STIMULATION OF DUODENAL MOTILITY BY HYPEROSMOLAR MANNITOL DEPENDS ON LOCAL OSMORECEPTOR CONTROL

Duodenal motility is stimulated by hyperosmolar solution. Since intest inal distension also stimulates intestinal motility, this increase in the motility response may be due to either stimulation of duodenal loc al osmoreceptor control or intestinal distension resulting from osmoti c equilibration. To test which mechanism is primarily responsible for this osmotically sensitive effect, we compared the number of duodenal spike bursts in five dogs equipped with duodenal fistulas that allowed for the preservation or removal of intestinal distension. The respons e to 300 vs. 1,200 mosM mannitol was compared under three experimental perfusion methods: 1) distension was preserved both proximal and dist al to the fistula (DD); 2) distension proximal to the fistula was remo ved (rD); and 3) distension both proximal and distal to the fistula wa s removed (rr). The test solutions had access to either the whole gut (DD and rD) or only the first 10 cm of the duodenum (rr). We found tha t 1) there were more spike bursts after the hyperosmolar solution (dos e effect, P < 0.05, analysis of variance); 2) there was no significant difference between the three experimental methods; and 3) the stimula ting effect of hyperosmolar solution depended on the first 10 em of th e duodenum. Thus, since hyperosmolar solution increased duodenal motil ity regardless of whether intestinal distension was preserved or remov ed, the stimulating effect of hyperosmolar solution on duodenal motili ty was primarily the result of a local osmoreceptor control mechanism located in the first 10 cm of the duodenum.