本文選題：慢性間歇低氧 + 血管內(nèi)皮��； 參考：《蘇州大學(xué)》2010年碩士論文

【摘要】： 第一部分慢性間歇低氧小鼠血管內(nèi)皮功能障礙及相關(guān)機(jī)制的探討 目的探討慢性間歇低氧(CIH)對(duì)小鼠血管內(nèi)皮功能的影響。 方法在我們前期研究已建立的間歇低氧小鼠模型基礎(chǔ)上,采用硝酸還原酶法檢測(cè)間歇低氧(CIH)1周、2周、3周、4周、6周后小鼠血清NO的水平,并應(yīng)用化學(xué)比色法測(cè)定小鼠血清e(cuò)NOS的活性,觀察低氧不同時(shí)間段NO體系的變化情況,并用透射電鏡觀察低氧6周小鼠肺動(dòng)脈內(nèi)皮細(xì)胞結(jié)構(gòu)的變化。 結(jié)果(1)在間歇低氧造模第1周時(shí),CIH組小鼠血清NO水平較對(duì)照組有所下降,但差異無統(tǒng)計(jì)學(xué)意義(p0.05);自低氧第2周始,小鼠血清NO下降水平較UC組比較差異有統(tǒng)計(jì)學(xué)意義,(CIH 78.96±9.93μmol/L UC 106.31±19.06μmol/L,p0.05)。隨著間歇低氧時(shí)間的延長,CIH組小鼠血清NO水平呈逐漸下降趨勢(shì),各造模時(shí)間段兩組之間比較,差異均有統(tǒng)計(jì)學(xué)意義(p0.05或p0.01)。另外,CIH各組小鼠血清e(cuò)NOS活性也隨造模時(shí)間呈逐漸下降趨勢(shì),自間歇低氧1周始,CIH組血清e(cuò)NOS活性較對(duì)照組有所下降,差異有統(tǒng)計(jì)學(xué)意義(CIH 22.26±2.96 UC 25.58±3.47 U/ml,p0.05);隨后低氧各組小鼠血清e(cuò)NOS活性均較UC組顯著下降,兩組間比較差異均有統(tǒng)計(jì)學(xué)意義(p0.05或p0.01)。 (2)低氧第6周后小鼠肺動(dòng)脈內(nèi)皮超微結(jié)構(gòu)的改變:電鏡下觀察發(fā)現(xiàn),間歇低氧小鼠肺動(dòng)脈內(nèi)皮細(xì)胞核膜模糊,染色質(zhì)邊集,內(nèi)膜向管腔內(nèi)突起,并可見內(nèi)皮細(xì)胞水腫,線粒體嵴稀疏,輕度腫脹,部分呈空泡變性。 結(jié)論隨著間歇低氧時(shí)間的延長,小鼠血清NO水平和eNOS活性逐漸下降,肺動(dòng)脈內(nèi)皮結(jié)構(gòu)受損。 第二部分阻塞性睡眠呼吸暫停低通氣綜合征患者血清NO水平的檢測(cè)及其臨床意義 目的探討不同程度阻塞性睡眠呼吸暫停低通氣綜合征(OSAHS)患者血清NO水平的變化的意義。 方法納入2008年6月-2009年2月在我院睡眠中心就診的73名男性成年打鼾患者,進(jìn)行多導(dǎo)睡眠圖(PSG)監(jiān)測(cè)。按照OSAHS診斷標(biāo)準(zhǔn),根據(jù)呼吸紊亂指數(shù)(AHI)將所有對(duì)象分為3組:單純鼾癥組(AHI5/h,12例),輕-中度(AHI 5-40/h,36例)和重度OSAHS組(AHI40/h,25例),采用硝酸還原酶法測(cè)定其血清NO水平,比較血清NO水平、高血壓發(fā)生率、體重指數(shù)(BMI)和PSG監(jiān)測(cè)的睡眠呼吸參數(shù)(最低氧飽和度(L-SaO2)、SaO290%的時(shí)間(min)、平均氧飽和度(M-SaO2)以及AHI)在不同嚴(yán)重程度的OSAHS患者間的差異,同時(shí)分析血清NO水平和各參數(shù)之間的相關(guān)性。 結(jié)果各組研究對(duì)象的年齡、BMI之間的差異無統(tǒng)計(jì)學(xué)意義(p0.05)。隨著OSAHS嚴(yán)重程度加重,高血壓發(fā)生率逐步上升;重度OSAHS組氧減指標(biāo)較其他兩組加重,差異有顯著統(tǒng)計(jì)學(xué)意義(均p0.01),血清NO水平隨著OSAHS嚴(yán)重程度逐漸降低,組間比較有顯著統(tǒng)計(jì)學(xué)意義(p0.01),OSAHS患者的血清NO水平與AHI、SaO290%的時(shí)間呈負(fù)相關(guān)(r分別為-0.83,-0.54,p0.01),與M-SaO2、L-SaO2呈正相關(guān)(r分別為0.48和0.52,均p0.01)。 結(jié)論阻塞性睡眠呼吸暫停低通氣綜合征(OSAHS)患者高血壓發(fā)生率隨著OSAHS的嚴(yán)重程度而升高,OSAHS患者血清NO水平隨病情嚴(yán)重程度的加重而降低,這可能是高血壓病發(fā)生、發(fā)展的重要因素之一。
[Abstract]:Part 1: endothelial dysfunction and related mechanisms in chronic intermittent hypoxia mice
Objective to investigate the effects of chronic intermittent hypoxia (CIH) on vascular endothelial function in mice.
Methods on the basis of our pre established intermittent hypoxia mice model, the serum levels of NO in mice were measured by the nitrate reductase method for 1 weeks, 2 weeks, 3 weeks, 4 weeks and 6 weeks, and the activity of eNOS in the serum of mice was measured by chemical colorimetry, and the changes of NO system in different periods of hypoxia were observed and the transmission electron microscope was used. The changes of pulmonary artery endothelial cell structure in 6 week hypoxia were observed.
Results (1) at first weeks of intermittent hypoxia, the serum level of NO in CIH group was lower than that of the control group, but the difference was not statistically significant (P0.05). Since the second weeks of hypoxia, the decrease of serum NO in mice was statistically significant compared with that of the UC group (CIH 78.96 + 9.93 mu mol/L UC 106.31 + 19.06 mol/L, P0.05). The level of serum NO in the CIH group was gradually decreasing. The difference between the two groups was statistically significant (P0.05 or P0.01). In addition, the serum eNOS activity of all CIH mice decreased gradually with the time of modeling, and the activity of eNOS in the CIH group decreased from 1 weeks to the intermittent hypoxia, and the difference was statistically significant. Significance (CIH 22.26 + 2.96 UC 25.58 + 3.47 U/ml, P0.05), and then the serum eNOS activity of the mice in each group was significantly lower than that in the UC group, and the difference was statistically significant between the two groups (P0.05 or P0.01).
(2) ultrastructural changes in the pulmonary artery endothelium of mice after sixth weeks of hypoxia: under the electron microscope, it was found that the nuclear membrane of the pulmonary artery endothelial cells in the intermittent hypoxic mice was blurred, the chromatin was set, the endometrium protruded into the lumen, the edema of the endothelial cells, the sparsity of the crista, the slight swelling of the mitochondria, and some vacuolated degeneration.
Conclusion with the prolongation of intermittent hypoxia time, serum NO level and eNOS activity in mice gradually decrease, and the structure of pulmonary artery endothelium is impaired.
The second part of serum NO level in patients with obstructive sleep apnea hypopnea syndrome and its clinical significance
Objective to explore the significance of changes of serum NO levels in patients with obstructive sleep apnea hypopnea syndrome (OSAHS).
Methods the polysomnography (PSG) was carried out in 73 male adult snoring patients in the sleep center of our hospital in February -2009 June 2008. According to the OSAHS diagnostic criteria, all the objects were divided into 3 groups: simple snoring group (AHI5/h, 12 cases), mild to moderate (AHI 5-40/h, 36 cases) and severe OSAHS group (AHI40/h, 25 cases). The serum level of NO was measured with nitrate reductase, and the difference in the serum NO level, the incidence of hypertension, the body mass index (BMI) and PSG monitoring of the sleep breathing parameters (L-SaO2), the time of SaO290% (min), the average oxygen saturation (M-SaO2) and AHI) in the OSAHS patients with different severity, and the analysis of the serum NO level were compared. Correlation with each parameter.
Results there was no significant difference in age and BMI between the subjects of each group (P0.05). As the severity of OSAHS aggravated, the incidence of hypertension increased gradually, and the oxygen reduction index in the severe OSAHS group was heavier than the other two groups, and the difference was statistically significant (P0.01). The serum NO level gradually decreased with the severity of OSAHS, and there was a significant difference between the groups. Statistical significance (P0.01), the level of serum NO in OSAHS patients was negatively correlated with the time of AHI, SaO290% (R respectively -0.83, -0.54, P0.01), and was positively correlated with M-SaO2, L-SaO2 (r was 0.48 and 0.52 respectively).
Conclusion the incidence of hypertension in patients with obstructive sleep apnea hypopnea syndrome (OSAHS) increases with the severity of OSAHS, and the level of serum NO in OSAHS patients decreases with the severity of the disease, which may be one of the important factors for the development of hypertension.
【學(xué)位授予單位】：蘇州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2010
【分類號(hào)】：R766

