[Impact of glutamine and ω-3 polyunsaturated fatty acids on intestinal permeability and lung cell apoptosis during intestinal ischemia-reperfusion injury in a rat model].

OBJECTIVE: To investigate the impact of intestinal lymphatic vessels ligation and different enteral nutrition support during ischemia/reperfusion on intestinal permeability, systemic inflammatory response and pulmonary dysfunction in a rat model. METHODS: Seventy-two Sprague-Dawley male rats were randomized into normal diet group, regular enteral nutrition group, glutamine-enriched group, 0-3 polyunsaturated fatty acids (wo-3PUFA) group, and sham control after gastrostomy. All the enteral nutrition group were isocaloric (1046 kJ kg-' d-1) and isonitrogenous (1.8 g N kg-' d-'). After enteral nutrition for 7 days, the rats were subjected to intestinal ischemia for 60 min, or ischemia plus mesenteric lymph duct ligation except for the sham group followed by 3 days of nutrition (72 h). Intestinal permeability (lactose/mannitol ratio in the urine, L/M) was determined on the 5th, 7th and 9th day after gastrostomy. The levels of serum diamine oxidase, endotoxin, cytokines, ALT and AST were detected at the 11th day after gastrostomy. Mucosal thickness was measured using small intestine and villusheight. Myeloperoxidase (MPO), nitric oxide (NO), NO synthase, and apoptotic index were detected in lung tissue. RESULTS: Ischemia for 60 min could cause intestinal injury. Intestinal permeability(L/M)was increased significantly in every group on the first day after ischemia (P<0.05). However, L/M decreased significantly 3 days after ischemia (P<0.05). The groups with Glu and o-3PUFA-enriched nutrition almost restored to normal level (P>0.05). The level of L/M in lymphatic ligation group was significantly lower than non-ligation group (P<0.05). The levels of endotoxin and cytokine were reduced, mucosal thickness and villous height were significantly higher (P<0.05) in the groups of Glu and o-3PUFA-enriched nutrition compared with enteral nutrition and normal diet groups during intestinal ischemia-reperfusion injury. MPO, NO, NOS and the apoptosis index of lung tissue decreased in the groups of Glu and o-3PUFA-enriched as well as after lymph duct ligation (P<0.05). CONCLUSIONS: The distant tissue-lung damage and systemic inflammation caused by intestinal ischemia-reperfusion injury may be related to some factors in the intestinal lymph. Blocking the gut-lymph pathway and/or adding Glu and o-3PUFA in enteral nutrition may reduce intestinal permeability and endotoxin, increase mucosal thickness, attenuate the systemic inflammatory reaction, and prevent lung injury

Lymph duct ligation during ischemia/reperfusion prevents pulmonary dysfunction in a rat model with ω-3 polyunsaturated fatty acid and glutamine.

OBJECTIVE: The release of injurious factors into the mesenteric lymph from the ischemic intestine has been shown to contribute to lung injury and systemic inflammation after severe injury. We studied the effects of lung injury and systemic inflammatory reaction after intestinal ischemia/reperfusion and mesenteric lymph duct ligation with different nutritional statuses. METHODS: Rats (n = 72) were fed with a normal diet or received one of three diets (enteral nutrition, glutamine, or ω-3 polyunsaturated fatty acid) that were isocaloric and isonitrogenous. After 7 d, rats were subjected to 60 min of intestinal ischemia, ischemia plus mesenteric lymph duct ligation, or sham procedures. After 3 d of ischemia, the lymph nodes, lung, intestinal, liver, and blood were harvested and analyzed. RESULTS: In the different groups, lung injury, including levels of myeloperoxidase, nitric oxide, nitric oxide synthase, and the index of alveolar apoptosis, were partly prevented by mesenteric lymph duct ligation (P < 0.05). Likewise, the rats with ischemia/reperfusion, but not those with duct ligation plus ischemia/reperfusion, had a significant increase in intestinal permeability and decreased mucosal thickness. The serum cytokine and endotoxin concentrations were also lower in the lymph duct ligation groups, although there was no significant difference between lymph duct ligation and sham procedure. The lung and intestinal injuries were attenuated in the groups fed with glutamine and ω-3 polyunsaturated fatty acid. CONCLUSION: These results indicate that lymph duct ligation prevents lung injury, a systemic inflammation reaction, and gut-barrier dysfunction. Enteral glutamine and ω-3 polyunsaturated fatty acid modified the gut inflammation, prevented lung injury, and attenuated the systemic inflammation reaction.

