慢性肺源性心脏病患者血清TGF-β1水平与动脉血氧分压及心脏超声右心指标相关性的研究
发布时间：2018-07-31 08:32
【摘要】：目的:慢性肺源性心脏病,简称慢性肺心病,是一种常见的呼吸系统慢性疾病。患者肺、心功能均受到不同程度的损害,病情逐渐进展,对患者的生活质量及生存寿命造成严重影响。目前,慢性肺心病的发病机制尚未完全明确,但得到广泛认同的是,低氧性肺动脉高压是其发生、发展的中心环节。低氧性肺动脉高压包含两方面重要的病理生理学改变,即低氧性肺血管收缩和低氧性肺血管重构,后者使肺动脉的解剖结构发生变化,形成肺循环血流动力学的障碍。低氧性肺血管重构是肺动脉高压由可逆性转变为持续存在的决定因素,也是临床上血管舒张药物治疗肺动脉高压需要攻克的难点。转化生长因子b1(transforming growth factorβ1,TGF-β1)是新近发现的一种调节细胞生长和分化的细胞因子,在促纤维化及组织结构重构方面作用显著,可以引起血管壁实质细胞的增殖、肥大、重排、迁移、凋亡和细胞外基质增加。现有研究表明TGF-β1的蛋白、m RNA在低氧诱导的慢性肺心病动物模型的支气管粘膜、肺组织、肺血管管壁及支气管肺泡灌洗液、血清中均处于高表达,提示低氧可能导致TGF-β1表达水平增加,活化的TGF-β1在推动肺动脉高压及肺心病的形成和发展过程中扮演着重要角色,由此推测TGF-β1水平在慢性肺心病患者血清中也可能是升高的。本研究测定了90例慢性肺心病患者在不同时期下(急性加重期和缓解期)血清TGF-β1的表达水平,并将其与动脉血氧分压(Pa O2)及反映肺动脉高压、右心室扩大的超声指标—主肺动脉内径(MPAD)、右室内径(RVD)、肺动脉收缩压(PASP)进行相关性分析,进一步探究TGF-β1在慢性肺源性心脏病中的作用,为其防治提供新的临床思路。方法:慢性肺心病急性加重期患者90例,男62例,女28例,年龄58~83岁,平均(69.77±7.24)岁,经常规治疗症状、体征等病情稳定后2周作为缓解期组。选取性别、年龄等一般资料相匹配的90例健康人为健康对照组。各组血清TGF-β1的测定采用酶联免疫吸附法(ELISA),并应用SPSS19.0统计软件进行one-way ANOVA。患者急性加重期和缓解期均行彩色超声心动图检查,测量MPAD、RVD、PASP参数指标,并行动脉血气分析测定Pa O2,上述检测指标均与血清TGF-β1水平行相关分析。结果:1.一般资料慢性肺心病急性加重期患者90例,其中男62例,女28例,平均年龄(69.77±7.24)岁,彩色超声心动图测得的平均主肺动脉内径(MPAD)为(25.97±3.37)mm,平均右室内径为(26.43±2.99)mm,平均肺动脉收缩压(PASP)为(54.41±6.85)mm Hg。急性加重期患者经常规治疗病情缓解后测得的平均主肺动脉内径(MPAD)为(25.07±3.38)mm,平均右室内径为(26.45±3.67)mm,平均肺动脉收缩压(PASP)为(49.36±6.86)mm Hg。健康对照组90例,其中男60例,女30例,平均年龄(68.90±5.79)岁,平均主肺动脉内径(MPAD)为(19.13±2.84)mm,平均右室内径为(20.31±4.11)mm。2.各组血清TGF-β1水平TGF-β1在慢性肺心病患者急性加重期、缓解期及健康对照组受试者血清中的表达水平分别为(306.12±27.04)pg/ml、(161.16±24.00)pg/ml、(82.15±24.34)pg/ml。三组间血清TGF-β1水平差异均有统计学意义(P0.05)。3.慢性肺心病患者血清TGF-β1水平与Pa O2的相关性慢性肺心病患者急性加重期和缓解期血清TGF-β1水平均与Pa O2呈负相关(r=-0.739,P0.05;r=-0.619,P0.05)。且急性加重期Pa O2水平明显低于缓解期,差异有统计学意义(P0.05)。4.慢性肺心病患者血清TGF-β1水平与心脏超声右心参数MPAD、RVD、PASP的相关性慢性肺心病患者急性加重期血清TGF-β1水平与MPAD、RVD、PASP均呈正相关(r=0.740,P0.05;r=0.792,P0.05;r=0.878,P0.05);缓解期血清TGF-β1水平也与MPAD、RVD、PASP均呈正相关(r=0.600,P0.05;r=0.718,P0.05;r=0.630,P0.05)。结论:1.慢性肺心病患者血清TGF-β1水平明显高于健康对照组,且与反应肺动脉高压、右心室扩大的超声指标呈正相关,表明TGF-β1极有可能参与了慢性肺心病的病理生理过程。2.慢性肺心病患者血清TGF-β1水平与Pa O2呈负相关,表明TGF-β1水平升高可能与缺氧刺激有关。3.慢性肺心病患者急性加重期血清TGF-β1水平显著高于缓解期,提示TGF-β1水平监测可为慢性肺心病患者病情评估、观察疗效提供一种新的可能手段。4.慢性肺心病患者血清TGF-β1水平升高与低氧和右心系统病变关系密切,拮抗TGF-β1信号传导途径或抑制其活性有可能为慢性肺心病的防治提供新的思路。
[Abstract]:Objective: chronic pulmonary heart disease (CCHD), referred to as chronic cor pulmonale, is a common chronic respiratory disease. The lung and heart function of the patients are impaired in varying degrees, and the disease progresses gradually. The quality of life and life life of the patients is seriously affected. Hypoxic pulmonary hypertension is the central part of its development. Hypoxic pulmonary hypertension contains two important pathophysiological changes, namely hypoxic pulmonary vasoconstriction and hypoxic pulmonary vascular remodeling. The latter causes changes in the anatomical