Abstract
INHIBITION OF GASTRIC EMF’TYING BY HYPEROSMOLAR SOLUTION DEPENDS ON DUODENAL RESISTANCE. H. C. Lin and J. H. Meyer. Dept. of Medicine, Cedars-Sinai Medical Center and Sepulveda VA Medical Center, UCLA, Los Angeles, CA. Osmotic control of gastric emptying (GE) has been postulated to be dependent on duodenal osmoreceptors (Gastro 68:1144, 1975). Contradicting this idea was our earlier finding that the osmolality within the range of 0.25M-l.OM glucose meals was an unimportant factor in the regulation of GE when thyme was diverted out of the proximal duodenum to eliminate duodenal resistance (even when the proximal 65cm of gut was exposed to chyme)(AJP 256: G404,1989). Since duodenal resistance to GE is caused by limitations in duodenal capacity (J Lab Clin Med 111:654, 1988), inhibition of GE by a hyperosmolar solution may depend primarily on the duodenal resistance and not on the feedback from duodenal osmoreceptors. We tested this idea by tracking GE in dogs with duodenal fistulas in which duodenal resistance was either eliminated (by temporarily diverting all thyme from the fistulas before reperfusing the output back into the distal limb of the fistula) or preserved (duodenal fistulas were corked). In 4 dogs, using a gamma camera and Tc-99m labeled solutions, we compared the GE of 5OOml of 1200mOsm mannitol and 0.15M NaCl (300mOsm). RESULTS; Areas Under 60-min GE courses. AUC varies between 0 (complete emptying at time 0) and 550 (no emptying), Values are means + SE. mOsm NaCl 1200mOsm Mannitol Resist. Eliminated 210.5 f 55.7 286.9 + 39.7 Resist. Preserved 322.6 + 41.2 450.1 + 19.7 1) In the absence of duodenal resistance, GE of 1200mOsm mannitol was the same as 300mOsm NaCl (p>O.25); and 2) GE of 1200 mOsm mannitol was slower than 300mOsm NaCl only when duodenal resistance was preserved (~~0.05). aNCLUSION: Inhibition of GE by hyperosmolar solution depends on duodenal resistance.
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