Abstract

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.