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目的探讨急性低压缺氧对大鼠及溃疡模型大鼠下消化道生长抑素（ＳＳ） 分布的影响及生理意义。方法３６ 只雄性Ｗｉｓｔｅｒ 大鼠随机分成６ 组，其中３ 组为对照组，３ 组为急性溃疡模型实验组。在低压舱内模拟上升至５０００ ｍ 、１００００ ｍ 各停留３０ ｍｉｎ ，取消化道粘膜，用放免法测定胃肠道粘膜ＳＳ 含量。结果对照组小肠ＳＳ 含量，５０００ ｍ 组明显高于地面组（ Ｐ＜ ０ ．０５） 。对照组盲肠ＳＳ含量，５０００ ｍ 组明显高于１００００ ｍ 组和地面组（ Ｐ＜ ０ ．０１ ，Ｐ＜ ０ ．０５） ，对照组小肠粘膜、盲肠ＳＳ含量１００００ ｍ 组与地面组间无显著性差异。实验组小肠ＳＳ含量，５０００ ｍ 组明显高于地面组（ Ｐ＜ ０ ．０１） ，与１００００ ｍ 组间无显著性差异，１００００ ｍ 组与地面组ＳＳ含量间无显著性差异。实验组盲肠ＳＳ 含量５０００ ｍ 组、１００００ ｍ 组均明显高于地面组（ Ｐ＜ ０ ．０１ ，Ｐ＜ ０ ．０５） 。而５０００ ｍ 与１００００ ｍ 组盲肠ＳＳ 含量间无显著性差异。结论模拟上升至５０００ ｍ 急性低压缺氧引起小肠、盲肠粘膜ＳＳ 含量明显升高。模拟上升至１００００ ｍ 急性低压缺氧，引起实验组盲肠粘膜ＳＳ含量增高，对小肠、对照组盲
Objective To investigate the effect of acute hypobaric hypoxia on somatostatin (SS) distribution in lower gastrointestinal tract of rat and ulcer models and its physiological significance. Methods Thirty-six male Wister rats were randomly divided into 6 groups, of which 3 were control group and 3 were experimental group of acute ulcer model. In the low-pressure cabin simulation increased to 5000 m, 10000 m each stay for 30 min, mucosa removed, radioimmunoassay determination of gastrointestinal mucosa SS content. Results In the control group, the content of SS in the small intestine was significantly higher in the 5000 m group than in the ground group (P <0.05). The content of SS in cecal of control group was significantly higher than that of 10000 m group and ground group (P <0.01, P <0.05) in 5000 m group. There was no significant difference between SS group of control group and ground group difference. The content of SS in small intestine in experimental group was significantly higher than that in ground group (P <0. 01) in 5000 m group, but no significant difference with 10000 m group. There was no significant difference in SS content between 10000 m group and ground group. In the experimental group, the content of SS in the cecum of 5000e and 10000m groups was significantly higher than that of the ground group (P <0.01, P <0.05). There was no significant difference in SS content of cecum between 5000 m and 10000 m groups. Conclusions The simulated rise to 5000 m acute hypobaric hypoxia caused small intestinal and cecal mucosal SS content was significantly increased. The simulation rose to 10000 m acute hypobaric hypoxia, causing the experimental group cecal mucosa increased SS content, small intestine, control group blind