缺氧性肺动脉高压大鼠肺腺泡内动脉肌化与内皮结构变化的关系

RELATIONSHIP BETWEEN MUSCULARITY OF PULMONARY INTRA-ACINAR ARTERIES AND STRUCTURAL CHANGES OF ARTERIAL ENDOTHELIUM IN RATS WITH HYPOXIC PULMONARY HYPERTENSION

利用右心导管术、光镜、微机辅助测量及透射电镜,综合观察分析了不同时间减压缺氧(5000m高度)对大鼠肺腺泡内动脉(IAA)内皮结构和肌化的影响及与肺动脉高压(PH)的关系。发现:(1)缺氧24h,IAA即有明显肌化;随缺氧时间延长,ф<50μm的外周血管肌化百分率持续增加,与肺动脉压增高及右室肥厚密切相关。揭示IAA肌化为PH形成的重要原因。(2缺氧24h,IAA内皮是显著胞内水肿;缺氧7d,出现内皮下水肿,内皮增生、肥厚;缺氧14d,内皮下水肿严重,内弹力层大部消失,内皮增生、肥厚继续加重;缺氧21及40d,内皮下水肿减轻,但增生、肥厚更重。结合肺动脉压及IAA肌化变化分析,提示因不同缺氧时间段IAA内皮结构不同程度的变化,其参与导致动脉肌化的机制有所不同。

The effect of hypobaric hypoxia (5 000m) on the endothelium of pulmonary intra-acinar arteries (IAA) and its relations with arterial muscularity and pulmonary hypertension (PH) were studied. The results were as follows: (1) Along with the prolongation of hypoxic exposure, the muscularity of IAA was enhanced and closely related with the increment in pulmonary arterial pressure (PAP) and hypertrophy of right ventricle, indicating its important role in the development of PH. (2)After 24h of exposure, notable intracellular edema of endothlium occurred. From 7 to 14 days of exposure, subendothelial edema took place and gradually deteriorated and internal elastic laminae eventually disappeared. From 21 to 40 days of exposure, subendothelial edema was alleviated whereas the proliferation and hypertrophy of endothelium were getting more severe. The results obtained indicated that the endothelium of IAA might have different roles in the arterial muscularization in the different stages of hypoxia.