Cheng Jun-tao, Xiao Guang-xia, Xia Pei-yuan, Yuan Jian-cheng, Qin Xiao-jian
Institute of Burn Research, Southwest Hospital, The Third Military Medical University, Chongqing, PR China.
Zhonghua Shao Shang Za Zhi. 2003 Aug;19(4):229-32.
To observe different degrees of intra-abdominal pressure and different duration on the intestinal permeability and endotoxin/bacteria translocation in rabbit model, so as to explore the mechanism of the development of abdominal compartment syndrome (ACS) and MODS.
Rabbit model of intra-abdominal hypertension was established by injection of gaseous nitrogen into the peritoneal cavity. Thirty-nine New Zealand white rabbits were employed in the study. The change in intestinal permeability was determined by fluorescein isothiocyanate dextran (FITC-D) and two kinds of molecular probes of type II horseradish peroxidase (HRP-II). The effects of intra-abdominal hypertension on the endotoxin/bacteria translocation were also detected.
The contents of FITC-D and HRP-II in portal veins increased evidently (P < 0.01) when intra-abdominal pressure (IAP) was higher than 20 mmHg. The endotoxin (ET) content in portal vein in rabbits with IAP of 10 mmHg for 1, 2 and 4 hours exhibited no difference compared with that in normal control, while the ET content increased obviously after 1 hour with IAP of 20 mmHg and increased thereafter along with the prolongation of IAP, and increase in pressure. The bacterial translocation rates were 33.3%, 66.7% and 100% when IAP was maintained at 20 mmHg for 1, 2 and 4 hours, respectively, and there was evidence of bacterial translocation to the liver. The rate of bacterial translocation to intestinal mesenteric lymph nodes was 100% when IAP was 30 mmHg for 1 and 2 hours. There was no bacterial translocation to the spleen in all experimental rabbits.
Intestinal mucosal permeability increased significantly with increased endotoxin content in portal vein when IAP was higher than 20 mmHg. At the sane time, the bacteria could be translocate to intestinal mesenteric lymph nodes and liver, which might be constitute one of the important factors leading to the development of ACS and MODS.
观察兔模型中不同程度的腹腔内压力及不同作用时间对肠道通透性和内毒素/细菌移位的影响，以探讨腹腔间隔室综合征（ACS）和多器官功能障碍综合征（MODS）的发病机制。
通过向腹腔内注入气态氮建立兔腹腔高压模型。本研究采用39只新西兰白兔。采用异硫氰酸荧光素葡聚糖（FITC-D）和Ⅱ型辣根过氧化物酶（HRP-II）两种分子探针测定肠道通透性的变化。同时检测腹腔高压对内毒素/细菌移位的影响。
腹腔内压力（IAP）高于20 mmHg时，门静脉中FITC-D和HRP-II的含量明显增加（P<0.01）。IAP为10 mmHg持续1、2和4小时的兔门静脉内毒素（ET）含量与正常对照组相比无差异，而IAP为20 mmHg 1小时后ET含量明显增加，此后随IAP升高及压力持续时间延长而增加。IAP维持在20 mmHg 1、2和4小时时，细菌移位率分别为33.3%、66.7%和100%，并有细菌移位至肝脏的证据。IAP为30 mmHg持续1和2小时时，细菌移位至肠系膜淋巴结的发生率为100%。所有实验兔均无细菌移位至脾脏。
当IAP高于20 mmHg时，肠道黏膜通透性显著增加，门静脉内毒素含量升高。同时，细菌可移位至肠系膜淋巴结和肝脏，这可能是导致ACS和MODS发生发展的重要因素之一。
