Takuo Fujita

Effect of Antisomatostatin γ-Globulin on Gastrin Release in Rats

In order to determine the mechanism of endogenous gastric somatostatin in the regulation of gastrin release, antisomatostatin rabbit γ-globulin was administered in vivo and in vitro in the rat. First, in rats anesthetized by chloral hydrate, intravenous injection of 1 ml antisomatostatin rabbit γ-globulin had no significant effect on plasma gastrin levels. Second, basal gastrin release from the isolated perfused rat stomach was not affected by the administration of antisomatostatin rabbit γ-globulin (1:99 and 1:1 dilutions). Third, the addition of antisomatostatin rabbit γ-globulin (1:99) to incubated rat antral mucosa, however, significantly increased the basal gastrin release. From these results, it is concluded that antral somatostatin exerts its inhibitory effect on basal gastrin release mainly not through the circulation but via paracrine pathways.

Epidermal growth factor stimulates prostaglandin E release from isolated perfused rat stomach.

Summary Effect of epidermal growth factor, a potent stimulator of growth in many tissues, on immunoreactive-prostaglandin E secretion from isolated perfused rat stomach was investigated. Both mouse and human epidermal growth factor (10 −7 M) evoked a marked increase in immunoreactive prostaglandin E secretion from the rat stomach. Since prostaglandin E is a potent inhibitor of gastric acid secretion, the present study suggests that the increase in prostaglandin E secretion from the stomach may be responsible for the antisecretory effect of epidermal growth factor on gastric acid.

Plasma immunoreactive somatostatin levels in rat hypophysial portal blood: Effect of glucagon administration

Abstract Plasma somatostatin levels of the hypophysial portal blood was examined in urethane-anesthetized rats. Portal blood was withdrawn at a rate of 4.7 μl/min via a cannula placed over the stump of the pituitary stalk, collected into the ice-cold tube at 20min intervals before and after the intraventricular injection of test materials. Immunoreactive somatostatin extracted from the plasma with acid acetone was measured by a specific radioimmunoassay. Basal plasma somatostatin concentrations, 778±52pg/ml (means±SE), did not significantly change after the administration of control solution (0.1N acetic acid in physiological saline), while intraventricular injection of glucagon (2, 10 and 50 μg) caused a significant and dose-related increase in plasma somatostatin during the first 20min. These results suggested that somatostatin release from the median eminence into the hypophysial portal vessel was stimulated by glucagon, although the physiologycal significance remains to be clarified.