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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。
Right heart catheterization, light microscopy, computer-assisted measurement and transmission electron microscopy were used to observe the effect of hypobaric hypoxia (5000m altitude) on the endothelial structure and muscle formation of rat pulmonary alveolar septum (IAA) Pulmonary hypertension (PH) relationship. The results showed that: (1) IAA had obvious muscle formation after hypoxia for 24 hours. With the prolongation of hypoxia time, the percentage of peripheral arterialization of ф <50μm continued to increase, which was closely related to pulmonary hypertension and right ventricular hypertrophy. Revealing the formation of IAA muscle PH important reason. (2) Hypoxia 24h, IAA endothelium was marked intracellular edema; hypoxia 7d, subependymal edema, endothelial hyperplasia, hypertrophy; hypoxia 14d, subepithelial edema serious, most of the disappearance of the internal elastic layer, endothelial hyperplasia, hypertrophy continued to increase Hypoxia 21 and 40d, subendothelial edema reduced, but hyperplasia, hypertrophy heavier.Combined with pulmonary arterial pressure and IAA muscle changes, suggesting that due to different hypoxia IAA endothelium changes in varying degrees, its involvement leads to arterialization The mechanism is different.