低剂量亚硝酸钠对失血性休克大鼠肠屏障功能的影响

发布时间：2018-02-01 15:00

本文关键词： 亚硝酸钠失血性休克肠屏障　出处：《山西医科大学》2013年硕士论文　论文类型：学位论文

【摘要】：目的(1)通过对肿瘤坏死因子α (tumor necrosis factor-α, TNF-α)的含量、髓过氧化物酶(myeloperoxidase, MPO)的含量,及肠粘膜屏障完整性的病理学观察和评分,探讨失血性休克大鼠的复苏过程中,在亚硝酸钠的参与下,是否可以对肠粘膜屏障的功能起到保护作用。 (2)通过测定失血性休克大鼠肠粘膜中一氧化氮(nitric oxide, NO)的含量变化,观察亚硝酸钠对肠粘膜的作用是否与NO的含量有关。方法清洁级健康雄性Sprague-Dawley (SD)大鼠40只,随机分为4组。体重200～250g,每组十只：即假手术组(S组)、失血性休克组(HS组)、亚硝酸钠组(NI组)、酚妥拉明组(PI组)。肝素化大鼠0.1mg/kg,暴露左侧颈总动脉并插管,待血压稳定后,经颈动脉放血(0.5ml/min)诱导休克,10min达到休克状态,休克的标准为平均动脉压(mean artery pressure, MAP)维持在35～40mm Hg之间,若MAP低于此水平,则回输自体血,若MAP高于此水平,继续放血,维持休克状态60min,放出的自体血回收,常温保存。经股静脉首先回输自体血进行复苏,若输入自体血后,血压不能维持在理想水平,则加用生理盐水复苏,速度均为0.2ml/min,20min复苏结束,并维持MAP在休克前的80%。NI组、PI组分别于复苏后10min给予药物干预亚硝酸钠(4.8mmol)酚妥拉明(0.123mg),假手术组动物除不放血和输液外,其他处理与失血性休克组相同。复苏2h后,处死大鼠,取肠组织。肠组织粘膜在光镜下对进行分析、评分。使用免疫组织化学法测定肠组织TNF-α的含量,制备组织匀浆测定MPO、NO的含量。结果与S组相比,HS组肠黏膜破坏严重,组织损伤评分高,TNF-α、MPO和NO含量增高(P0.05)；与HS组相比,NI组和PI组损伤程度略轻于HS组,并且TNF-α、MPO含量下降,NO含量增高(P0.05),其中NI组损伤程度最轻,NO含量最高(P0.05)；与HS组相比,PI组的NO含量无明显差异。结论(1)失血性休克后,可引起肠道炎症反应,肠粘膜屏障损伤。 (2)大鼠肠道炎症反应的引起及屏障的破坏可能与TNF-α及中性粒细胞增多有关。 (3)复苏过程中,若使用亚硝酸钠,可使肠道炎症反应减轻,肠道屏障功能改善,这些作用与NO含量增高、TNF-α减低、中性粒细胞减少有关。
[Abstract]:Objective to investigate the effect of tumor necrosis factor- 伪 (TNF- 伪) on tumor necrosis factor 伪 (TNF- 伪). The contents of myeloperoxidase (MPO) and the integrity of intestinal mucosal barrier were observed and scored in order to explore the process of resuscitation in hemorrhagic shock rats. Whether, with the participation of sodium nitrite, the function of intestinal mucosal barrier can be protected. The contents of nitric oxide (no) in intestinal mucosa of hemorrhagic shock rats were determined. To observe whether the effect of sodium nitrite on intestinal mucosa is related to the content of no. Methods 40 healthy male Sprague-Dawley rats of clean grade were used. They were randomly divided into 4 groups, weighing 200,250g, with 10 rats in each group: sham operation group (S group), hemorrhagic shock group (HS group) and sodium nitrite group (NI group). Heparinized rats (0.1 mg / kg) were exposed to the left common carotid artery and intubated. After stable blood pressure, shock was induced through carotid artery bleeding (0.5 ml / min). The standard of shock was mean artery pressure (MAPP) between 35 and 40 mm Hg. If MAP is below this level, autologous blood is reinfused. If MAP is above this level, continue to bleed, maintain shock state for 60 minutes, and recover the released autologous blood. The blood was resuscitated through the femoral vein. If the blood pressure could not be maintained at the ideal level after the autologous blood was infused, the blood pressure could be resuscitated with physiological saline at a speed of 0.2 ml / min. After 20 minutes of resuscitation, MAP was maintained in the 80.NI group before shock. Pi group was given drug intervention with sodium nitrite 4.8mmol / L) Phenodol Lemine 0.123 mg / g after resuscitation 10 minutes after resuscitation, except for no bleeding and transfusion in sham operation group. The other treatments were the same as those in the hemorrhagic shock group. After resuscitation for 2 hours, the rats were killed and the intestinal tissues and mucosa were analyzed under light microscope. The content of TNF- 伪 in intestinal tissue was determined by immunohistochemical method, and the content of MPON- 伪 in tissue homogenate was determined by immunohistochemical method. Results compared with S group, the intestinal mucosal damage in HS group was serious, and the tissue injury score was higher than that in S group. The contents of TNF- 伪 MPO and no in HS group were higher than those in S group (P 0.05). Compared with HS group and Pi group, the degree of injury was slightly lighter, and the content of TNF- 伪 -MPO decreased and the content of no increased (P 0.05), among which the injury degree of NI group was the least. The content of no was the highest (P 0.05). There was no significant difference in no content in Pi group compared with HS group. Conclusion 1) hemorrhagic shock can induce intestinal inflammation and injury of intestinal mucosal barrier. 2) the intestinal inflammatory reaction and barrier damage in rats may be related to the increase of TNF- 伪 and neutrophils. During the course of resuscitation, sodium nitrite could relieve the inflammatory reaction and improve the intestinal barrier function. These effects were related to the increase of no content and the decrease of TNF- 伪 and neutrophils.
【学位授予单位】：山西医科大学
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R459.7

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