Background. Clinical data suggest enteral nutrition prevents stress ulcerat
ion and intragastric nutrients prevent restraint-induced gastric injury. Th
e purpose of these studies was to determine if jejunal nutrients can protec
t without gastric contact and to determine if gastric pH, motility, or muco
sal perfusion is affected.
Methods. In Experiment 1, 27 rats were restrained for 2 h at room temperatu
re followed by 2 h in cold (4 degrees C), with intragastric (IG) or intraje
junal (IJ) 2 ml/h infusions of saline or 25% glucose. Gastric lesions, pH,
volumes, and glucose concentrations were measured postmortem. In Experiment
2, 23 rats had gastric strain gauges implanted >5 days prior to a 0.5 ml/h
IG or IJ infusion during stress. In Experiment 3, 40 rats were anesthetize
d for laser Doppler measurements of gastric mucosal perfusion and arterial
catheter monitoring of systemic hemodynamics. Rats received 0.5-ml boluses
of concentrated glucose or saline IG or IJ, and were monitored for 60 min.
Results. (1) The 2 ml/h IJ and IG glucose infusions prevented gastric injur
y, but the elevated gastric glucose concentrations suggested equal gastric
contact. (2) The 0.5 ml/h glucose IG and IJ infusions decreased gastric inj
ury without reflux of the IJ glucose into the stomach and suppressed stress
-induced hypercontractility, but not acidity. (3) Systemic perfusion pressu
res were unaffected by enteral glucose. IG glucose had little effect on gas
tric mucosal perfusion, while IJ glucose decreased gastric perfusion within
5 min.
Conclusions. These studies show that large volumes of enteral glucose preve
nt restraint injury but IJ glucose refluxes into the stomach. The gastropro
tective effects of small, nonrefluxing volumes of IJ glucose associated wit
h suppression of stress-induced gastric hypercontractility, but not with su
ppressed acidity or enhanced perfusion. (C) 2000 Academic Press.