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用氨基甲酸乙酯麻醉的大鼠,探讨了丘脑下部食欲中枢和迷走神经以及胃运动之间的功能联系。刺激饱中枢,主要引起迷走神经胃支离中性冲动的增加和胃运动的抑制。这种效应不受静脉注射呱乙啶的影响。刺激摄食中枢,通常引起迷走神经胃支离中性冲动的增加和胃运动的亢进。阿托品可消除胃运动的亢进效应,但是不影响迷走神经胃支离中性冲动的增加效应。根据实验结果初步认为,饱中枢通过迷走神经主要与非肾上腺素能抑制性神经元形成突触联系,引起胃运动的抑制,摄食中枢则通过迷走神经,主要与胆硷能神经元形成突触联系,引起胃运动的亢进。
Rat anesthetized with urethane, the functional relationship between the appendix and the vagus nerve and gastric motility in the lower part of the hypothalamus was examined. Stimulation of the full central nervous system, mainly caused by vagus nerve stagnation of the increase in neutral impulses and gastric motility inhibition. This effect is not affected by intravenous guanethidine. To stimulate the feeding center, usually caused by vagus nerve stagnation of the increase in neutral impulses and gastric motility hyperthyroidism. Atropine can eliminate the hyperthyroidism effect of gastric motility, but does not affect the increase of gastric vagal nerve neutral impulses. According to the experimental results, it is preliminarily thought that the saturated center mainly forms synaptic connection with non-adrenergic inhibitory neurons through the vagus nerve and causes gastric motility inhibition. The feeding center passes the vagus nerve and mainly forms synaptic connection with cholinergic neurons, causing Stomach hyperactivity.