本文選題：慢性低氧性肺動脈高壓　切入點(diǎn)：肺損傷　出處：《南華大學(xué)》2015年碩士論文

【摘要】：目的:探索吸入氫氣對慢性低氧性肺動脈高壓的影響。方法:(1)動物的分組及缺氧處理:將30只,4-6周大健康雄性清潔級C57小鼠(四川省實(shí)驗(yàn)動物中心),重量(18-22)g,隨機(jī)分為3組:空白對照組(Control)、缺氧組(Hypoxia)、缺氧+氫氣吸入組(Hypoxia+H2)每組10只。空白組不做任何處理;缺氧組予置于氧倉吸入低氧混合氣體(10%O2+90%N2),每天8小時,其余時間置于常氧,持續(xù)28天;缺氧+氫氣吸入組在低氧混合氣體中加入氫氣(10%O2+4%H2+86%N2),其他與缺氧組相同。低氧處理28天后,取組織標(biāo)本檢查;(2)慢性缺氧模型檢驗(yàn):28天缺氧暴露結(jié)束后,予3%戊巴比妥鈉(25mg/kg)腹腔注射,氣管插管,頸動脈采血后,即查血常規(guī),統(tǒng)計三組的紅細(xì)胞、血紅蛋白;(3)評估肺動脈高壓(Pulmonary arterial hypertension,PAH)模型:造模完成后,開胸取出心臟組織,分離左右心室并稱重,求得心室肥厚指數(shù)。取同一側(cè)同一肺段,4%多聚甲醛固定后,切片,HE染色,使用image processing program6.0測量小血管內(nèi)外徑,通過心室肥厚指數(shù)和肺微小動脈增生兩項(xiàng)間接指標(biāo)來反映;(4)肺損傷評估:肺組織HE染色后。使用光學(xué)顯微鏡進(jìn)行觀察,參照Mikawa方法進(jìn)行肺病理評分;(5)肺組織炎性因子測定:肺組織勻漿后,提取組織液,應(yīng)用酶聯(lián)免疫吸附試驗(yàn)(Enzyme linked immunosorbent assay,ELISA)法檢測。(6)肺組織丙二醛(malondialdehyde,MDA)測定:肺組織勻漿后,提取組織液,定量肺組織MDA。結(jié)果:(1)紅細(xì)胞、血紅蛋白測定:缺氧組與缺氧+氫氣吸入組紅細(xì)胞數(shù)目和血紅蛋白量均增高,符合慢性缺氧血液系統(tǒng)變化,但缺氧組的變化最為顯著;(2)心室肥厚指數(shù)(Right Ventricular Hypertrophy Index,RVHI)和肺血管中膜厚度百分比(Wall thickness percentage,MT%)測定:缺氧組和缺氧+氫氣吸入組與對照組相比,RVHI均增高。缺氧組MT%增高,符合肺動脈高壓的病理學(xué)改變,氫氣吸入可改善PAH;(3)肺損傷評估:缺氧組肺病理評分較對照組增高,出現(xiàn)了肺組織間隙的充血和炎細(xì)胞的浸潤。缺氧+氫氣吸入組無明顯的肺損傷表現(xiàn);(4)炎性因子和MDA的檢測:Elisa測得腫瘤壞死因子(Turmor necrosis factor-α,TNF-α)和中性粒細(xì)胞彈性蛋白酶(Neutrophil elastase,NE)以及肺組織MDA定量,在缺氧組和缺氧+氫氣吸入組均有增高,但缺氧+氫氣治療組較輕。結(jié)論:吸入氫氣通過抗氧化、抗炎作用保護(hù)肺組織并改善肺動脈高壓。
[Abstract]:Objective: to explore the effect of hydrogen inhalation on chronic hypoxic pulmonary hypertension. Methods: 30 healthy male C57 mice aged 4-6 weeks (Sichuan Experimental Animal Center, weighing 18-22g) were divided into groups and treated with hypoxia. The rats were divided into 3 groups: control group (n = 10), control group (n = 10), hypoxia group (n = 10) and hypoxic hydrogen inhalation group (n = 10). Hypoxia group was placed in oxygen chamber and inhaled hypoxia mixture gas 10O290N _ 2 for 8 hours per day, the rest of the time was placed in normoxic for 28 days. The hypoxic hydrogen inhalation group added 10O2 4%H2 86N 2 to the hypoxic mixture gas, and the others were the same as the hypoxia group. After 28 days of hypoxia treatment, tissue specimens were taken for examination. 3% pentobarbital sodium (25 mg / kg) was injected intraperitoneally, endotracheal intubation was performed, blood routine was checked immediately after carotid artery blood sampling, the red blood cells and hemoglobin of the three groups were counted to evaluate pulmonary arterial hypertensionPAH) model: after the model was made, the heart tissue was taken out by thoracotomy. The left and right ventricle were separated and weighed, and the ventricular hypertrophy index was obtained. After fixed with 4% paraformaldehyde in the same lung segment, the sections were stained with HE, and the diameter of small vessels was measured by image processing program6.0. The evaluation of lung injury was reflected by two indirect indexes of ventricular hypertrophy index and pulmonary arteriolar hyperplasia: lung tissue was stained with HE and observed with optical microscope. According to Mikawa method, lung tissue inflammatory factors were measured: after lung tissue homogenate, tissue extract was extracted. Enzyme linked immunosorbent assay (Elisa) was used to detect malondialdehyde malondialdehyde (MDA) in lung tissue. Results quantitative lung tissue MDA.Results erythrocyte and hemoglobin measurement: the number of red blood cells and hemoglobin content in hypoxia group and hypoxia hydrogen inhalation group were increased, which were consistent with the changes of chronic hypoxia blood system. However, the changes of right Ventricular Hypertrophy index (RVHI) and the percentage of pulmonary vascular mesenchymal thickness (RVHI) in hypoxia group and hypoxic hydrogen inhalation group were higher than those in control group, and that in hypoxia group was higher than that in control group, and that in hypoxia group was higher than that in control group. In accordance with the pathological changes of pulmonary hypertension, hydrogen inhalation could improve the assessment of pulmonary injury: the lung pathological score of hypoxia group was higher than that of control group. Hyperemia and infiltration of inflammatory cells occurred in lung tissue space. There were no obvious lung injury manifestations in hypoxic hydrogen inhalation group. (4) inflammatory factors and MDA were detected. Tumor necrosis factor Turmor necrosis factor- 偽 (TNF- 偽) and neutrophil were detected by MDA. And MDA in lung tissue. Conclusion: hydrogen inhalation can protect lung tissue and improve pulmonary hypertension by anti-oxidation, anti-inflammatory effect.
【學(xué)位授予單位】：南華大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2015
【分類號】：R544.1

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