【參考文獻(xiàn)】

相關(guān)期刊論文 前6條

1 田蓉;平芬;高鳳岐;趙景春;韓書芝;馬秀芬;;阻塞性睡眠呼吸暫停低通氣綜合征合并高血壓患者血內(nèi)皮素、一氧化氮及腫瘤壞死因子-α水平的變化[J];國際呼吸雜志;2006年06期

2 宋愛玲;曾奕明;陳曉陽;;慢性缺氧/再氧合小鼠模型實(shí)驗(yàn)研究[J];國際呼吸雜志;2006年06期

3 袁志明,陳寶元,王佩顯,蔣漢濤,張敬霞;慢性間歇低氧誘發(fā)大鼠高血壓發(fā)病過程中一氧化氮和一氧化氮合酶的變化[J];臨床心血管病雜志;2005年08期

4 中華醫(yī)學(xué)會(huì)呼吸病學(xué)分會(huì)睡眠呼吸疾病學(xué)組;阻塞性睡眠呼吸暫停低通氣綜合征診治指南(草案)[J];中華結(jié)核和呼吸雜志;2002年04期

5 王贊峰;馮學(xué)威;康健;;阻塞性睡眠呼吸暫停低通氣綜合征患者的血管內(nèi)皮舒張功能[J];中華結(jié)核和呼吸雜志;2006年11期

6 陳寶元;何權(quán)瀛;;重視睡眠呼吸暫停模式的間歇低氧研究[J];中華結(jié)核和呼吸雜志;2007年12期

，

本文編號(hào)：1952428