论文部分内容阅读
目的探讨慢性间歇性低压低氧(CIHH)对大鼠胸主动脉环舒张活动的影响及其一氧化氮相关机制。方法成年雄性SD大鼠80只,随机分为对照组(CN组)和慢性间歇性低压低氧组(CIHH组),每组40只。CIHH组给予模拟海拔5 000 m(PB=404 mm Hg,PO2=84 mm Hg)的低压低氧处理,6 h/d,共28 d。对照组处于常压常氧环境,平行饲养。应用离体血管环灌流记录胸主动脉的舒缩活动;采用Western blotting法检测胸主动脉组织中eNOS和PI3K的表达水平。结果与CN组相比,CIHH组乙酰胆碱引起的胸主动脉舒张明显增强(P<0.05),胸主动脉组织中eNOS的表达增多(P<0.05);M EK阻断剂PD98059孵育,对CN组和CIHH组无影响;PI3K阻断剂LY294002孵育,可阻断CIHH组胸主动脉舒张增强和eNOS表达增多(P<0.05);且CIHH组胸主动脉组织中PI3K的表达升高(P<0.05)。结论 CIHH处理可通过PI3K途径活化血管内皮eNOS,增强乙酰胆碱诱导的大鼠胸主动脉舒张。
Objective To investigate the effect of chronic intermittent hypobaric hypoxia (CIHH) on diastolic activity of the thoracic aorta and its related mechanism of nitric oxide in rats. Methods Eighty adult male Sprague-Dawley rats were randomly divided into control group (CN group) and chronic intermittent hypobaric hypoxia group (CIHH group), 40 rats in each group. Hypoxic hypoxia treatment was performed in the CIHH group at a simulated altitude of 5 000 m (PB = 404 mm Hg, PO2 = 84 mm Hg) for 6 h / d for 28 days. The control group was under normobaric atmosphere and fed in parallel. The vasoconstrictor activity of the thoracic aorta was recorded by perfusion in vitro. The expression of eNOS and PI3K in the thoracic aorta was detected by Western blotting. Results Compared with CN group, the relaxation of thoracic aorta induced by acetylcholine in CIHH group was significantly increased (P <0.05), and the expression of eNOS in thoracic aorta was increased (P <0.05). Compared with CN group, PDK8059 (P <0.05). The PI3K inhibitor LY294002 could block the increase of thoracic aorta and eNOS expression in CIHH group (P <0.05), and the expression of PI3K in thoracic aorta of CIHH group was increased ). Conclusion CIHH treatment can activate vascular endothelial eNOS through PI3K pathway and enhance acetylcholine-induced relaxation of thoracic aorta in rats.