Sympatho‐adrenergic inhibition of basal and acid‐induced changes in duodenal motility, mucosal net fluid and alkaline secretion in the anaesthetized cat

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Abstract
Experiments were performed on chloralose anaesthetized cats. A 2‐cm segment of the proximal duodenum was isolated between two luminally situated balloons and perfused with isotonic saline containing [14C]‐PEG 4000 as a non‐absorbable marker. The perfusate was analysed with regard to alkalinity (back titration) and concentration of marker (liquid scintillation). Net alkalinization and net fluid transport were calculated with conventional equations. Motor activity in the duodenal wall was recorded as changes in volume of the proximal balloon. In presence of sympathetic neural activity (spontaneous or electrically stimulated) basal motor of sympathetic neural activity (spontaneous or electrically stimulated) basal motor activity and mucosal alkaline secretion was and increased minimally in response to luminal HCl (30 mM). Net fluid transport was in an absorptive state and shifted to a small secretion upon the acid‐exposure. Subsequent to bilateral acute splanchnicotomy, or the administration of the adrenolytic guanethidine (3–4 mg kg‐1, i. v.), spontaneous duodenal contractions occurred and the alkaline secretion was increased. Furthermore, both parameters were then markedly stimulated by luminal perfusion with 30 mM HCl. Basal net fluid transport was zero and turned into secretion upon the acid‐exposure. No morphological changes of the duodenal surface epithelium could be detected. The study demonstrates the existence of splanchnic nerve‐mediated, adrenergic inhibition of basal, as well as of acid‐induced duodenal motility, fluid and alkaline secretion.

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