NUTRITION METABOLISM OF HIGHER ANIMALS IN HYPOXIA

高等动物缺氧时的营养代谢

基本信息

批准号：
05660146
负责人：
NAKANO Yoshihisa
金额：
$ 1.47万
依托单位：
Osaka Prefecture University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1993
资助国家：
日本
起止时间：
1993 至 1995
项目状态：
已结题

项目摘要

This study examined the effects of hypoxia on the gastric function in conscious rats in a series of experiments. Hypoxia delayd the excretion rats of urinary urea until after 12h of hypoxia and the delay was more remarkable in rats subjected to 7.6%O_2 hypoxia than in those subjected to 10.5%O_2 hypoxia. In Experiment 2, when rats fed the high protein diet for 4h were exposed to 7.6%O_2, a delay in gastric emptying was found in the hypoxic rats. In Experiment 3, when rats fed the normal protein diet for 4h were exposed to 7.6%O_2 hypoxia, the rats of urea excretion in the hypoxic rats were not significantly different from that in the normoxic rats until after 24h of hypoxia. However, rats fed the normal protein diet for 4h werecaused a delay of gastric emptying by 10.5%O_2 hypoxia. In Experiment 4, when rats fed the high protein diet for 4h were exposed to 7.6%O_2 or 10.5%O_2 hypoxia, the plasma gastrin concentration in the 7.6%O_2 hypoxic rats was 2.3-fold that in the normoxic rats after 6h of hypoxia although the gastrin level did not differ between the 10.5%O_2 hypoxic and the normoxic rats during 6h of hopoxia. Furthermore, when food-deprived rats were exposed to 7.6%O_2 or 10.5%O_2 hypoxia, the gastrin concentration was higher in both hypoxic groups than in the normoxic group after 3h of hypoxia. In Experiment 5, food-deprived rats with pylous ligation were exposed to 7.6%O_2 or 10.5%O_2 hypoxia for 3h. Both hypoxia inhibited the secretion of gastric acid and stimulated the gastrin release. In Experiment 6, food-deprived rats with pylorus ligation were orally administered HC1 and then exposed to 7.6%O_2 hypoxia for 3h. The rise of the gastrin concentration due to hypoxia was completely inhibited by the oral administration of HC1. These results demonstrate that hypoxia inhibits gastric emptying and secretion and that the inhibitory effect of hypoxia on gastric acid secretion stimulates gastrin release through positive feedback regulation.

这项研究检查了一系列实验中缺氧对有意识大鼠胃功能的影响。缺氧延迟尿液的排泄大鼠直到缺氧12h后，延迟在患有7.6％O_2低氧的大鼠中比患有10.5％O_2缺氧的大鼠更为明显。在实验2中，当将高蛋白饮食喂4H的大鼠暴露于7.6％O_2时，在低氧大鼠中发现了胃排空的延迟。在实验3中，当将正常蛋白质饮食的大鼠暴露于7.6％O_2缺氧时，低氧大鼠的尿素排泄大鼠与正常氧性大鼠直到24H低氧后的大鼠没有显着差异。但是，喂养正常蛋白质饮食的大鼠以4H的速度延迟了胃排空的延迟10.5％O_2缺氧。在实验4中，当大鼠将高蛋白饮食喂入4H时，暴露于7.6％O_2或10.5％O_2缺氧时，在6H中，在6H中的7.6％O_2低氧大鼠中的血浆胃蛋白浓度为2.3倍，尽管在6H中，但在6H中，在胃动力蛋白水平之间没有差异为6H，但在10.5％O_2下方的脉冲及其之间没有差异。此外，当食物缺乏的大鼠暴露于7.6％O_2或10.5％O_2缺氧时，两个低氧组的胃蛋白浓度均高于3H缺氧后的常氧组。在实验5中，将具有leo孔连接的食物剥夺大鼠暴露于3H的7.6％O_2或10.5％O_2缺氧。两种缺氧都抑制了胃酸的分泌，并刺激了胃酸释放。在实验6中，口服HC1的食物剥夺大鼠，然后暴露于3H 3H中的7.6％O_2缺氧。 HC1的口服给药完全抑制了由于缺氧引起的胃蛋白浓度的升高。这些结果表明，缺氧抑制胃排空和分泌，并且缺氧对胃酸分泌的抑制作用会通过正反馈调节刺激胃蛋白释放。