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In acute experiments on chloralosed cats gastric motility was recorded with a rubber balloon system kept at constant intragastric pressure under experimental conditions not requiring abdominal surgery.-Electric stimulation of the central end of either a small vagal branch at the level of the diaphragm or of one vagal nerve at the level of the neck, while the opposite vagal nerve was left intact produced profound reflex relaxation of the stomach. Also the efferent pathway of the relaxatory reflex was in the vagal nerves.-The reflex relaxation persisted after administration of atropine, which shows that it was not due to reflex suppression of prevailing activity of the vagal cholinergic motor fibres. It was also independent of adrenergic mechanisms, since it persisted after administration of guanethidine in doses known effectively to block the adrenergic intestino-gastric inhibitory reflex. This vago-vagal relaxatory reflex response thus showed the same characteristics as the gastric response elicited by efferent stimulation of the high-threshold vagal relaxatory fibres.-It is concluded that this vago-vagal reflex originates, at least partly, from abdominal structures, with the efferent pathway consisting of the relaxatory, high-threshold fibres producing pronounced gastric relaxation. This vago-vagal relaxatory reflex may be involved in receptive relaxation of the stomach.

The effect of distension of a small or large intestinal loop on the ileo-cecal sphincter (ICS) in the cat was studied with a flow-recording technique. Distension of a small or large intestinal loop, isolated from the adjacent intestine, but with its mesenteric vascular and nervous supply intact, elicited a contraction of the ICS concomitant with an inhibition of the adjacent large and small intestinal motility. Vagal and pelvic nerve section did not affect the response to distension of the ICS nor exclusion of the adrenal glands from the circulation. The sphincter reflex could be entirely or almost entirely eliminated by cutting both the splanchnic and lumbar colonic nerves, but not one or the other. Spinal anesthesia bocked the reflex response indicating a spinal reflex arc. The reflex persisted after atropine and propranolol, while both guanethidine and phenoxybenzamine completely abolished the reflex contraction of the sphincter. The present results indicate that the excitatory intestino-ileo-cecal sphincteric reflex is a spinal reflex with the main afferent and/or efferent fibres located within the major splanchnic and lumbar colonic nerves. The excitatory motor response in the sphincter is adrenergic and mediated via alpha-receptors.

The reflex effects of distension and contraction of the gastric antrum on corpus-fundus motility were studied in anesthetized cats. Besides a vagally mediated reflex corpus-fundus relaxation, antral distension elicited a prompt reflex inhibition of corpus-fundus contractions that was present also after vagotomy. In vagotomized animals this inhibitory reflex persisted also after cervical spinal cord transection, but was abolished by spinal anrsthesia or by guanethidine. Stepwise increases of antral distension revealed that the reflex corpus-fundus inhibition appeared already at distending pressures of 5–10 cm H2O, then increased in a graded fashion and could be maintained for at least 10 min if a steady distension was applied. Also “isometric” antral contractions were effective in eliciting the reflex corpus-fundus inhibition. — It is concluded that activation of slowly adapting “tension receptors” in the antral gastric wall inhibits gastric (corpus-fundus) motility via a spinal reflex mechanism, mediated by splanchnic adrenergic fibres that seem to suppress the intramural excitatory cholinergic neurons. This gastro-gastric adrenergic inhibitory reflex seems to be activated concomitantly with a vago-vagal gastro-gastric relaxatory reflex. It is suggested that these two suppressive reflex mechanisms play an important role in regulation of gastric motor functions.