中文摘要：

目的 研究硫氢化钠（NaHS）对慢性间歇性低氧（CIH）大鼠离体胸主动脉血管张力的影响。方法 将雄性SD大鼠随机分成对照（Sham）组和慢性间歇性低氧（CIH）组,用无创套尾法测大鼠的尾动脉收缩压（SBP）,用离体血管张力实验观察NaHS对大鼠胸主动脉血管张力的影响。结果 与Sham组相比,在苯肾上腺素（Phe）预收缩的大鼠胸主动脉中,CIH组乙酰胆碱（ACh）引起的舒张作用显著减弱（P〈0.01）。Sham组在累积浓度NaHS为50~100μmol/L时引起血管收缩,NaHS为300~1000μmol/L时引起血管舒张;CIH组在累积浓度NaHS为50~300μmol/L时引起血管收缩,500~1000μmol/L时引起血管舒张。与Sham组（100μmol/L）相比,CIH组（300μmol/L）低浓度NaHS引起的血管收缩作用显著增加（P〈0.01）;与Sham组（1000μmol/L）相比,CIH组（1000μmol/L）高浓度NaHS引起的血管舒张作用显著减弱（P〈0.01）。结论 在Phe预收缩的大鼠胸主动脉中,累积浓度的NaHS在Sham组和CIH组均可引起双向作用,即在低浓度时产生血管收缩,高浓度时产生血管舒张,两组之间差异有显著性（P〈0.01）;同时CIH可使大鼠血管内皮依赖性舒张功能下降,其机制可能与血管对硫化氢的反应异常有关。

英文摘要：

Objective To investigate the effect of NariS on the tension of thoracic aorta in a rat model of chronic intermittent hypoxia（CIH）. Methods Male SD rats were randomly divided into Sham and CIH groups. The con- scious noninvasive method with tail cuff was performed in rats to record the systolic blood pressure （SBP）. The ex- periment of vascular tension in vitro was carried out to observe the effects from Naris on thoracic aorta rings. Re- sults Compared with Sham thoracic arteries, the relaxant effect induced by acetylcholine （ACh） was decreased markedly in CIH thoracic arteries preeontracted with phenylephrine（Phe） （P 〈 0. 01 ）. NariS caused contraction at low concentrations （50 - 100 p~mol/L in Sham arteries and 50 - 300 ~mol/L in CIH arteries） and relaxation at high concentrations （300 ~ 1 000 ~moL/L in Sham arteries and 500 - 1 000 ~mo]/L in CIH arteries）. Compared with Sham thoracic arteries （100 ~xmol/L）, the maximum contractile effect at low concentrations （300 ~xmol/L） in- creased notably in CIH arteries （P 〈0. 01 ）. Compared with Sham thoracic arteries（ 1 000 i.~mol/L）, the relaxant effect at high concentrations （ 1 000 I~mol/L） decreased significantly in CIH arteries （ P 〈 0. 01 ）. Conclusion Cumulative concentrations of NariS can cause contractile and relaxant effects in the precontracted with Phe of the thoracic arteries both Sham and CIH groups. However, there is a significant difference between two groups （P 〈 0. 01 ）. Meanwhile, CIH can induce endothelium-dependent vasodilatation function decline. The mechanism may be involved in abnormal vascular reaction to hydrogen sulfide.