structure of the pulmonary artery, the obstacle of pulmonary circulation hemodynamics, and hypoxic pulmonary vessels. Remodeling is the determinant of the reversible transformation of pulmonary artery hypertension, and it is also a difficult problem to be tackled by clinical vasodilator in the treatment of pulmonary hypertension. Transforming growth factor B1 (transforming growth factor beta 1, TGF- beta 1) is a newly discovered cytokine that regulates cell growth and differentiation, in the promotion of fibrosis and tissue Structural remodeling has a significant role in the proliferation, hypertrophy, rearrangement, migration, apoptosis and the increase of extracellular matrix in the parenchymal cells of the vascular wall. The present study shows that the TGF- beta 1 protein, m RNA, is in the bronchial mucosa, lung tissue, pulmonary vascular wall and bronchoalveolar lavage fluid in the hypoxic induced chronic cor pulmonale animal models. It is suggested that hypoxia may lead to an increase in the expression level of TGF- beta 1. The activated TGF- beta 1 plays an important role in promoting the formation and development of pulmonary hypertension and cor pulmonale. Thus, it is suggested that the level of TGF- beta 1 in chronic cor pulmonale may also be elevated. This study measured 90 patients with chronic cor pulmonale in different cases. The expression level of serum TGF- beta 1 during the period (acute exacerbation and remission) and its correlation with arterial blood oxygen pressure (Pa O2) and pulmonary arterial hypertension, right ventricular enlargement, the main pulmonary artery internal diameter (MPAD), right ventricle diameter (RVD) and pulmonary artery systolic pressure (PASP) were analyzed to further explore the TGF- beta 1 in chronic pulmonary heart. Methods: 90 cases of acute exacerbation of chronic cor pulmonale, 62 men, 28 women, age 58~83 years, average age (69.77 + 7.24) years, regular treatment of symptoms, and signs and other conditions after the 2 weeks as remission group. Select the sex, age and other general data matching the health of healthy people in 90 cases. The serum TGF- beta 1 was measured by enzyme linked immunosorbent assay (ELISA), and the SPSS19.0 statistical software was applied to the acute exacerbation and remission period of one-way ANOVA. patients with color echocardiography. The parameters of MPAD, RVD, PASP were measured and Pa O2 was measured in parallel with arterial blood gas analysis. The above indexes were all with the level of serum TGF- beta 1. Results: 1. general data of 90 patients with acute exacerbation of chronic cor pulmonale, including 62 male and 28 female, average age (69.77 + 7.24) years, the average main pulmonary artery diameter (MPAD) was (25.97 + 