Modulation of gastric distension-induced sensations by small intestinal receptors

Duodenal lipid exacerbates gastrointestinal sensations during gastric diste nsion. Using luminal application of the local anesthetic benzocaine, we inv estigated the role of intestinal receptors in the induction of these sensat ions. Nine healthy subjects were studied on five occasions, during which is otonic saline or 20% lipid (2 kcal/min), combined with (duodenal or jejunal ) 0.75% benzocaine or vehicle at 2.5 ml/min, was infused intraduodenally be fore and during gastric distension. Intragastric pressures and volumes, gas trointestinal sensations, and plasma CCK levels were determined. Duodenal l ipid combined with vehicle increased gastric volume (in ml: saline, -10 +/- 18; lipid/vehicle, 237 +/- 30) and plasma CCK [mean levels (pmol/l): salin e, 2.0 +/- 0.2; lipid/vehicle, 8.0 +/- 1.6] and, during distensions, induce d nausea (scores: saline, 3 +/- 2: lipid/vehicle, 58 +/- 19) and decreased pressures at which fullness and discomfort occurred. Duodenal but not jejun al benzocaine attenuated the effect of lipid on gastric volume, plasma CCK, and nausea during distension (135 +/- 38 and 216 +/- 40 ml, 4.6 +/- 0.6 pm ol/l and not assessed, and 37 +/- 12 and 64 +/- 21 for lipid + duodenal ben zocaine and lipid + jejunal benzocaine, respectively) and on pressures for sensations. In conclusion, intestinal receptors modulate gastrointestinal s ensations associated with duodenal lipid and gastric distension. There is a lso the potential for local neural mechanisms to regulate CCK release and t hereby reduce afferent activation indirectly.