论文部分内容阅读
一般认为,水及电解质稳态的破坏不仅是急性高山病(AMS)和高原肺水肿(HAPE)的病因学机制,而且尿量减少及体重增加与AMS和HAPE的关系促使这一假说的提出:因低氧效应诱发的抗利尿激素(ADH)释放所致的水储留可能是这类疾病的加速机制。为阐明这一问题,我们研究了正常Long—Evans大鼠(N)及患先天性尿崩症的大鼠(DI)暴露于低压性低氧(0.5atm)环境4天其肺的水平衡状况。结果发现,急性暴露期间,两组大鼠水摄入量及尿量均显著下降;N组鼠体重增加,肺水量亦升高,而DI组鼠体重及肺水量均未改变;任何一组鼠在高原环境
It is generally accepted that the destruction of water and electrolyte homeostasis is not only the etiological mechanism of acute mountain sickness (AMS) and high altitude pulmonary edema (HAPE), but also that the relationship between reduced urine volume and weight gain and AMS and HAPE motivates this hypothesis: Water retention due to hypoxia-induced release of antidiuretic hormone (ADH) may be an acceleration mechanism for these diseases. To elucidate this issue, we investigated the water balance in the lungs of normal Long-Evans rats (N) and rats with congenital diabetes insipidus (DI) exposed to hypobaric hypoxia (0.5 atm) for 4 days . The results showed that water intake and urine volume of rats in both groups decreased significantly during acute exposure. Rats in group N also increased body weight and lung water volume, while those in group DI did not change. In the plateau environment