Mechanisms in bile salt-induced secretion in the small intestine. An experimental study in rats and cats

The present study was designed to test whether fluid and electrolyte secretion evoked in the small intestine by the dihydroxy bile salt sodium deoxycholate could be due to activation of a nervous reflex mechanism. The effect of the bile salt on small intestinal motility was also investigated, and an analysis was made of factors involved in passive and active transport mechanisms relevant to bile salt-induced secretion. Luminal perfusion with sodium deoxycholate changed net fluid transport from absorption to secretion. Hexamethonium, a ganglionic receptor blocker, lidocaine, a local anaesthetic and tetrodotoxin, a sodium channel blocker, inhibited the induced fluid secretion. The inhibitory effect increased in proportion to the rate of secretion. Elimination of the bile salt from the perfusate also inhibited the secretion. A minor part of the induced change in net fluid transport was resistant to nerve blockade or to bile salt elimination. The change of net fluid transport was paralleled by a change of sodium and chloride transport from absorption to secretion. The change of net sodium transport was due to both a reduced uptake and increased losses. Villus tissue hyperosmolality was reduced by the bile salt. Hexamethonium inhibited the electrolyte secretion. The bile salt caused epithelial lesions in the upper parts of the villi. The lesions persisted also after the bile salt-induced secretion had been inhibited by nerve blockade or by bile salt elimination. Lesions also appeared in intestines which failed to develop net fluid secretion. The bile salt also induced characteristic intestinal contractions which showed a good correlation with the rate of net fluid secretion. The motility was also inhibited by nerve blockade or bile salt elimination. Atropine abolished the induced motility but did not influence the secretion. Indomethacin, a prostaglandin synthesis inhibitor, or pyrilamine, a histamine 1-receptor antagonist, did not inhibit either motility or secretion. The bile salt caused a mucosal vasodilatation, total blood flow increasing about 50%. Capillary filtration coefficient remained unchanged. Lymph flow did not increase. No correlation was found between the change of intestinal blood flow and the change of net fluid transport. Hexamethonium and tetrodotoxin inhibited the induced secretion without influencing blood flow. It is concluded that sodium deoxycholate evokes intestinal secretion and motility via an enteric nervous reflex arch consisting of a presynaptic cholinergic neuron and two postganglionic neurons, one cholinergic innervating the intestinal smooth muscle cell and the other non-cholinergic, non-adrenergic influencing intestinal flu