Schröder J, Kahlke V, Fändrich F, Gebhardt H, Erichsen H, Zabel P, Schroeder P
Department of General and Thoracic Surgery, University of Kiel, Germany.
Shock. 1998 Jul;10(1):26-31. doi: 10.1097/00024382-199807000-00005.
Glutamine is an essential substrate for gut mucosal structure, but the role for gut immune function is not fully known. To determine the effect on gut cytokine release in relation to bacterial translocation and gut morphology, a nonlethal hemorrhagic shock (30 min, 30 mmHg) was performed in male Wistar rats followed by 4 days of different way of feeding. A conventional total parenteral nutrition (TPN) solution was compared with an isocaloric and isonitrogenous TPN solution supplemented with alanin-L-glutamine and glycyl-L-glutamine. An enteral chow-fed control group was included. Gut mononuclear cells and splenic macrophages were obtained and endotoxin-induced supernatant tumor necrosis factor-alpha (TNF) and interleukin-6 (IL-6) bioactivity was measured. Histological specimen of the small bowel were taken and mesenteric lymph nodes (MLN) were separated. Enteral feeding following hemorrhagic shock was accompanied by a normal mucosal structure and no bacterial translocation could be detected. TPN was characterized by suppression of cytokine release in gut mononuclear cells and splenic macrophages compared with the enteral-fed control (p < .05). Decreased TNF and IL-6 release was associated with a significantly increased mucosal injury score (p < .05) and a high incidence of bacterial translocation to MLN (66%, p < .05 vs. control). Supplementation of glutamine-dipeptides did not prevent TPN-induced bacterial translocation to MLN (p < .05 vs. control) but significantly improved mucosal injury (p < .05 vs. TPN). Down-regulation of TNF release in TPN-fed rats could not be reversed by glutamine dipeptides while IL-6 release was significantly increased compared with TPN-fed animals (p < .05), and no difference to enteral-fed controls could be found. Enteral nutrition following hemorrhagic shock is superior to parenteral nutrition with regard to mucosal structure, cytokine release, and bacterial translocation. Supplementation of TPN with glutamine dipeptides could reverse TPN-induced suppression of IL-6 release and improved mucosal structure, which may be beneficial in various disease conditions in which TPN is an integrated part of patients management.
谷氨酰胺是肠道黏膜结构的必需底物,但其对肠道免疫功能的作用尚不完全清楚。为了确定其对与细菌移位和肠道形态相关的肠道细胞因子释放的影响,对雄性Wistar大鼠进行非致死性失血性休克(30分钟,30 mmHg),随后采用不同的喂养方式持续4天。将传统的全胃肠外营养(TPN)溶液与补充了丙氨酰-L-谷氨酰胺和甘氨酰-L-谷氨酰胺的等热量、等氮量TPN溶液进行比较。纳入经口给予食物的对照组。获取肠道单核细胞和脾巨噬细胞,测量内毒素诱导的上清液肿瘤坏死因子-α(TNF)和白细胞介素-6(IL-6)的生物活性。采集小肠组织学标本并分离肠系膜淋巴结(MLN)。失血性休克后经口喂养伴随着正常的黏膜结构,且未检测到细菌移位。与经口喂养的对照组相比,TPN的特征是肠道单核细胞和脾巨噬细胞中的细胞因子释放受到抑制(p < 0.05)。TNF和IL-6释放减少与黏膜损伤评分显著增加(p < 0.05)以及细菌移位至MLN的高发生率(66%,与对照组相比p < 0.05)相关。补充谷氨酰胺二肽并不能预防TPN诱导的细菌移位至MLN(与对照组相比p < 0.05),但显著改善了黏膜损伤(与TPN相比p < 0.05)。谷氨酰胺二肽不能逆转TPN喂养大鼠中TNF释放的下调,而与TPN喂养的动物相比,IL-6释放显著增加(p < 0.05),且与经口喂养的对照组无差异。在黏膜结构、细胞因子释放和细菌移位方面,失血性休克后的肠内营养优于肠外营养。用谷氨酰胺二肽补充TPN可逆转TPN诱导的IL-6释放抑制并改善黏膜结构,这在TPN是患者治疗组成部分的各种疾病状况中可能有益。