抄録
Gastric acid secretion is suppressed, resulting in a significant rise in gastric pH, when conscious rats are exposed to hypoxia (Yamaji et al., 1996). When adrenal medullectomized rats were exposed to moderate (10.5% O2) hypoxia for 3 h, gastric acid secretion was restored to nearly the level in normoxia by the adrenal medullectomy. In severe (7.6% O2) hypoxia, the operation also caused an increase in the level of gastric acid output, although the extent was lower than that under 10.5% O2 hypoxic conditions. Gastric pH was normalized by the operation even with 7.6% O2 hypoxia. Similar results were obtained when reserpine, which causes an adrenergic discharge, was administered. When an α2-adrenoceptor blocking agent, yohimbine, was administered, the inhibitory effect of 10.5% and 7.6% O2 hypoxia on gastric acid secretion was almost completely removed. However, neither prazosin (an α1-adrenoceptor blocker) nor propranolol (a β-adrenoceptor blocker) showed any significant effects on gastric acid output in hypoxia. These results indicate that acute hypoxia stimulated the adrenergic response from the adrenal medulla, and that gastric acid secretion was consequently suppressed through α2-adrenoceptor.
