Foitzik T, Stufler M, Hotz H G, Klinnert J, Wagner J, Warshaw A L, Schulzke J D, Fromm M, Buhr H J
Department of Surgery, Universitätsklinikum Benjamin Franklin, Freie Universität Berlin, Berlin, Germany.
J Gastrointest Surg. 1997 Jan-Feb;1(1):40-6; discussion 46-7. doi: 10.1007/s11605-006-0008-8.
Intestinal barrier failure and subsequent translocation of bacteria from the gut play a decisive role in the development of systemic infections in severe acute pancreatitis. Glutamine (GLN) has been shown to stabilize gut barrier function and to reduce bacterial translocation in various experimental settings. The aim of this study was to evaluate whether GLN reduces gut permeability and bacterial infection in a model of acute necrotizing pancreatitis. Acute necrotizing pancreatitis was induced in 50 rats under sterile conditions by intraductal infusion of glycodeoxycholic acid and intravenous infusion of cerulein. Six hours after the induction of pancreatitis, animals were randomly assigned to one of two groups: standard total parental nutrition (TPN) or TPN combined with GLN (0.5 g/kg(-1)/day(-1)). After 96 hours, the animals were killed. The pancreas was prepared for bacteriologic examination, and the ascending colon was mounted in a Ussing chamber for determination of transmucosal resistance and mannitol flux as indicators of intestinal permeability. Transmucosal resistance was 31% higher in the animals treated with GLN- supplemented TPN compared to the animals given standard TPN. Mannitol flux through the epithelium was decreased by 40%. The prevalence of pancreatic infections was 33% in animals given GLN-enriched TPN as compared to 86% in animals receiving standard TPN (P < 0.05). Adding GLN to standard TPN not only reduces the permeability of the colon but decreases pancreatic infections in acute necrotizing pancreatitis in the rat. This confirms previous reports that GLN decreases bacterial translocation by stabilizing the intestinal mucosal barrier. The present findings provide the first evidence suggesting that stabilizing the intestinal barrier can reduce the prevalence of pancreatic infection in acute pancreatitis and that GLN may be useful in preventing septic complications in clinical pancreatitis.
肠道屏障功能衰竭以及随后细菌从肠道的移位在重症急性胰腺炎全身感染的发生中起决定性作用。在各种实验条件下,谷氨酰胺(GLN)已被证明可稳定肠道屏障功能并减少细菌移位。本研究的目的是评估GLN在急性坏死性胰腺炎模型中是否能降低肠道通透性和细菌感染。在无菌条件下,通过导管内注入甘氨胆酸和静脉注入蛙皮素,诱导50只大鼠发生急性坏死性胰腺炎。胰腺炎诱导6小时后,将动物随机分为两组之一:标准全胃肠外营养(TPN)或TPN联合GLN(0.5 g/kg⁻¹/天⁻¹)。96小时后,处死动物。制备胰腺进行细菌学检查,并将升结肠安装在Ussing室中,以测定跨粘膜电阻和甘露醇通量作为肠道通透性的指标。与给予标准TPN的动物相比,接受补充GLN的TPN治疗的动物跨粘膜电阻高31%。通过上皮的甘露醇通量降低了40%。给予富含GLN的TPN的动物胰腺感染发生率为33%,而接受标准TPN的动物为86%(P<0.05)。在标准TPN中添加GLN不仅可降低结肠通透性,还可减少大鼠急性坏死性胰腺炎中的胰腺感染。这证实了先前的报道,即GLN通过稳定肠粘膜屏障减少细菌移位。目前的研究结果提供了首个证据,表明稳定肠道屏障可降低急性胰腺炎中胰腺感染的发生率,并且GLN可能有助于预防临床胰腺炎中的感染性并发症。