严重烧伤后高代谢反应机理的研究

Study on preserving intestinal function and the possiblemechanism of hypermetabolic response following severe burn Injury

我们设计了一个小香猪实验模型，以便获取门静脉、肠系膜下静脉及中心静脉等不同区域的血标本，术后７天造成３０％Ⅲ度烧伤，并随机分为早期喂养（伤后两小时开始喂养）和延迟喂养（伤后４天开始喂养）进行观察。结果表明，与延迟喂养比较，早期肠道营养可增强肠粘膜屏障功能，减少肠道细菌及毒素移位，使肿瘤坏死因子、分解代谢激素明显降低，最终使代谢率、３－甲基组氨酸排量明显降低。结果还表明，在高代谢期间的代谢反应中，经肠道途径介导的至少约占１／３。实验结果提示：“肠道－肝单核吞噬细胞系－高代谢反应”是严重烧伤高代谢反应的另一重要机理。经肠入血的细菌、毒素及由肝枯否氏细胞释放的活性介质则是这一机理的介导因产。

AbstractIn order to approach the mechanism of hypermetabolic response following severe burn injury,a newanimal model was developed with a specially bred mini-swine(Guizhou;pecies ).Multiple catheterizationswere applied for sampling different blood from portal,inferior mesenteric as will as jugular(central)veins.The animals were sustained with 30/Ⅲburn of TB-SA and divided randomly into early feeding group,giv-en a complete diet beginning from 2 hours postburn(N=6),and delayed feeding group,given the same dietinitiating on 4 day postburn(N=6).The resultsshowed that compared with delayed feeding,early enteral feeding could strengthen the barrier function,decline the rate of translocation of bacteria and endotoxinfrom the gut to portal vein,reduce obviously bloodTNF, CRP and catabolic-hormones,and significantlydecrease REE(resting energy expenditure) and urinary3-Mehis excretion.During the hypermetabolism(PBD7-10),the metabolic response mediated by“intestinal way”was at least 35%. The way of“intestinaltract-macrophages in liver-Hypermetabolism”is apossible mechanism of hypermetabolic response follow-ing severe burn injury, and the bacteria and endotoxintranslocated from the gut,the active products(IL-I,TNF, etc ) released by Kupffer’s cells might be themediating factors of the mechanism.