[Method for drainage of lymph fluid and determining the change of active materials in lymph fluid after rat ischemia-reperfusion injury].

OBJECTIVE: To set up a method for the drainage of lymph fluid and explore the change of active materials in lymph fluid and serum after rat ischemia-reperfusion injury. METHODS: The method of the drainage of lymph fluid was well established. Sixteen healthy male rats of SPF grade were selected and randomly divided into 2 groups: intestinal ischemia-reperfusion + drainage group (I/R + drainage group) and drainage group. All the rats were subjected to superior mesenteric artery occlusion for 60 minutes, followed by 120 minutes of reperfusion. We compared the change of high mobility group box-1 (HMGB1) protein, endotoxin tumor necrosis factor alpha (TNF-alpha), interleukin (IL) -1 beta, IL-6, and soluble vascular cell adhesion molecular-1 (sICAM-1) by draining lymph fluid and collecting serum in 2 groups. RESULTS: The drainage of lymph fluid was successfully performed. The HMGB1, endotoxin, and cytokines in serum and lymph fluid were significantly higher in ischemia-reperfusion group than in drainage group (P < 0. 05). CONCLUSIONS: The method for drainage of lymph fluid is simple and feasible. Endotoxin, HMGB1, and some cytokines in serum and lymph fluid may mediate the ischemia-reperfusion injury.

[Effect of mesenteric lymphatic duct ligation on the system inflammation during the intestinal ischemia-reperfusion].

OBJECTIVE: To estimate the effect of the lymph duct ligation on systemic inflammatory factors and endotoxins during intestinal ischemia-reperfusion (I/R). METHODS: Male SD rats underwent occlusion of superior mesenteric artery for 60 min followed by reperfusion for 120 min plus lymph duct ligation or not. Forty rats were randomly divided into 4 groups: group A (blank); group B (sham); group C (intestinal I/R); group D (intestinal I/R plus lymph duct ligation). Mesenteric lymph nodes were harvested for standard bacteriologic cultures. The endotoxin, D-lactate, diamine oxidase (DAO), and cytokines in serum were detected. RESULTS: The rates of bacterial translocation to mesenteric lymph nodes were 40% in group C and 20% in group D. No positive lymph node cultures were encountered in any of group A and B. The serum cytokines (except for sICAM-1) , D-lactate, DAO and endotoxin levels were lower in group D than those in group C (P<0.05), but both were higher than those in group A and B (P<0.05). CONCLUSION: During intestinal I/R injury, blockage the lymph flow from gut into bloodstream decreases the levels of cytokines, and significantly attenuates the increase in intestinal permeability.

[Analysis of maltose clearance in plasma and urine of healthy volunteers with high-performance liquid chromatography].

OBJECTIVE: To analyze the maltose clearance in plasma and urine of healthy volunteers with high-performance liquid chromatography. METHODS: Maltose solution was infused to 12 healthy volunteers during a 4-hour period at an infusion rate of 0.2, 0.3, and 0.5 g/(kg x h), Plasma and urine specimens were collected at different time points before and after infusion, and then analyzed with high-performance liquid chromatography. RESULTS: The coefficients of variation of the precision and accuracy of the analysis method ranged 3.68%-4.58% and 0.44%-4.83% for plasma, respectively, and 2.91%-7.62% and 0.95%-8.27% for urine, respectively. The plasma maltose concentration increased in a dose-dependent manner (r > 0.99). The plasma maltose concentrations returned to the baseline levels 12 hours later. Two hours after injection, the urinary excretion of maltose increased, reached the peak value within 2-4 hours, began to decrease 6 hours later, and became zero 24 hours later. CONCLUSIONS: An infusion rate of 0.2-0.5 g/(kg x h) of maltose will not remarkably increase the blood glucose level in healthy people. The routine infusion rate should below 0.3 g/(kg x h), unless an emergency exists.

[Application of nutrigenomics in clinical nutrition].

In the past decade, the focus of nutritional study shifted from epidemiology and physiology to molecular biology. Advanced research strategies and technologies including genomics, transcriptomics, proteomics, metabolomics, and system biology have been gradually applied in clinical nutrition. This article reviews the effects of nutrients on gene expressions, application of modern molecular biology in clinical nutrition, as well as the advances and challenges in recent years..