Objective To investigate the effect of hydrogen sulfide ( H2 S) on hypoxic pulmonary hyperten-sion rats and the expressions of some apoptosis related genes Bax mRNA and Bcl-2mRNA in lung tissues. Methods 30 male Wistar rats were randomly divided into 3 groups: the normoxia control group ( the group A ) , the hypoxia group (the group B), and the hypoxia+NaHS group (the group C). NaHS solution was injected intraperitoneally everyday before hypoxic challenge for rats. The model of rat hypoxic pulmonary hypertension was established by at-mospheric intermittent hypoxia method. Their mean pulmonary artery pressure ( mPAP) was detected by right cardiac catheterization. Their right ventricle and left ventricle plus septum were weight, and the ratio of the weight of right ventricle to left ventricle plus septum ( right ventricle hypertrophy index, RVHI) were also determined. The expres-sion of BaxmRNA and Bcl-2mRNA was detected by RT-PCR. Results ① After model established, the bodyweight decreased significantly in the groups B and C (P<0. 05), but the weight was significantly higher in the group C than in the group B. ②The level of mPAP increased obviously, and the R/L+S ratio increased in the groups B and C ( P<0. 05). ③ Under optical microscope, the walls of pulmonary arterioles were thin and the lumens were large in the control group. In the hypoxia group, the walls were thicker and the lumens were narrower than those of the control groups. The thickened caliberwas relieved significantly in the group C. ④ Compared with the groups B and C, the expression of BaxmRNA decreased, but the expression of Bcl-2 mRNA increased in the control group ( P<0. 05 ) . Conclusion H2 S can regulate the expression of BaxmRNAand Bcl-2mRNA, and alleviate the hypoxic pulmonary vascular reconstruction, which plays an important protect role in hypoxic pulmonary hypertension.%目的：研究H2 S对大鼠低氧性肺动脉高压及凋亡相关基因BaxmRNA、Bcl-2mRNA表达的影响,探讨其在低氧性肺动脉高压发病中的作用。方法将30只雄性Wistar大鼠随机分为三组：常氧对照组、低氧组及低氧+NaHS组(腹腔注射NaHS并进行低氧处理)。常压间歇低氧法建立大鼠低氧性肺动脉高压模型,右心导管法检测平均肺动脉压(mPAP)；分别称量大鼠右心室(RV)和左心室加室间隔(LV+S)的质量,计算出右心室肥厚指数RV/( LV+S)；HE及弹力纤维+VG染色光镜下观察肺血管形态及肺小动脉平滑肌结构,弹力纤维、肌纤维及胶原纤维增生情况；RT-PCR方法检测BaxmRNA、Bcl-2mRNA在肺组织中的表达。结果①低氧各组较对照组体重明显减轻(P<0．05),但低氧+NaHS组明显高于低氧组(P<0．05),造模前各组大鼠体重无差别(P>0．05)。②低氧各组较对照组mPAP明显升高(P<0．05)、RV/(LV+S)明显增加(P<0．05)。低氧+NaHS组较低氧组mPAP明显降低(P<0．05),RV/(LV+S)明显减少(P<0．05)。③光镜下观察,对照组肺动脉管壁较薄,薄厚均匀,管腔较大。内弹力膜呈平缓波浪状,管壁层次结构清晰；低氧组肺小动脉平滑肌增生,胶原纤维增多,管壁增厚,管腔狭窄。内弹力膜增厚,外膜胶原纤维增生、沉积,外弹力膜也增厚,内外弹力板间距离均增宽；中膜平滑肌细胞也增生明显,管壁增厚,管腔明显变小,管周水肿。低氧+NaHS组较低氧组上述表现有所缓减。④低氧各组较对照组肺组织BaxmRNA表达均显著降低,Bcl-2 mR-NA表达均显著增加(P<0．05)。低氧+NaHS组较低氧组肺组织BaxmRNA表达显著升高,Bcl-2mRNA表达明显降低(P<0．05),低氧+NaHS组较对照组大鼠肺组织BaxmRNA、Bcl-2 mRNA表达无统计学差异(P>0．05)．结论 H2 S可以调节低氧性肺动脉高压细胞大鼠肺组织凋亡相关基因BaxmRNA、Bcl-2mRNA的表达,缓解低氧性肺血管重建,对低氧性肺动脉高压的发病起到保护作用。
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