Jj. Cullen et al., Gastric emptying of liquids and postprandial pancreatobiliary secretion are temporarily impaired during endotoxemia, DIG DIS SCI, 44(11), 1999, pp. 2172-2177
The aims of our study were to determine mechanisms by which pancreatobiliar
y secretion is altered during endotoxemia. Dogs underwent placement of duod
enal perfusion and aspiration catheters and antral manometry catheters. Gas
tric emptying of liquids, antral motility, output of bile acids and amylase
, and serum levels of enteric hormones were determined after ingestion of a
360-kcal mixed-nutrient liquid meal. Each dog was then given a single dose
of E. coli lipopolysaccharide (200 mu g/kg, intravenously) and the studies
repeated for the next three days. Endotoxin slowed gastric emptying of liq
uids and decreased amylase output for two days. Bile acid output was decrea
sed on postendotoxin day 1. Pancreatic polypeptide alone was decreased on p
ostendotoxin day 1. We conclude that the decrease in pancreatobiliary outpu
t is probably due to decreased nutrient flow into the duodenum and not due
to decreased production of hormones that influence pancreatobiliary secreti
on. The delayed gastric emptying, decreased pancreatobiIiary output, and de
creased postprandial levels of pancreatic polypeptide suggest diminished va
gal output as a possible explanation for the effects of endotoxin on upper
gut function.