Bülbüller Nurullah, Pektaş Bahattin, Ozdarendeli Aykut, Doğru Osman, Aygen Erhan, Akpolat Nusret
Department of General Surgery, Firat University Medical Center, Elaziğ, Turkey.
J Surg Res. 2005 Feb;123(2):194-9. doi: 10.1016/j.jss.2004.08.028.
Hemorrhagic shock causes mucosal damage in intestine and it results in translocation of bacteria to distant organs. In this study, effects of various doses of L-Tryptophan on the prevention of bacterial translocation in hemorrhagic shock induced rabbits were investigated. This study was carried out on six groups, each was consisting of 10 rabbits. While any procedure was conducted on the rabbits in group 1 (as a control group), 1 x 10(10)Escherichia coli isolate were administered rabbits in the other groups by gavage. In groups 3, 4, 5, and 6, hemorrhagic shock was induced. After induction of hemorrhagic shock, 10, 50, and 200 mg/kg L-Tryptophan were intragastrically administered to animals in groups 4, 5, and 6, respectively. Blood and terminal ileum samples were taken to detect bacterial translocation by polymerase chain reaction and mucosal damage by histopathological examination at 24 h after hemorrhagic shock. The occurrence of bacterial translocation increased as well when intestinal bacterial intensity was increased (P < 0.05). The most intensive bacterial translocation was formed in group 3 as a result of the additive effect of hemorrhagic shock to bacterial augmentation. It was observed that bacterial translocation was significantly reduced in groups 5 and 6 that are 50 and 200 mg/kg L-Tryptophan were administered (P < 0.01). Histopathological changes on mucosa and submucosa support these results. As a result, we concluded that augmentation of intestinal bacterial intensity induces bacterial translocation, the addition of hemorrhagic shock to bacterial augmentation makes more excessive translocation and mucosal changes have effective roles in these events. L-Tryptophan decreased the intestinal mucosal damage and bacterial translocation induced by hemorrhagic shock, in a dose-dependent manner.
失血性休克会导致肠道黏膜损伤,进而致使细菌易位至远处器官。在本研究中,研究了不同剂量的L-色氨酸对预防失血性休克诱导的家兔细菌易位的作用。本研究在六组家兔中进行,每组10只。第1组家兔不进行任何处理(作为对照组),其他组家兔通过灌胃给予1×10¹⁰大肠杆菌分离株。第3、4、5和6组诱导失血性休克。在诱导失血性休克后,分别向第4、5和6组动物胃内给予10、50和200mg/kg的L-色氨酸。在失血性休克24小时后采集血液和回肠末端样本,通过聚合酶链反应检测细菌易位,并通过组织病理学检查检测黏膜损伤。随着肠道细菌强度增加,细菌易位的发生率也增加(P<0.05)。由于失血性休克对细菌增殖的叠加作用,第3组形成了最严重的细菌易位。观察到给予50和200mg/kg L-色氨酸的第5和6组细菌易位明显减少(P<0.01)。黏膜和黏膜下层的组织病理学变化支持这些结果。因此,我们得出结论,肠道细菌强度增加会诱导细菌易位,失血性休克叠加细菌增殖会使易位更加严重,并且黏膜变化在这些事件中起重要作用。L-色氨酸以剂量依赖的方式减少了失血性休克诱导的肠道黏膜损伤和细菌易位。