Tsubomura T, Okamoto T, Kurahashi K, Fujiwara M
J Pharmacol Exp Ther. 1987 May;241(2):650-4.
Experiments were performed on cats anesthetized with thiopental sodium and gallamine triethiodide and ventilated artificially. Gastric motility was recorded by a balloon method. Electrical stimulation of the vagal trunk in cats with chronic supranodose vagotomy for 11 to 32 days caused an excitatory response of the stomach. The pulse duration of electrical stimulation to obtain a maximal excitatory response of the stomach was 3 msec. Administration of hexamethonium (10 mg/kg i.v.) did not inhibit but enhanced the excitatory response of stomach. Atropine (3, 10 and 30 micrograms/kg i.v.), hemicholinium (10 mg/kg i.v.) and morphine (5 mg/kg i.v.) inhibited this hexamethonium-resistant excitatory response of the stomach, whereas treatment with physostigmine (300 mu/kg i.v.) augmented it. A substance P antagonist, (D-Pro2, D-Trp7.9)-substance P (250 and 500 micrograms/kg i.v.), did not affect the hexamethonium-resistant excitatory response. Acetylcholine content of the nodose ganglion 6 to 8 days after supranodose vagotomy was assayed using the radioenzymatic method, and the level was about 48% that of the intact ganglion. These results suggest that the gastric excitatory response to stimulation of the supranodose denervated vagal trunk is produced by activation of vagal afferent fibers probably originating from the nodose ganglion; the fibers involved are cholinergic.
实验在使用硫喷妥钠和三碘季铵酚麻醉并进行人工通气的猫身上进行。采用气囊法记录胃动力。对慢性切断迷走神经结上神经干11至32天的猫的迷走神经干进行电刺激，可引起胃的兴奋反应。获得胃最大兴奋反应的电刺激脉冲持续时间为3毫秒。静脉注射六甲铵（10毫克/千克）并未抑制反而增强了胃的兴奋反应。静脉注射阿托品（3、10和30微克/千克）、半胆碱（10毫克/千克）和吗啡（5毫克/千克）可抑制胃的这种六甲铵抵抗性兴奋反应，而静脉注射毒扁豆碱（300微克/千克）则增强了该反应。P物质拮抗剂（D - Pro2，D - Trp7,9） - P物质（250和500微克/千克静脉注射）不影响六甲铵抵抗性兴奋反应。采用放射酶法测定迷走神经结上神经切断术后6至8天结状神经节的乙酰胆碱含量，其水平约为完整神经节的48%。这些结果表明，对迷走神经结上失神经支配的迷走神经干刺激产生的胃兴奋反应是由可能起源于结状神经节的迷走传入纤维激活所致；所涉及的纤维是胆碱能的。
