[Effects of intermittent hypoxia intestinal bacterial translocation on mesenteric lymph node injury].

Objective: To observe the effect of intermittent hypoxia on intestinal bacterial translocation and mesenteric lymph node (MLN) structure and explore its mechanism. Methods: Twenty-four adult male Wistar rats were randomly divided into an experimental group (HI group) and a control group (UC group), with 12 rats in each. During the experiment, both groups were fed under the same conditions, but the HI group received simulated sleep apnea with hypoxic treatment. On the last day of the 2nd and 4th week of the experiment, 20% urethane(0.7 ml/100g) was used for anesthesia, and MLNs and corresponding small intestinal tissues were aseptically collected.HE staining was used to observe the microscopic changes of the tissues. The lymph node tissue was sent for pathogenic culture. The levels of oxide dismutase (SOD), lipid peroxide (MDA) and reactive oxygen species (ROS) were measured for the extent of oxidative stress. Serum diamine oxidase (DAO) was measured to assess the extent of intestinal mucosal damage. Result: MLNs and their corresponding small intestines were damaged in the HI group as compared to the UC group. With the prolongation of intermittent hypoxic time, the number of germinal centers in MLNs was significantly reduced, with the volume reduced, cortical medullary fusion aggravated, and the area ratio increased. The intestinal tissue showed severe damage to the intestinal epithelium, increased permeability, mucosal edema, and changes of the crypts. At the 4th week, MLNs in the HI group grew Clostridium perfringens under anaerobic conditions, confirming intestinal bacterial translocation. The contents of ROS, SOD and MDA in MLNs of the HI group were significantly higher than those in the UC group ( P <0.05). At the 2nd week and the 4th week, the contents of ROS, SOD and MDA were not significantly changed in the UC group( P >0.05). While the content of ROS and MDA in MLNs of the HI group at 4th week was significantly higher than that in the second week ( P <0.05), but no change of SOD was observed ( P >0.05). Serum DAO levels in the HI group were higher than those in the UC group at week 2 and week 4 ( P <0.05), suggesting that the degree of intestinal mucosal injury in the HI group was more serious than that in the UC group. Conclusion: Hypoxic exposure aggravated the degree of oxidative stress in rats. With the prolongation of intermittent hypoxia, the intestinal mucosa of rats was seriously damaged. The intestinal flora shifted to damage the structure of mesenteric lymph nodes, and oxidative stress was further aggravated, which in turn affected the integrity of the intestinal autoimmune function.