Objective To study the protective effect of glutamine on the intestinal mucosal antioxidation in endotoxemic rats. Methods Twenty-eight male Wistar rats were randomly divided into three groups, group A:parenteral nutrition supplemented with glutamine, group B:TPN without glutamine,and group C:normal control. Endotoxemia was induced by continous intravenous infusion of lipopolysaccharide(LPS) at a dose of 2 mg/kg per day throughout the 5-day study period. The mucosal protein、DNA、ATP、SOD、MDA、GSH、sIgA were determined. Results The mucosal protein、DNA、ATP、SOD、GSH and sIgA content in endotoxic rats were markedly decreased, MDA was increased as compared with normal control(P＜0.05). The former indices in group A were improved and MDA content was decreased as compared with group B(P＜0.05). Conclusion Glutamine can improve gut energy metabolism, decrease the extent of mucosal injury of free radicals, and give an protective effect on the mucosal probably by increasing GSH.
ObjectiveTo determine the effects of different volume fluid resuscitation on intestinal injury and the permeability of intestine in hemorrhagic shock rats. MethodsSprague-Dawley male rats(n=72) were randomly equally divided into 4 groups after the model establishment of blood pressure-controlled hemorrhage, 45, 30, and 15 mL/(kg·h) of fluid resuscitation were performed in high dosage of resuscitation(HLR), moderate dosage of resuscitation(MLR), and low dosage of resuscitation(LLR) group respectively, but rats of Sham group didn't accept fluid resuscitation. After resuscitation, ten centimeters ileum was harvested for testing intestinal permeability. Then 6 rats of each group were sacrificed at 24, 48, and 72 hours after fluid resuscitation respectively. Over the specified time interval, blood was collected for testing levels of lactic acid and plasma tumor necrosis factor-α(TNF-α). The ileums of 3 resuscitation groups were obtained for testing the ratio of wet weight to dry weight and observing the histological changes. ResultsAfter resuscitation, the intestinal permeability was higher in HLR group(P<0.05). At 3-8 hours after resuscitation, rats of Sham group were all died, and the other rats of 3 groups were all alive. The level of plasma lactic acid was lower in LLR group than those of other 2 groups at 24 hours(P<0.05). The levels of TNF-α were higher in HLR group than those of other 2 groups at 24, 48, and 72 hours(P<0.05), and at 48 hours, level of TNF-α in LLR group was lower than MLR group(P<0.05). At 24 hours after resuscitation, ratio of intestinal wet weight to dry weight in LLR group was the lowest, and HLR group was the highest(P<0.05). According to the histopathology, intestinal injuries of the 3 groups were tend to be remission with the time, and at 48 and 72 hours after resuscitation, intestinal villus of LLR group appeared to be normal. ConclusionLimited fluid resuscitation of 15 mL/(kg·h) could not only decrease the levels of lactic acid and TNF-α, but also moderate the intestinal permeability and the intestinal injury in early stage after shock and surgery.
ObjectivesTo systematically review the risk factors for intestinal injury induced by non-steroidal anti-inflammatory drugs(NSAIDs).MethodsWe comprehensively searched WanFang Data, CNKI, Web of Science, EBSCO, PubMed and The Cochrane Library databases to collect studies on risk factors of NSAIDs-induced intestinal injury. Two reviewers independently screened literature, extracted data and assessed risk of bias, and then, meta-analysis was performed by using RevMan 5.2 and STATA 12.0 software.ResultsA total of 6 case-control studies were included, in which 265 patients were in the case group and 301 patients in the control group. The results of meta-analysis showed that PPI was an independent risk factor for NSAIDs-induced intestinal injury (OR=1.59, 95%CI 1.07 to 2.35, P=0.02). In addition, patients with osteoarthritis (OR=2.44, 95% CI 1.11 to 5.36, P=0.03) or rheumatoid arthritis (OR=3.04, 95% CI 1.31 to 7.03, P=0.01) was associated with intestinal mucosal injury induced by NSAIDs. Gender, age, smoking history, drinking history, H2RA and rebamipide medication history, cardiovascular disease and cerebrovascular disease were not associated with intestinal injury.ConclusionsPPI is an independent risk factor for NSAIDs-induced intestinal injury. However, studies with high-quality, larger sample size are required to further verify that PPI increases the prevalence of intestinal injury.