低O_2高CO_2性肺动脉高压大鼠血浆内皮素和肺细小动脉超微结构的研究

THE STUDY OF THE ENDOTHELIN AND THE PULMONARY ARTERIOLE ULTRASTRUCTURE IN PULMONARY HYPERTENSION RATS INDUCED BY HYPOXIA AND HYPERCAPNIA

为探讨低Ｏ２高ＣＯ２性肺动脉高压形成的机制，对血浆内皮素（ＥＴ）和肺细小动脉超微结构改变进行研究。应用低Ｏ２高ＣＯ２性肺动脉高压大鼠模型，观察了不同ＥＴ浓度时肺细小动脉超微结构改变。实验组①ＥＴ浓度明显升高，②肺细小动脉内皮细胞（ＥＣ）水肿，内质网扩张，内皮下水肿明显，内膜增厚；③肺细小动脉中膜平滑肌细胞（ＳＭＣ）竖立，微丝束增多，ＳＭＣ数目增多，细胞面积增大；④外膜纤维母细胞（ＦＩＢ）增生，胶原纤维密集。结果表明低Ｏ２高ＣＯ２引起的血浆ＥＴ增高，可致肺动脉内膜增厚、平滑肌细胞和纤维母细胞增生，可能是肺动脉高压形成的重要机制之一。

? Objective to study the pathogenetic mechanism of hypoxia and hypercapnia pulmonary hypertension,the endothelin and the ultrastructure in pulmonary arteriole was investigated in rats with hypoxia and hypercapnia pulmonary hypertension.The endothelin level of plasma and the ultrastructural changes of pulmonary arteriole were observed. Results in experimental groups:①The endothelin level is increased.②The intracellular edema of endthelium and subendothelial edema occurred,the endoplasmic reticulum expanded,the hypertrophy of endothelium was getting more severe.③The smooth muscle cell was standed.The quantity was increased and the area was expanded.④The fibroblast showed apparent proliferation.Conclusion:the increasing of endothelin of plasma is related to hypertrophy of endothelium and proliferation of smooth muscle cell and fibroblast.It is one of the important mechanism of pulmonary hypertension.