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急性胰腺炎实验模型中肠道功能的改变

Alterations in intestinal function in acute pancreatitis in an experimental model.

作者信息

Wang X D, Wang Q, Andersson R, Ihse I

机构信息

Department of Surgery, Lund University Hospital, Sweden.

出版信息

Br J Surg. 1996 Nov;83(11):1537-43. doi: 10.1002/bjs.1800831113.

DOI:10.1002/bjs.1800831113
PMID:9026331
Abstract

Gastrointestinal tract failure may be involved in the development of systemic septic complications in acute pancreatitis. Systemic and intestinal circulation, intestinal permeability and absorptive function were evaluated in the early course of acute pancreatitis induced in rats by retrograde intraductal injection of 0.2 ml of 5 per cent sodium taurodeoxycholate and 0.4 nmol trypsin. A decrease in systemic arterial pressure and intestinal blood flow and an increase in intestinal permeability as measured by the leakage of 125I-labelled human serum albumin from blood to lumen were noted in the distal ileum and colon, reaching statistically significant differences 6 h after induction of pancreatitis. The transport of small molecular markers (sodium fluorescein and 51Cr-labelled ethylenediamine tetra-acetic acid) through the distal ileum and colon in vitro from the mucosal to the serosal site in Ussing chambers significantly increased in the early periodic (20-60 min) of incubation, while the passage of a macromolecular marker (ovalbumin) demonstrated a definite increase at 60-120 min of incubation. D-Xylose absorption from the gut lumen to the portal vein was significantly less in acute pancreatitis than after sham operation. Intravenous administration of the hydroxyl radical scavenger dimethylsulphoxide prevented the compromised intestinal permeability and gut absorptive capacity induced by acute pancreatitis, but did not affect the reduced arterial pressure and intestinal microcirculation. Cytotoxic oxygen-derived free radicals may contribute to the development of alterations in intestinal permeability and absorptive function found in the early stage of acute pancreatitis in the rat.

摘要

胃肠道功能衰竭可能参与急性胰腺炎全身感染性并发症的发生发展。通过向大鼠胰管逆行注射0.2 ml 5%牛磺脱氧胆酸钠和0.4 nmol胰蛋白酶诱导急性胰腺炎,在其病程早期评估全身和肠道循环、肠道通透性及吸收功能。观察到胰腺炎诱导6小时后,大鼠回肠末端和结肠出现全身动脉压和肠道血流量下降,以及125I标记的人血清白蛋白从血液渗漏至肠腔所测得的肠道通透性增加,差异具有统计学意义。在体外孵育早期(20 - 60分钟),乌氏腔中小分子标志物(荧光素钠和51Cr标记的乙二胺四乙酸)从回肠末端和结肠黏膜向浆膜部位的转运显著增加,而大分子标志物(卵清蛋白)在孵育60 - 120分钟时出现明显增加。急性胰腺炎时肠道腔向门静脉的D - 木糖吸收明显少于假手术后。静脉注射羟自由基清除剂二甲亚砜可预防急性胰腺炎诱导的肠道通透性受损和肠道吸收能力下降,但不影响动脉压降低和肠道微循环。细胞毒性氧衍生的自由基可能在大鼠急性胰腺炎早期肠道通透性和吸收功能改变的发生中起作用。

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