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本研究旨在探讨慢性间歇性低压低氧(chronic intermittent hypobaric hypoxia,CIHH)对大鼠胸主动脉和肺动脉收缩功能的影响及其机制。雄性Sprague-Dawley大鼠随机分为4组:CIHH处理14天组(CIHH14)、28天组(CIHH28)、42天组(CIHH42)和对照组(CON)。CIHH大鼠分别给予14、28和42天相当于海拔5000m高度、每天6h的CIHH处理;常规制备胸主动脉和肺动脉环,通过离体动脉环灌流和描记方法记录动脉的收缩活动。结果显示:(1)CIHH各组大鼠由去甲肾上腺素(noradrenaline,NA)和KCl诱发的胸主动脉和肺动脉环收缩幅度与对照大鼠无显著差异。(2)CIHH各组大鼠由血管紧张素Ⅱ(angiotensinⅡ,ANGⅡ)诱发的胸主动脉环收缩幅度较对照大鼠明显降低,而由ANGⅡ诱发的肺动脉环收缩幅度与对照大鼠无显著差异;CIHH14、28和42三组大鼠由ANGⅡ诱发的胸主动脉环收缩幅度无显著差异。(3)CIHH对ANGⅡ诱发的胸主动脉环收缩的抑制作用呈非内皮依赖性,此作用可被ATP敏感钾通道(KATP)阻断剂格列苯脲、一氧化氮合酶抑制剂L-NAME所逆转,而不被环氧合酶抑制剂吲哚美辛所阻断。结果提示,CIHH处理可非内皮依赖性地降低ANGⅡ诱发的大鼠胸主动脉收缩反应,此作用可能与KATP通道开放和NO生成增多有关。
This study aimed to investigate the effects of chronic intermittent hypobaric hypoxia (CIHH) on the contractile function of the thoracic and pulmonary arteries in rats. Male Sprague-Dawley rats were randomly divided into 4 groups: CIHH-treated 14-day group (CIHH14), 28-day group (CIHH28), 42-day group (CIHH42) and control group (CON). CIHH rats were given CIHH treatment at the altitude of 5000m for an altitude of 5000m for 14, 28 and 42 days respectively, and the thoracic aorta and pulmonary artery rings were routinely prepared. The contractile activity of the arteries was recorded by ex vivo perfusion and tracing methods. The results showed that: (1) There was no significant difference in contraction amplitude between the thoracic aorta and pulmonary artery rings induced by noradrenaline (NA) and KCl in CIHH rats. (2) The contraction amplitude of thoracic aorta induced by angiotensin Ⅱ (ANGⅡ) in CIHH groups was significantly lower than that in control rats, while the contraction amplitude of pulmonary rings induced by angiotensin Ⅱ was not significantly different from that in control rats. There was no significant difference in the contraction amplitude of thoracic aorta induced by ANGⅡ in CIHH14, 28 and 42 groups. (3) The inhibitory effect of CIHH on angiotensin Ⅱ-induced thoracic aortic ring contraction was non-endothelium-dependent, and this effect could be blocked by glibenclamide, an inhibitor of ATP-sensitive potassium channel (KATP), nitric oxide synthase inhibitor L- NAME reversed without being blocked by the cyclooxygenase inhibitor indometacin. The results suggest that CIHH treatment may reduce ANG Ⅱ-induced thoracic aortic contractile response in a non-endothelium-dependent manner, which may be related to the opening of KATP channels and the increase of NO production.