Abstract

The aim of this work was to characterize the discharge pattern of vagal efferent fibers supplying the stomach, and the modifications of this pattern induced by stimulation of oesophageal or intestinal receptors. The experiments were performed on dogs in which the central end of the left thoracic vagus had been sutured to the peripheral end of the left phrenic nerve. In such preparations, the activity of the motor units of the reinnervated left hemidiaphragm indicated the activity of vagal efferent fibers. After the left hemidiaphragm had been transformed into subcutaneous muscle, it was possible to study, using electromyography, in the conscious dog, the discharge of efferent vagal fibers which originally supplied the stomach. All the gastric vagal efferent fibers presented a spontaneous discharge with a very low frequency (0.1 Hz < f < 5 Hz). The firing of some fibers was increased each time the gastric motility was enhanced: these fibers were considered to be excitatory fibers. In contrast, other fibers exhibited an opposite discharge pattern and they were considered to be inhibitory fibers. Among all the gastric fibers whose activity was recorded in this study, some of them presented a modification of discharge during the receptive relaxation of the proximal stomach produced by an oesophageal distension. The discharge of excitatory fibers was suppressed while that of the inhibitory fibers was markedly increased. Taking into account these modifications of discharge, parallel to the relaxation of the proximal stomach, it was assumed that these fibers originally supplied the gastric fundus. Other fibers whose discharge remained unchanged during receptive relaxation were supposed to supply the distal stomach, i.e. the gastric antrum. During gastric emptying, when a small inflated baloon, propelled by gastric peristalsis entered the duodenum, the discharge frequency of all the excitatory fibers was decreased whereas that of the inhibitory fibers was enhanced. Similar variations of discharge were observed during the enterogastric inhibitory reflex, caused by an intraduodenal infusion of hydrochloric acid.

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