代谢支持，这表现为氨清除和糖异生增强。
