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首页> 外文期刊>Life sciences >N-acetylcysteine inhibits hypoxic pulmonary hypertension most effectively in the initial phase of chronic hypoxia.
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N-acetylcysteine inhibits hypoxic pulmonary hypertension most effectively in the initial phase of chronic hypoxia.

机译：在慢性低氧的初期，N-乙酰半胱氨酸最有效地抑制低氧性肺动脉高压。

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Exposure to chronic hypoxia results in hypoxic pulmonary hypertension (HPH). In rats HPH develops during the first two weeks of exposure to hypoxia, then it stabilizes and does not increase in severity. We hypothesize that free radical injury to pulmonary vascular wall is an important mechanism in the early days of the hypoxic exposure. Thus antioxidant treatment just before and at the beginning of hypoxia should be more effective in reducing HPH than antioxidant therapy of developed pulmonary hypertension. We studied adult male rats exposed for 4 weeks to isobaric hypoxia (F(iO2) = 0.1) and treated with the antioxidant, N-acetylcysteine (NAC, 20 g/l in drinking water). NAC was given "early" (7 days before and the first 7 days of hypoxia) or "late" (last two weeks of hypoxic exposure). These experimental groups were compared with normoxic controls and untreated hypoxic rats (3-4 weeks hypoxia). All animals kept in hypoxia had significantly higher mean pulmonary arterial blood pressure (PAP) than normoxic animals. PAP was significantly lower in hypoxic animals with early (27.1 +/- 0.9 mmHg) than late NAC treatment (30.5 +/- 1.0 mmHg, P < 0.05; hypoxic without NAC 32.6 +/- 1.2 mmHg, normoxic controls 14.9 +/- 0.7 mmHg). Early but not late NAC treatment inhibited hypoxia-induced increase in right ventricle weight and muscularization of distal pulmonary arteries assessed by quantitative histology. We conclude that release of free oxygen radicals in early phases of exposure to hypoxia induces injury to pulmonary vessels that contributes to their structural remodeling and development of HPH.
机译：暴露于慢性缺氧会导致缺氧性肺动脉高压（HPH）。在大鼠中，HPH在暴露于缺氧的前两周内发展，然后稳定并没有增加严重性。我们假设在低氧暴露的早期，对肺血管壁的自由基损伤是重要的机制。因此，缺氧之前和开始时的抗氧化剂治疗应比发展性肺动脉高压的抗氧化剂治疗更有效地减少HPH。我们研究了暴露于等压低氧4周（F（iO2）= 0.1）并用抗氧化剂N-乙酰半胱氨酸（NAC，饮用水中20 g / l）处理的成年雄性大鼠。 NAC给予“早期”（缺氧之前7天和前7天）或“晚期”（缺氧暴露的最后两周）。将这些实验组与常氧对照组和未经治疗的低氧大鼠（缺氧3-4周）进行比较。保持缺氧的所有动物的平均肺动脉血压（PAP）明显高于正常氧动物。早期（27.1 +/- 0.9 mmHg）的低氧动物的PAP显着低于晚期NAC治疗（30.5 +/- 1.0 mmHg，P <0.05;无NAC的低氧动物32.6 +/- 1.2 mmHg，常氧对照组14.9 +/- 0.7毫米汞柱）。通过定量组织学评估，早期但非晚期NAC治疗抑制了低氧诱导的右心室重量增加和远端肺动脉肌肉化。我们得出的结论是，在暴露于缺氧的早期阶段释放游离氧自由基会诱导对肺血管的伤害，这有助于肺血管的结构重塑和发展。

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