Rauhofer E A, Greenberg D, Smith G P
Department of Psychiatry, New York Hospital-Cornell Medical Center, White Plains, NY 10605, USA.
Physiol Behav. 1996 Feb;59(2):237-40. doi: 10.1016/0031-9384(95)02132-9.
To investigate the role of gastric contractility in the prepyloric control of meal size, we administered atropine methyl nitrate (3 mg/kg,ip) or saline prior to 30-min tests on 3 separate days in which 0.8 M sucrose was ingested by rats after 1 h of food deprivation. Ingested 0.8 M sucrose accumulated in the stomach and did not empty into the small intestine during the test because the pylorus of each rat was closed by inflation of a chronic pyloric cuff. Atropine methyl nitrate had no significant effect on 30-min intake or on the pattern of intake observed at 3-min intervals during the test on any of the three test days. Thus, neither acute nor repetitive experience with atropine methyl nitrate changed the pattern or volume of intake. These results suggest that gastric contractile responses elicited by the intragastric accumulation of 0.8M sucrose during ingestion are not necessary for the control of meal size by prepyloric mechanisms.
为了研究胃收缩性在幽门前对进食量的控制作用，我们在3个不同的日子里，于禁食1小时后让大鼠摄入0.8M蔗糖进行30分钟测试之前，腹腔注射甲基硝酸阿托品（3mg/kg）或生理盐水。摄入的0.8M蔗糖在胃中积聚，且在测试期间未排入小肠，因为每只大鼠的幽门通过慢性幽门套囊充气而关闭。在三个测试日中的任何一天，甲基硝酸阿托品对30分钟摄入量或测试期间每隔3分钟观察到的摄入模式均无显著影响。因此，无论是急性还是反复接触甲基硝酸阿托品，都不会改变摄入模式或摄入量。这些结果表明，摄入期间胃内0.8M蔗糖积聚引发的胃收缩反应对于幽门前机制控制进食量并非必需。
