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目的观察急性低压缺氧后内皮素前体原（ｐｐＥＴ）和内皮素－１（ＥＴ－１）的变化规律，探讨ＥＴ－１升高的机理。方法将实验大鼠分成三组，观察急性中度低压缺氧３０ｍｉｎ时及６ｈ后ｐｐＥＴ和ＥＴ－１的含量变化，分析其相关性。结果①急性中度低压缺氧３０ｍｉｎ后ｐｐＥＴ和ＥＴ－１均明显升高（Ｐ＜０．０５或０．０１），脱离缺氧后６ｈ，ｐｐＥＴ和ＥＴ－１有轻度下降，但仍未恢复到对照组水平（Ｐ＜０．０５）。②缺氧前对照组ｐｐＥＴ与ＥＴ－１呈明显正相关（ｒ＝０．９３，Ｐ＜０．００１），缺氧３０ｍｉｎ后，ＥＴ－１和ｐｐＥＴ虽明显升高，但二者仍呈明显正相关（ｒ＝０．９０，Ｐ＜０．００１），脱离缺氧后６ｈ，二者有轻度下降，但二者亦呈明显正相关（ｒ＝０．８０，Ｐ＜０．０１）。结论急性低压缺氧可启动ＥＴ基因系统，ＥＴ－１的升高是ｐｐＥＴ合成和释放增加的结果。急性中度低压缺氧对ＥＴ基因启动的时间较长，至少可维持６ｈ以上。
Objective To observe the changes of endothelin (PPET) and endothelin-1 (ET-1) after acute hypobaric hypoxia and to explore the mechanism of ET-1 elevation. Methods The experimental rats were divided into three groups. The levels of ppET and ET-1 in acute moderate hypobaric hypoxia 30min and 6h were observed, and their correlations were analyzed. Results ① The levels of ppET and ET-1 in acute moderate hypobaric hypoxia were significantly increased after 30min hypoxia (P <0.05 or 0.01), but there was a slight decrease in ppET and ET-1 after 6h hypoxia Recovery to the control group level (P <0.05). ② Before hypoxia, there was a significant positive correlation between ppET and ET-1 in the control group (r = 0.93, P <0.001). After hypoxia for 30min, ET-1 and ppET were significantly increased (R = 0.90, P <0.001), and there was a slight decrease after 6h hypoxia (r = 0.80, P <0.01) . Conclusions Acute hypobaric hypoxia can activate the ET gene system. The increase of ET-1 is the result of the increase of ppET synthesis and release. Acute moderate hypobaric hypoxia activates the ET gene longer, at least for more than 6h.