营养支持途径对严重烧伤后肠黏膜上皮细胞增生的影响

目的:探讨肠道喂养及静脉营养对严重烧伤早期肠黏膜上皮细胞增生功能的影响.方法:将30%TBSAⅢ度烧伤大鼠行颈外静脉插管后,随机分为肠道喂养组(EF组)及静脉营养组(PN组),伤后2 h分别采用灌喂和颈外静脉输入方法给予等氮、等热卡的营养液.分别于伤前、伤后6,12,24,48和72 h处死动物,检测肠黏膜蛋白质含量、胸腺嘧啶核苷激酶活性、增生指数及PCNA表达.结果:烧伤后两组大鼠肠黏膜蛋白质含量均降低,EF组在伤后24,48和72 h分别为262±24mg/m,283±29mg/m,282±18 mg/m,明显高于PN组的195±45 mg/m,194±41 mg/m,143±19 mg/m.烧伤后肠黏膜胸腺嘧啶核苷激酶活性多较伤前降低,EF组在伤后72 h明显高于PN组(分别为88±19 nmol/m,35±7 nmol/m).PN组肠黏膜细胞增生指数在伤后6,12 h分别为78.4±3.4%,89.9±1.3%,明显高于EF组的60.4±10.1%,75.7±6.9%;而在伤后48,72 h分别为25.9±12.7%,12.5±8.6%,显著低于EF组的78.9±1.6%,56.9±5.6%.EF组肠黏膜PCNA表达明显多于PN组.结论:早期肠道喂养较静脉营养更能促进严重烧伤后肠黏膜上皮细胞增生,利于受损肠黏膜的修复.

Objective: To introduce a safe and specific approachof 13C magnetic resonance spectrum (13C MRS )spectroscopy and investigate the alterations in hepaticanabolism.Methods: Relative anaplerotic, pyruvate recyclingand gluconeogenic fluxes were measured by 13C MRSisotopomer analysis of blood glucose from rats with 40%body surface area burn injury, and from rats exposed tosham injury. A short chain fatty acid, [U-13C] propionatewhich was avidly extracted by the liver, was infusedintravenously to deliver 13C into the citric acid cycle.Proton-decoupled 13C MRS of deproteinized plasma orextracts of the freeze-clamped liver were used to determinethe distribution of 13C in blood or hepatic glucose.Results: There was no difference in the multipletsdetected in the glucose carbon-2 anomer from blood or liverafter 45 or 60 minutes of the infusion of the propionate,indicating that steady-state isotopic conditions wereachieved. Gluconeogenesis relative to citric acid cycle fluxwas not altered by burn injury; in both sham and burngroups the rate of glucose production was about equal toflux through citrate synthase. In the sham group ofanimals, the rate of entry of carbon skeletons into the citricacid cycle was about 4 times than that in the burn group.Similarly, flux through pyruvate kinase (again relative tocitrate synthase) was significantly increased after the burninjury.Conclusions: Since results from analysis of the bloodglucose are the same as that of the hepatic glucose, 13Cdistribution in the glucose and hepatic metabolism can beassessed based on the 13C MRS analysis of the bloodglucose.