谷氨酰胺强化的肠内营养对烧伤后肠源性高代谢的影响

目的:探讨谷氨酰胺强化的肠内营养对烧伤后肠源性高代谢的影响及机制。方法:将88只Wistar大鼠随机分为烧伤后常规肠内营养支持组(B)和谷氨酰胺(Gln)强化的肠内营养组,并与烧伤前指标作对照(PBD0)。烧伤大鼠均经占体表面积30%的全层皮肤烧伤,B组和Gln组采用等氮、等热卡的营养支持,Gln组予1.0g/(kg·d)的Gln,B组予等量的甘氨酸。观察烧伤前和烧伤后(PBD)1、3、5、7、10d大鼠静息能量代谢率(REE)的变化,同时检测了血浆Gln浓度、二胺氧化酶(DAO)活性、内毒素(LPS)、肿瘤坏死因子(TNF)和白细胞介素-1(IL-1)含量,并进行比较分析。结果:烧伤后两组大鼠血浆Gln浓度明显低于烧伤前,而REE、DAO、TNF、LPS及IL-1水平则明显高于烧伤前。两组相比,烧伤后Gln组大鼠的血浆Gln浓度明显高于B组,增幅约达40%,而REE、DAO、LPS、TNF及IL-1水平则明显低于B组。相关分析显示,REE与血浆Gln浓度呈显著负相关(r=-0.89,P<0.01)。结论:Gln强化的肠内营养可有效地提高烧伤大鼠的血浆Gln浓度,减轻肠道受损程度,抑制炎症介质的释放,从而降低肠源性高代谢。

Effect of enteral nutrition supplemented with glutamine on enterogenous hypermetabolism after severe burn injury

Objective To study the effect of enteral nutritional support supplemented with glutamine on enterogenous hypermetabolism after severe burn injury. Methods Eighty-eight Wistar rats were inflicted with 30% total body surface area full thickness burns and randomly divided into two groups of normal enteral nutrition (B) and enteral nutrition supplemented with glutamine treatment(Gln) group. Nitrogenous intake and caloric supply were identical in both groups , Gln and B group rats had been given glutamine or glycine at 1.0g/(kg.d), respectively. Parameters including the plasma glutamine concentration, resting energy expenditure (REE), activity of plasma DAO and levels of plasma TNF, LPS, IL-1 were determined. Results After burn injury, the glutamine concentration was significant decreased, and the REE, DAO activity and the levals of TNF, LPS, IL-1 were significantly increased. Compared with group B, the plasma glutamine concentration was markedly higher, and the level of REE, plasma DAO activity and TNF, LPS, IL-1 were significantly lower in group Gln. Correlation study showed that REE bears a negative correlationship with glutamine concentration (r=-0.89, P<0.01). Conclusions In severe burn injury, glutamine supplementation could abate the degree of intestine injury, lessen intestinal mucosal permeability, reduce the plasma inflammatory media and help to attenuate enterogenous hypermetabolism.