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急慢性门静脉高压症中的细菌移位

Bacterial translocation in acute and chronic portal hypertension.

作者信息

Garcia-Tsao G, Albillos A, Barden G E, West A B

机构信息

Hepatic Hemodynamic Laboratory, West Haven Veterans Affairs Medical Center, Connecticut 06516.

出版信息

Hepatology. 1993 Jun;17(6):1081-5.

PMID:8514258
Abstract

Patients with cirrhosis are predisposed to develop spontaneous bacteremias and peritonitis, mainly by enteric bacteria. Portal hypertension, by producing congestion and edema of the bowel wall, could increase the passage of bacteria from the intestinal lumen to regional lymph nodes to the systemic circulation or to both, a process termed bacterial translocation. The aim of this study was to investigate bacterial translocation at two stages of experimental portal hypertension: (a) acute (when shunting is minimal); and (b) chronic (when shunting is extensive and mimics the portal hypertension of cirrhosis). Rats were killed 2 days (acute) or 15 days (chronic) after partial portal vein ligation or control surgeries. Samples of mesenteric lymph nodes, blood, liver and spleen for standard bacteriological cultures and a fragment of ileum for histological examination were obtained. Two days after surgery, a significantly greater proportion of rats with acute portal hypertension (12 of 13 or 92%) had positive mesenteric lymph node cultures compared with both control groups: sham-operated (4 of 13 or 31%) and inferior vena cava-ligated (3 of 10 or 33%) animals (p < 0.01). However, 15 days after surgery no differences in translocation to mesenteric lymph nodes were found between rats with chronic portal hypertension (3 of 15 or 20%) and sham-operated controls (3 of 11 or 27%). In neither the acute nor the chronic rats were bacteria isolated from blood, spleen or liver. Rats with acute portal hypertension had significantly greater mesenteric inflammation than rats with chronic portal hypertension and control animals.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

肝硬化患者易发生自发性菌血症和腹膜炎,主要由肠道细菌引起。门静脉高压通过导致肠壁充血和水肿,可能会增加细菌从肠腔进入区域淋巴结再到体循环或两者的过程,这一过程称为细菌易位。本研究的目的是调查实验性门静脉高压两个阶段的细菌易位情况:(a)急性阶段(分流最少时);(b)慢性阶段(分流广泛且模拟肝硬化门静脉高压时)。在部分门静脉结扎或对照手术后2天(急性)或15天(慢性)处死大鼠。获取肠系膜淋巴结、血液、肝脏和脾脏样本进行标准细菌培养,并取一段回肠进行组织学检查。手术后2天,与两个对照组相比,急性门静脉高压大鼠(13只中有12只,即92%)肠系膜淋巴结培养呈阳性的比例显著更高:假手术组(13只中有4只,即31%)和下腔静脉结扎组(10只中有3只,即33%)动物(p<0.01)。然而,手术后15天,慢性门静脉高压大鼠(15只中有3只,即20%)和假手术对照组(11只中有3只,即27%)之间在肠系膜淋巴结易位方面未发现差异。在急性和慢性大鼠中,血液、脾脏或肝脏均未分离出细菌。急性门静脉高压大鼠的肠系膜炎症明显比慢性门静脉高压大鼠和对照动物更严重。(摘要截短至250字)

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