This study examines the effects of hypoxia on the gastric function in
conscious rats which adapted to a meal-feeding schedule, that allowed
free access to a high protein (HP) diet (550 g casein/kg diet, Exp. 1,
2 and 4), a normal protein (NP) diet (200 g casein/kg diet, Exp. 3) o
r a nonpurified rat (NPR) diet (Exp. 5 and 6) for 4 h every day for 2
wk. In Exp. 1, after 4 h of consuming the HP diet, rats were exposed t
o 7.6 or 10.5% O-2 normobaric hypoxia. Hypoxia delayed the excretion o
f urinary urea for 12 h. In Exp. 2 and 3, when rats were exposed to 7.
6% O-2 after 4 h of consuming the HP diet and exposed to 10.5% O-2 aft
er 4 h of consuming the NP diet, respectively, a significant delay in
gastric emptying was found in the hypoxic rats. In Exp. 4, when rats w
ere exposed to 7.6 O-2 hypoxia after 4 h of eating the HP diet, the pl
asma gastrin concentration in the 7.6% O-2 hypoxic rats was 2.3-fold t
hat of the normoxic rats after 6 h of hypoxia. Furthermore, when rats
that did not consume any HP diet on the day of the experiment were exp
osed to 7.6 or 10.5% O-2 hypoxia, the plasma gastrin concentration was
higher in both hypoxic groups than in the normoxic group after 3 and
6 h of hypoxia. In Exp. 5, rats that were not fed the NPR diet on the
day of study were exposed to 7.6 or 10.5% O-2 hypoxia for 3 h after py
lorus ligation. Hypoxia inhibited the secretion of gastric acid and el
evated the plasma gastrin concentration. In Exp. 6, unfed rats that ha
d been consuming the NPR diet were: exposed to 7.6% O-2 hypoxia for 3
h after pylorus ligation and were orally administered HCl. The rise of
the gastrin concentration due to hypoxia was completely inhibited by
oral HCl. These results demonstrate that hypoxia inhibits gastric empt
ying and gastric acid secretion and that the inhibitory effect of hypo
xia on gastric acid secretion stimulates gastrin release through posit
ive feedback regulation.