肝素对低氧性肺动脉平滑肌细胞血小板源生长因子表达的影响

Effect of heparin on platelet derived growth factor in the hypoxia - induced pulmonary hypertension

目的探讨肝素对低氧条件下大鼠肺动脉高压肺动脉平滑肌细胞（PASMC）血小板源生长因子（PDGF）表达的影响。方法建立低氧性肺动脉高压模型，24只雄性SD大鼠随机分为三组：常氧并注射生理盐水组（n=8）；低氧并注射生理盐水组（n=8）；低氧条件下应用肝素组（n=8）。3周后应用右心导管法测量右心室收缩压（RVSP），免疫组化法检测肺动脉平滑肌细胞内的PDGF，RT—PCR检测肺动脉平滑肌细胞中的PDGFmRNA。免疫组化结果用计算机进行灰度扫描分析，RT—PCR结果用目的片断与内参条带的吸光度之比值表示。结果RVSP：右心收缩压B组〉C组〉A组。组间比较P〈0．01。免疫组化结果灰度值B组〈C组〈A组，组间比较P〈0.01。RT—PCR结果显示与内参条带吸光度之比B组〉C组〉A组，组间比较P〈0．01。结论肝素作用的肺动脉平滑肌细胞中的PDGFmRNA和PDGF表达水平下降，这可能有利于抑制血管平滑肌细胞（VSMCs）的增生。

Objective To investigate the effects of heparin on platelet derived growth factor （PDGF） in pulmonary artery smooth muscle cell （PASMC） of hypoxia -induced pulmonary hypertension rats. Methods We built the modle of hypoxia - induced pulmonary hypertension. Twenty - four male SD rats were randomly divided into three groups. Group A： normoxia and injected normal saline, group B： hypoxia cage and injected normal saline, group C ： hypoxia cage and injected heparin. After three weeks, the right ventricular systolic pressure were measured by right -heart catheterization. Tested the content of PDGF in the lung by immunohistochemical test and analyse the images＇ gray scale by computor. Tested the content of PDGF mRNA in the lung by RT - PCR and display the results by the ratio of the strap of PDGF＇ s absorbance on that of GAPDH. Results The RVSP of both group A and group C were less than that of group B （P 〈 0. 01） ,and group C＇ s were higher than group A＇ s. In the immunohistochemical test, the group B＇ s gray scale were less than group C＇ s, and group C＇ s were less than group A＇ s. It was statistical significant when compared either two groups of the three （P 〈 0. 01 ） . The results of the RT - PCR test showed that the ratio of group B was higher than that of group C, and the ratio of group C was higher than that of group A. It was statistical significant when compared either two groups of the three （P 〈 0. 01 ） . Conclusion Pretreatment with heparin effectively prevents the formation of chronic hypoxic pulmonary hypertension. The mechanism may be relate to the inhibition of PDGF.