Detrimental Effects of Early Nutrition Administration After Severe Gut Ischemia-Reperfusion

BackgroundAlthough early enteral nutrition after insult has many advantages, effects of early nutritional manipulation on outcome after gut ischemia-reperfusion (I/R) remain unclear. We hypothesize that early enteral nutrition would improve survival after severe gut I/R by reducing organ injury and leukocyte activation.Materials and methodsMice were randomized to chow, intravenous (IV)-total parenteral nutrition (TPN), intragastric (IG)-TPN, or complex enteral diet (CED) for feeding after I/R. In experiment 1, 72 mice underwent both IV cannulation and gastrostomy before 45 or 10 min gut ischemia. At 12 (45 and 10 min ischemia) or 24 h (45 min ischemia) after I/R, mice were given one of the above diets. The chow group received IV saline and free access to chow was started at 12 or 24 h after I/R, i.e., no infusion of nutritional solutions. Survival was observed until 120 h. In experiment 2, 25 mice received one of the above diets at 12 h after 45 min gut I/R. Organ vascular permeability was assessed with Evans blue at 6 h after feeding. Reactive oxygen intermediate production with or without phorbol myristate acetate stimulation by circulating myeloid cells and expressions of CD11a and CD11b on these cells were also determined using flow cytometry.ResultsWhen feeding started at 12 h after 45 min ischemia, IV-TPN, IG-TPN, and CED significantly reduced survival time, as compared with chow. However, no significant difference was observed when feeding started at 24 h. There were no significant differences in survival times after 10 min ischemia among the four groups. Lung and small intestine vascular permeability was significantly higher in the IV-TPN group than in the other groups. There were no significant differences in reactive oxygen intermediate production or adhesion molecule expressions.ConclusionEarly nutrition administration after severe I/R reduces survival, possibly by increasing organ injury in IV-TPN and by other mechanisms in IG-TPN and CED.