3.37) mm, the mean right ventricle diameter was (26.43 + 2.99) mm, and the average systolic pressure of pulmonary artery (PASP) was (54.41 + 6.85) mm Hg The average main pulmonary artery diameter (MPAD) was (25.07 + 3.38) mm, the average right ventricle diameter was (26.45 + 3.67) mm, and the mean pulmonary artery systolic pressure (PASP) was (49.36 + 6.86) mm Hg. healthy control group, including 60 men and 30 women, with an average age of (68.90 + 3.38) years, and the average main pulmonary artery diameter (M). PAD) (19.13 + 2.84) mm, the mean right ventricular diameter was (20.31 + 4.11) mm.2. and TGF- beta 1 level TGF- beta 1 in the acute exacerbation of chronic cor pulmonale patients. The expression level of the serum in the remission stage and the healthy control group was (306.12 + 27.04) pg/ml, (161.16 + 24) pg/ml, and (82.15 + 24.34) pg/ml. three groups in the serum TGF- beta 1 level difference The levels of serum TGF- beta 1 and Pa O2 in patients with chronic pulmonary heart disease (P0.05).3. were negatively correlated with the level of TGF- beta 1 in the acute exacerbation and remission stage of chronic cor pulmonale patients (r=-0.739, P0.05; r=-0.619, P0.05). The serum levels of TGF- beta 1 in patients with chronic cor pulmonale and the right cardiac parameters of cardiac ultrasound, MPAD, RVD, PASP were correlated with the levels of TGF- beta 1 in the acute exacerbation period of chronic cor pulmonale patients with MPAD, RVD, PASP, and the level of serum beta 1 in the remission period was also positively correlated with the level of serum beta 1. R=0.718, P0.05, r=0.630, P0.05) conclusion: 1. the level of serum TGF- beta 1 in patients with chronic cor pulmonale was significantly higher than that in the healthy control group, and it was positively correlated with the ultrasound index of the pulmonary hypertension and the right ventricular enlargement, indicating that the TGF- beta 1 was very likely to be involved in the serum TGF- beta 1 level and Pa O2 of the chronic cor pulmonale patients with chronic cor pulmonale. Negative correlation shows that the elevated level of TGF- beta 1 may be significantly higher than the remission stage of serum TGF- beta 1 in patients with chronic pulmonary heart disease associated with.3. chronic cor pulmonale, suggesting that the monitoring of TGF- beta 1 can be used to evaluate the condition of chronic cor pulmonale patients. The observation of the curative effect provides a new level of serum TGF- beta 1 in patients with chronic cor pulmonale with.4.. Hyperoxia is closely related to hypoxia and right heart disease. Antagonizing TGF-beta 1 signaling pathway or inhibiting its activity may provide new ideas for the prevention and treatment of chronic pulmonary heart disease.
