收藏本站
《青藏铁路运营十周年学术研讨会卫生系统论文集》2016年
收藏 | 手机打开
二维码
手机客户端打开本文

Research on rat models of hypobaric hypoxia-induced pulmonary hypertension

T.-T.MA  Y WANG  X.-L.ZHOU  H.JIANG  R.GUO  L.-N.JIA  H.CHANG  Y GAO  X.-Y.YAO  Z.-M.GAO  L.PAN  
【摘要】:OBJECTIVE:Rat models of hypobaric hypoxia-induced pulmonary hypertension are commonly used in studies of chronic mountain sickness,while there are few researches specially focusing on these rats model.This study aims to exploring possible pathogenesis of hypobaric hypoxia-induced pulmonary hypertension by experimenting on hypobaric hypoxiainduced PH rat models at different simulate-altitudes.MATERIALS AND METHODS:32 healthy male SD rats were randomly divided into six groups of different degree and time period of hypobaric hypoxia.The mean pulmonary arterial pressure(m PAP),right ventricular pressure(RVSP),the right ventricle(RV),left ventricular(LV),ventricular septal(S),the right ventricular hypertrophy index(RVHI)[calculated under the formula of RV/(LV + S)],hematoxylin-eosin staining,elastic fibers staining,the ratio of the thickness of vascular wall to its outer diameter(MT%),the ratio of the cross-sectional area of the middle vascular wall to the total vascular cross-sectional area(MA%);the a-SMA,and the Ki6 expressions were detected to evaluated the pulmonary hypertension.RESULTS:There were significant differences of the mPAP,RVSP and RVHI value between the hypobaric hypoxia groups and the control group(p 0.05).The mPAP,RVSP,RVHI,MT%,MA%,α-SMA,and Ki6 of rats in model groups at an altitude of 3KM were higher than those of the control group,which raised gradually with the number of weeks increasing.The mPAP,RVSP,RV/(LV + S) value,MT%,MA%,a-SMA,and Ki67 of the 5KM-4W group were significantly higher than those of the control group(p 0.05).CONCLUSIONS:Rat models with pulmonary hypertension at different altitudes have been successfully established by automatic adjusting hypobaric hypoxia chamber.Exposure to a low oxygen environment at a simulate-altitude of 3km for 8 weeks have caused the pathological remodeling of pulmonary vascular walls and pulmonary hypertension,and further led to a series of pathological changes,including right ventricular hypertrophy.This model is easy to be replicated with good reproducibility and provides evidence for clinical trial of drugs.
【作者单位】:Department of Geriatric Medicine,Beijing Shijitan Hospital,Capital Medical University Department of Hypoxia Laboratory,Beijing Shijitan Hospital,Capital Medical University Department of Pathology,Beijing Shijitan Hospital,Capital Medical University Health Science Center of Peking University
【分类号】:R-332;R544.1
【正文快照】:
Introdurtinn^t ,Pulmonaiy hypertension is a disease Ihat can mduce pulmonary vascular remodeling and con- striction and dysfunction of pulmonary circula- tion.It can give rise to continuous overloading of right ventricular pressure,causing the right hear

【相似文献】
中国期刊全文数据库 前10条
1 王辰英;Microacupuncture therapy on 80 cases of chronic fasciitis at neck and back[J];中国临床康复;2002年22期
2 缪朝玉 ,苏定冯;The importance of blood pressure variability in rat aortic and left ventricular hypertrophy produced bysinoaortic denervation[J];第二军医大学学报;2002年12期
3 ;Arterial baroreflex function and leftventricular hypertrophy[J];第二军医大学学报;2004年04期
4 李拥军,崔炜,田泽君,郝玉明,都军,刘凡,张辉,祖秀光,刘素云,谢瑞琴,杨晓红,武宇洲,陈莉,安威;Crosstalk between ERK_(1/2) and STAT_3 in the modulation of cardiomyocyte hypertrophy induced by cardiotrophin-1[J];Chinese Medical Journal;2004年08期
5 刘华胜,马爱群,王春梅,刘勇,田红燕,白玲;Variation and significance of microtubules in rat volume overload cardiac hypertrophy[J];Chinese Medical Journal;2003年03期
6 黄俊,覃国辉,胡昌兴,龚丽娅,程芳舟,马业新,陆再英;Effects of transforming growth factor-β_1 and signal protein Smad3 on rat cardiomyocyte hypertrophy[J];Chinese Medical Journal;2004年10期
7 ;Different contributions of STAT3, ERK1/2, and PI3-K signaling to cardiomyocyte hypertrophy by cardiotrophin-1[J];Acta Pharmacologica Sinica;2004年09期
8 ;Portal vein embolization induces compensatory hypertrophy of remnant liver[J];World Journal of Gastroenterology;2006年03期
9 ;Ultrasonic evaluation of the relationship between left ventricular hypertrophy or left ventricular geometry and endothelial function in patients with essential hypertension[J];Journal of Nanjing Medical University;2009年06期
10 ;MiR-16 regulates CCND1 and CCND2 expression contributing to cardiac hypertrophy[J];岭南心血管病杂志;2011年S1期
中国重要会议论文全文数据库 前10条
1 朱大海;;Functional Role of Myostatin-induced Gene X in heart hypertrophy[A];中国遗传学会模式生物与人类健康研讨会会议论文集[C];2010年
2 Jie-Ning Zhu;Qiu-Xiong Lin;Xiao Zou;Ye-You Liang;Yong-Heng Fu;Chun-Yu Deng;Meng-Zhen Zhang;Xi-Yong Yu;单志新;;MicroRNA-16 represses myocardial hypertrophy by inhibiting CCND1,CCND2 and CCNE1 expression in cardiomyocytes[A];第十二届全国脂质与脂蛋白学术会议论文汇编[C];2014年
3 杨晓;;Function of a TGF-βregulated miRNA in cardiac hypertrophy[A];中国遗传学会模式生物与人类健康研讨会会议论文集[C];2010年
4 Zhalaga Bai;;Function of a TGF-β regulated miRNA in cardiac hypertrophy[A];第三届细胞结构与功能的信号基础研讨会论文摘要[C];2010年
5 Zhenyu Wang;Mingzhe Li;Jun Zhou;Xi Li;Tongcun Zhang;;The synergistic activation of histone acetylation p300 on the expression of marker gene of myocardial hypertrophy induced by MRTFs[A];生命的分子机器及其调控网络——2012年全国生物化学与分子生物学学术大会摘要集[C];2012年
6 ;Effect on hypertrophy scar fibroblasts proliferation by SiRNA which silences the expression of the TGF-βRⅡ[A];湖南省生理科学会2008年度学术年会论文摘要汇编[C];2008年
7 ;The Levels of MicroRNA-1 and MicroRNA-195 in Ault Rat Cardiac Fibroblasts[A];2008年全国生物化学与分子生物学学术大会论文摘要[C];2008年
8 ;Control of Malignant Arrhythmias by microRNAs[A];2008年全国生物化学与分子生物学学术大会论文摘要[C];2008年
9 王剑;Lagabaiyila Zha;;Cardiomyocyte Overexpression of miR-27b Induces Cardiac Hypertrophy and Dysfunction in Mice[A];第二届模式生物与人类健康研讨会会议论文集[C];2012年
10 ;High density lipoprotein downregulates angiotensin Ⅱ type 1 receptor and inhibits[A];第十三次全国心血管病学术会议论文集[C];2011年
 快捷付款方式  订购知网充值卡  订购热线  帮助中心
  • 400-819-9993
  • 010-62791813
  • 010-62985026