Rønholm E, Tomasdottir H, Runeborg J, Mattsby-Baltzer I, Olausson3 M, Aneman A, Bengtsson A
Department of Anaesthesiology & Intensive Care, Sahlgrenska University Hospital, Gothenburg, Sweden.
Acta Anaesthesiol Scand. 2000 Aug;44(7):850-7. doi: 10.1034/j.1399-6576.2000.440711.x.
Liver transplantation elicits a systemic inflammatory response and eventually a multiple organ failure syndrome. Gastro-intestinal inflammatory activation with release of proinflammatory cytokines and complement activation may occur. This study evaluates gastro-intestinal complement activation and the association with postoperative parenchymatous liver cell injury and liver dysfunction.
In 17 patients undergoing liver transplantation, blood samples were collected from radial artery and portal vein for analysis of complement SC5b-9 and endotoxin concentration. Portal venous-arterial SC5b-9 plasma concentration gradients at 30 min after reperfusion were calculated. Outcome parameters included postoperative organ failure and serum concentrations of aspartate aminotransferase, alanine aminotransferase, bilirubin and factor II-VII-X.
Patients with gastro-intestinal SC5b-9 release (n=7) had higher postoperative serum aspartate aminotransferase and alanine aminotransferase concentrations [49 (32-80) microkat/l vs 8 (6-14) microkat/l, P<0.01 and 33 (15-54) microkat/l vs 8 (4-23) microkat/l, P<0.04, respectively] and lower factor II-VII-X concentrations [46 (21-48)% vs 60 (47-69)%, P<0.02] compared to patients without gastro-intestinal SC5b-9 release (n=10). The ICU stay was prolonged in patients with gastro-intestinal complement release. There was no difference in number of organ failures and serum bilirubin concentration between the groups. The endotoxin concentration in arterial and portal vein blood was low and the association between endotoxaemia and complement activation was poor.
Gastro-intestinal complement activation may contribute to postoperative parenchymatous liver cell injury and liver dysfunction in patients undergoing liver transplantation.
肝移植引发全身炎症反应，并最终导致多器官功能衰竭综合征。可能会发生胃肠道炎症激活，伴有促炎细胞因子释放和补体激活。本研究评估胃肠道补体激活及其与术后实质肝细胞损伤和肝功能障碍的关联。
对17例接受肝移植的患者，从桡动脉和门静脉采集血样，分析补体SC5b-9和内毒素浓度。计算再灌注后30分钟时门静脉-动脉SC5b-9血浆浓度梯度。观察指标包括术后器官功能衰竭情况以及天冬氨酸转氨酶、丙氨酸转氨酶、胆红素和凝血因子II-VII-X的血清浓度。
发生胃肠道SC5b-9释放的患者（n = 7）术后血清天冬氨酸转氨酶和丙氨酸转氨酶浓度较高[分别为49（32 - 80）微卡/升对8（6 - 14）微卡/升，P < 0.01；33（15 - 54）微卡/升对8（4 - 23）微卡/升，P < 0.04]，而凝血因子II-VII-X浓度较低[46（21 - 48）%对60（47 - 69）%，P < 0.02]，与未发生胃肠道SC5b-9释放的患者（n = 10）相比。发生胃肠道补体释放的患者重症监护病房停留时间延长。两组间器官功能衰竭数量和血清胆红素浓度无差异。动脉血和门静脉血中的内毒素浓度较低，内毒素血症与补体激活之间的关联较弱。
胃肠道补体激活可能导致肝移植患者术后实质肝细胞损伤和肝功能障碍。