【学位授予单位】：承德医学院
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R541.5
本文编号：2155019
[Abstract]:Objective: chronic pulmonary heart disease (CCHD), referred to as chronic cor pulmonale, is a common chronic respiratory disease. The lung and heart function of the patients are impaired in varying degrees, and the disease progresses gradually. The quality of life and life life of the patients is seriously affected. Hypoxic pulmonary hypertension is the central part of its development. Hypoxic pulmonary hypertension contains two important pathophysiological changes, namely hypoxic pulmonary vasoconstriction and hypoxic pulmonary vascular remodeling. The latter causes changes in the anatomical structure of the pulmonary artery, the obstacle of pulmonary circulation hemodynamics, and hypoxic pulmonary vessels. Remodeling is the determinant of the reversible transformation of pulmonary artery hypertension, and it is also a difficult problem to be tackled by clinical vasodilator in the treatment of pulmonary hypertension. Transforming growth factor B1 (transforming growth factor beta 1, TGF- beta 1) is a newly discovered cytokine that regulates cell growth and differentiation, in the promotion of fibrosis and tissue Structural remodeling has a significant role in the proliferation, hypertrophy, rearrangement, migration, apoptosis and the increase of extracellular matrix in the parenchymal cells of the vascular wall. The present study shows that the TGF- beta 1 protein, m RNA, is in the bronchial mucosa, lung tissue, pulmonary vascular wall and bronchoalveolar lavage fluid in the hypoxic induced chronic cor pulmonale animal models. It is suggested that hypoxia may lead to an increase in the expression level of TGF- beta 1. The activated TGF- beta 1 plays an important role in promoting the formation and development of pulmonary hypertension and cor pulmonale. Thus, it is suggested that the level of TGF- beta 1 in chronic cor pulmonale may also be elevated. This study measured 90 patients with chronic cor pulmonale in different cases. The expression level of serum TGF- beta 1 during the period (acute exacerbation and remission) and its correlation with arterial blood oxygen pressure (Pa O2) and pulmonary arterial hypertension, right ventricular enlargement, the main pulmonary artery internal diameter (MPAD), right ventricle diameter (RVD) and pulmonary artery systolic pressure (PASP) were analyzed to further explore the TGF- beta 1 in chronic pulmonary heart. Methods: 90 cases of acute exacerbation of chronic cor pulmonale, 62 men, 28 women, age 58~83 years, average age (69.77 + 7.24) years, regular treatment of symptoms, and signs and other conditions after the 2 weeks as remission group. Select the sex, age and other general data matching the health of healthy people in 90 cases. The serum TGF- beta 1 was measured by enzyme linked immunosorbent assay (ELISA), and the SPSS19.0 statistical software was applied to the acute exacerbation and remission period of one-way ANOVA. patients with color echocardiography. The parameters of MPAD, RVD, PASP were measured and Pa O2 was measured in parallel with arterial blood gas analysis. The above indexes were all with the level of serum TGF- beta 1. Results: 1. general data of 90 patients with acute exacerbation of chronic cor pulmonale, including 62 male and 28 female, average age (69.77 + 7.24) years, the average main pulmonary artery diameter (MPAD) was (25.97 + 3.37) mm, the mean right ventricle diameter was (26.43 + 2.99) mm, and the average systolic pressure of pulmonary