缺氧性肺动脉高压与肺腺泡内动脉构型重组  

HYPOXIC STRUCTURAL REMODELING OF INTRA-ACINAR PULMONARY ARTERY AND PULMONARY HYPERTENSION

作　　者：席思川 车东媛[1] 张婉蓉 

机构地区：[1]中国医学科学院心血管研究所病理科,中国医学科学院阜外心血管病医院病理科,武汉同济医科大学病理教研室

出　　处：《中国循环杂志》1995年第5期287-290,共4页Chinese Circulation Journal

基　　金："八五"攻关资助

摘　　要：用光镜与电镜观察、形态测量等方法，研究了缺氧大鼠腺泡内肺动脉（ＩＡＰＡ）构型重组的发展过程及其与肺动脉高压（ＰＨＴ）之间的关系。结果发现，慢性缺氧能引起大鼠肺动脉压升高、ＩＡＰＡ构型重组和右心室肥大等３种改变密切相关。ＩＡＰＡ构型重组首先是内皮细胞肿胀增生，继而是中膜平滑肌细胞增生肥大，细胞外基质增多，以及无肌型动脉肌化等结构改变。本文认为，内皮细胞在ＩＡＰＡ构型重组中可能起关键性作用。ＩＡＰＡ构型重组是持续性ＰＨＴ的形态学基础。Morphological observation and measurement together with statistical analysis were applied to investigate the hypoxic structural remodeling of intra-acinat pulmonaty artery(IAPA) and its relationship with pulmonary hypertension(PHT). The results indicated that chronic hypoxia could cause PHT, structural remodeling of IAPA and right ventricular hypertrophy, which are correlated with one another. The structural remodeling of IMA began with swelling and proliferation of endothelial cells(EC), then the proliferation and hypertrophy of smooth muscle cells in the media of IAPA with much more extracellular matrix, and muscularization of pulmonary nonmuscular artery became obvious in the meantime. All the above changes suggest that EC play a key role in the structural remodeling of IAPA which results in PHT.

关 键 词：缺氧 肺动脉高压 内皮细胞 病理 腺泡内动脉 

分 类 号：R543.202[医药卫生—心血管疾病]