P. Leveau et al., ALTERATIONS IN INTESTINAL MOTILITY AND MICROFLORA IN EXPERIMENTAL ACUTE-PANCREATITIS, International journal of pancreatology, 20(2), 1996, pp. 119-125
Conclusion, A delay in intestinal transit time appears as an early eve
nt in acute pancreatitis, preceding intestinal bacterial overgrowth an
d translocation,Background, Septic complications, primarily caused by
bacteria of enteric origin, are frequent in severe acute pancreatitis.
Impairment in intestinal motility probably plays a pathophysiological
role in the development of bacterial overgrowth and ensuing transloca
tion. Methods, In the present study, the influence of acute pancreatit
is on intestinal motility was evaluated by measuring small intestinal
transit time in the rat. Acute pancreatitis was induced by the retrogr
ade intraductal infusion of 0.2 mt taurodeoxycholate. Intestinal trans
it time was studied by intraduodenal injection of Krebs' phosphate-buf
fered solution labeled with (Na2CrCO4)-Cr-51, and 1 h small intestinal
transit was measured at 1, 3, 12, and 24 h, after induction of pancre
atitis. Bacterial overgrowth was evaluated by measuring Escherichia co
li counts in the colon and distal small intestine, and bacterial trans
location to mesenteric lymph nodes, the liver, spleen, and pancreas wa
s determined. Results, A delayed small intestinal transit time was not
ed from 3 h on after induction of acute pancreatitis, with most of the
radioactivity retained in the first two intestinal segments. Overgrow
th of E. coil was noted 12 h after induction of pancreatitis in both t
he colon and distal small intestine, and at the same time-point, a sig
nificant increase in the incidence of bacterial translocation to mesen
teric lymph nodes was seen.