artery (PASP) was (54.41 + 6.85) mm Hg The average main pulmonary artery diameter (MPAD) was (25.07 + 3.38) mm, the average right ventricle diameter was (26.45 + 3.67) mm, and the mean pulmonary artery systolic pressure (PASP) was (49.36 + 6.86) mm Hg. healthy control group, including 60 men and 30 women, with an average age of (68.90 + 3.38) years, and the average main pulmonary artery diameter (M). PAD) (19.13 + 2.84) mm, the mean right ventricular diameter was (20.31 + 4.11) mm.2. and TGF- beta 1 level TGF- beta 1 in the acute exacerbation of chronic cor pulmonale patients. The expression level of the serum in the remission stage and the healthy control group was (306.12 + 27.04) pg/ml, (161.16 + 24) pg/ml, and (82.15 + 24.34) pg/ml. three groups in the serum TGF- beta 1 level difference The levels of serum TGF- beta 1 and Pa O2 in patients with chronic pulmonary heart disease (P0.05).3. were negatively correlated with the level of TGF- beta 1 in the acute exacerbation and remission stage of chronic cor pulmonale patients (r=-0.739, P0.05; r=-0.619, P0.05). The serum levels of TGF- beta 1 in patients with chronic cor pulmonale and the right cardiac parameters of cardiac ultrasound, MPAD, RVD, PASP were correlated with the levels of TGF- beta 1 in the acute exacerbation period of chronic cor pulmonale patients with MPAD, RVD, PASP, and the level of serum beta 1 in the remission period was also positively correlated with the level of serum beta 1. R=0.718, P0.05, r=0.630, P0.05) conclusion: 1. the level of serum TGF- beta 1 in patients with chronic cor pulmonale was significantly higher than that in the healthy control group, and it was positively correlated with the ultrasound index of the pulmonary hypertension and the right ventricular enlargement, indicating that the TGF- beta 1 was very likely to be involved in the serum TGF- beta 1 level and Pa O2 of the chronic cor pulmonale patients with chronic cor pulmonale. Negative correlation shows that the elevated level of TGF- beta 1 may be significantly higher than the remission stage of serum TGF- beta 1 in patients with chronic pulmonary heart disease associated with.3. chronic cor pulmonale, suggesting that the monitoring of TGF- beta 1 can be used to evaluate the condition of chronic cor pulmonale patients. The observation of the curative effect provides a new level of serum TGF- beta 1 in patients with chronic cor pulmonale with.4.. Hyperoxia is closely related to hypoxia and right heart disease. Antagonizing TGF-beta 1 signaling pathway or inhibiting its activity may provide new ideas for the prevention and treatment of chronic pulmonary heart disease.
【学位授予单位】：承德医学院
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R541.5
【参考文献】
相关期刊论文 前10条
1 刘云;朱金权;孙增先;;转化生长因子β1抑制肺动脉平滑肌细胞凋亡的机制研究[J];中国药房;2016年34期
2 吴松;项炜;朱滨;;脓毒症所致急性呼吸窘迫综合症患者血清转化生长因子β-1的表达[J];系统医学;2016年11期
3 葛锐;陈中文;吕晓东;;转化生长因子β1基因多态性与哮喘易感性Meta分析[J];中国预防医学杂志;2016年10期
4 王焕;曾玉兰;彭红星;杨荣时;;TGF-β_1在烟雾暴露大鼠肺血管的表达及其与肺血管重塑的关系[J];华中科技大学学报(医学版);2016年01期
5 姜君;;血清转化生长因子β1水平与肺结核活动性的关系[J];贵州医药;2015年10期
6 姚丽霞;;老年肺炎支原体肺炎患者IL-10、TNF-α、TGF-β1的变化及其临床意义分析[J];临床肺科杂志;2015年07期
7 刘岚;张永林;顾志娟;常红生;;兔煤工尘肺模型高分辨率CT表现与血清转化生长因子β_1表达水平相关研究[J];实用医学影像杂志;2015年03期
8 葛正行;周洵;高瑞;李波;;rHSG对COPD大鼠小气道阻力及成纤维细胞TGF-β1表达的影响[J];基础医学与临床;2014年11期
9 袁宝军;李超;王冬梅;邹吉敏;马毅华;朱秀萍;;煤工尘肺患者血清TGF-β1和IL-17A水平及其与肺功能关系[J];中国实验诊断学;2014年06期
10 管频;陈娟;冯光球;吴洁;;COPD患者肺组织中Smad蛋白、TGF-β_1表达与气道重塑的关系[J];海南医学;2014年12期
相关硕士学位论文 前1条
1 吴茜;急性肺血栓栓塞动物模型的建立与IL-13、TGF-β在肺栓塞中的作用初步探讨[D];天津医科大学;2011年
，本文编号：2155019
本文链接：https://www.wllwen.com/yixuelunwen/xxg/2155019.html
最近更新
教材专著
