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早在1904年Plumier观察到低氧性肺动脉高压,其后在很多哺乳动物(包括人类)亦有同样发现。低氧性肺血管收缩的结果使血流从低氧的肺泡区转移到通气较好的肺泡区,以改善通气灌注关系和气体交换,使血液得到充分氧合。这本是机体的适应性代偿机制,但如果广泛的肺泡低氧(高原或慢性阻塞性肺疾患)则可导致肺动脉高压。近几十年来的研究证明,急、慢性低氧性肺血管收缩是肺动脉高压的主要病因,是高山病或肺心病的主要发病学环节。由于急、慢性低氧是最直接、最有效和可重复地诱发肺动脉高压的方法,因此大量的研究工作者均以低氧为手段来复制急、慢性肺动脉高压的动物模型,以探讨高山病或肺心
As early as 1904, Plumier observed hypoxic pulmonary hypertension, followed by many mammals (including humans) also found the same. As a result of hypoxic pulmonary vasoconstriction, blood flow is diverted from the hypoxic alveolar region to the well-aerated alveolar region to improve ventilation and gas exchange and provide adequate oxygenation of the blood. This is the body’s adaptive compensatory mechanism, but can lead to pulmonary hypertension if extensive alveolar hypoxia (high altitude or chronic obstructive pulmonary disease). In recent decades, studies have shown that acute and chronic hypoxic pulmonary vasoconstriction is the main cause of pulmonary hypertension is the main pathogenesis of mountain sickness or pulmonary heart disease. Due to acute and chronic hypoxia is the most direct, most effective and reproducible method of inducing pulmonary hypertension, a large number of researchers hypoxia as a means to reproduce the acute and chronic pulmonary hypertension in animal models to explore the disease or Pulmonary heart