本文關鍵詞： 亞硝酸鈉 失血性休克 腸屏障　出處：《山西醫(yī)科大學》2013年碩士論文　論文類型：學位論文

【摘要】：目的(1)通過對腫瘤壞死因子α (tumor necrosis factor-α, TNF-α)的含量、髓過氧化物酶(myeloperoxidase, MPO)的含量,及腸粘膜屏障完整性的病理學觀察和評分,探討失血性休克大鼠的復蘇過程中,在亞硝酸鈉的參與下,是否可以對腸粘膜屏障的功能起到保護作用。 (2)通過測定失血性休克大鼠腸粘膜中一氧化氮(nitric oxide, NO)的含量變化,觀察亞硝酸鈉對腸粘膜的作用是否與NO的含量有關。方法清潔級健康雄性Sprague-Dawley (SD)大鼠40只,隨機分為4組。體重200～250g,每組十只：即假手術組(S組)、失血性休克組(HS組)、亞硝酸鈉組(NI組)、酚妥拉明組(PI組)。肝素化大鼠0.1mg/kg,暴露左側頸總動脈并插管,待血壓穩(wěn)定后,經(jīng)頸動脈放血(0.5ml/min)誘導休克,10min達到休克狀態(tài),休克的標準為平均動脈壓(mean artery pressure, MAP)維持在35～40mm Hg之間,若MAP低于此水平,則回輸自體血,若MAP高于此水平,繼續(xù)放血,維持休克狀態(tài)60min,放出的自體血回收,常溫保存。經(jīng)股靜脈首先回輸自體血進行復蘇,若輸入自體血后,血壓不能維持在理想水平,則加用生理鹽水復蘇,速度均為0.2ml/min,20min復蘇結束,并維持MAP在休克前的80%。NI組、PI組分別于復蘇后10min給予藥物干預亞硝酸鈉(4.8mmol)酚妥拉明(0.123mg),假手術組動物除不放血和輸液外,其他處理與失血性休克組相同。復蘇2h后,處死大鼠,取腸組織。腸組織粘膜在光鏡下對進行分析、評分。使用免疫組織化學法測定腸組織TNF-α的含量,制備組織勻漿測定MPO、NO的含量。 結果與S組相比,HS組腸黏膜破壞嚴重,組織損傷評分高,TNF-α、MPO和NO含量增高(P0.05)；與HS組相比,NI組和PI組損傷程度略輕于HS組,并且TNF-α、MPO含量下降,NO含量增高(P0.05),其中NI組損傷程度最輕,NO含量最高(P0.05)；與HS組相比,PI組的NO含量無明顯差異。 結論(1)失血性休克后,可引起腸道炎癥反應,腸粘膜屏障損傷。 (2)大鼠腸道炎癥反應的引起及屏障的破壞可能與TNF-α及中性粒細胞增多有關。 (3)復蘇過程中,若使用亞硝酸鈉,可使腸道炎癥反應減輕,腸道屏障功能改善,這些作用與NO含量增高、TNF-α減低、中性粒細胞減少有關。
[Abstract]:Objective to investigate the effect of tumor necrosis factor- 偽 (TNF- 偽) on tumor necrosis factor 偽 (TNF- 偽). 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- 偽 in intestinal tissue was determined by immunohistochemical method, and the content of MPON- 偽 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- 偽 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- 偽 -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- 偽 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- 偽 and neutrophils.
【學位授予單位】：山西醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2013
【分類號】：R459.7

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