Curran T J, Uzoaru I, Das J B, Ansari G, Raffensperger J G
Children's Memorial Hospital, Chicago, IL 60614, USA.
J Pediatr Surg. 1995 Feb;30(2):242-6; discussion 246-7. doi: 10.1016/0022-3468(95)90568-5.
Patients on total parenteral nutrition (TPN) commonly have hepatobiliary dysfunction. Interruption of the enterohepatic circulation (EHC) and gallbladder stasis are part of the pathogenesis. Cholecystokinin-octapeptide (CCK-OP), by emptying the gallbladder, stimulates the EHC. This study was performed to determine whether daily CCK-OP infusions can ameliorate the hepatobiliary dysfunction caused by TPN.
Rabbits maintained on a standard TPN for 12 days were divided into two groups. One group (n = 6) received daily intravenous doses of CCK-OP, and the other (n = 13) received TPN only. A lab-chow-fed (LCF) group (n = 8) served as controls. The authors studied bile flow and bile acid secretion rates, sulfobromophthalein (BSP) secretion, gallbladder emptying in response to CCK-OP, and liver histology.
The LCF group had a bile flow of 82.3 microL/kg/min; that for the TPN-only group was 45.7 microL/kg/min (P < .001). The daily CCK-OP group did not improve more than the TPN-only group, with a bile flow of 45.8 microL/kg/min (P = NS). Bile acid secretion was 0.64 mumol/kg/min for the LCF group, 0.46 for the TPN-only group (P = NS), and 0.46 for the daily CCK-OP group (P = NS). TPN impaired the ability of the gallbladder to empty, and this was restored with daily CCK-OP. In the LCF group, the mean BSP secretion was 81.7% of a 5-mg/kg bolus within 60 minutes, compared with 72.5% in the daily CCK-OP group (P = NS) and 63.5% in the TPN-only group (P < .01). Histological examination of the liver showed that daily CCK-OP produced less periportal inflammation and fibrosis, although all TPN groups had hepatocyte damage in the centrilobular area.
Stimulation of the EHC with daily CCK-OP infusions during TPN decreased periportal inflammation and fibrosis, maintained gallbladder emptying capacity, and improved organic anion (BSP) secretion, although bile flow and bile acid secretion were not improved, and hepatocyte damage persisted.
接受全胃肠外营养（TPN）的患者常出现肝胆功能障碍。肠肝循环（EHC）中断和胆囊淤滞是发病机制的一部分。八肽胆囊收缩素（CCK-OP）可通过排空胆囊来刺激肠肝循环。本研究旨在确定每日输注CCK-OP是否能改善TPN所致的肝胆功能障碍。
将维持标准TPN 12天的兔子分为两组。一组（n = 6）每日静脉注射CCK-OP，另一组（n = 13）仅接受TPN。一组实验室常规喂养（LCF）的兔子（n = 8）作为对照。作者研究了胆汁流量、胆汁酸分泌率、磺溴酞钠（BSP）分泌、胆囊对CCK-OP的排空反应以及肝脏组织学。
LCF组的胆汁流量为82.3微升/千克/分钟；仅接受TPN组为45.7微升/千克/分钟（P <.001）。每日注射CCK-OP组的改善情况并不优于仅接受TPN组，胆汁流量为45.8微升/千克/分钟（P = 无显著性差异）。LCF组的胆汁酸分泌为0.64微摩尔/千克/分钟，仅接受TPN组为0.46（P = 无显著性差异），每日注射CCK-OP组为0.46（P = 无显著性差异）。TPN损害了胆囊的排空能力，而每日注射CCK-OP可使其恢复。在LCF组中，5毫克/千克推注剂量的BSP在60分钟内的平均分泌率为81.7%，每日注射CCK-OP组为72.5%（P = 无显著性差异），仅接受TPN组为63.5%（P <.01）。肝脏组织学检查显示，尽管所有TPN组在小叶中心区域都有肝细胞损伤，但每日注射CCK-OP组的门静脉周围炎症和纤维化较轻。
在TPN期间每日输注CCK-OP刺激肠肝循环可减轻门静脉周围炎症和纤维化，维持胆囊排空能力，并改善有机阴离子（BSP）分泌，尽管胆汁流量和胆汁酸分泌未得到改善，且肝细胞损伤仍然存在。
