RESUMO
It has been clearly documented that Elaeagnus angustifolia [E.A.] have variety of medicinal uses including anti - ulcerogenic activity. Our recent study demonstrates that intragastric administration of E.A. blocked the carbachol - induced gastric acid secretion, completely. The aim of this work therefore is to evaluate the role of oral administration of E.A. on carbachol - induced gastric acid secretion in order to compare with intragastric effect of the drug. We also hypothesized that E.A. fruit might be involved in control of basal acid secretion and juice volume. To address this question, we investigated the oral effect of E.A. fruit extract on basal acid secretion on pylorous - ligated conscious rats. In this study we used pylorus ligation method. Briefly, animals were anesthetized and two cannulas were introduced into the stomach through esophagus to wash the stomach and pylorousdodenal junction to collect the stomach juice. Carbachol was infused into jugular vein and gastric juice was collected in 10 - min periods to titrate with NaOH 0.01 N. To concider the effect of the E.A. extraction on basal acid secretion, all experiments were performed in conscious rats who received the E.A. extract or saline 1.5 hours before pylorus-ligation. Ligation of pylorus was performed under brief ether anesthetized. Two and half hours after treatment, the stomach was removed, juice volume was measured and acid output was determined as above. Statistical analysis was performed by analysis of variance and subsequent tukey test. Our results showed that the E.A. fruit extract dose dependently decreased the carbachol - induced gastric acid secretion. Stimulated acid secretion was suppressed%52 +/- 4 at a dose 600 mg/kg and this inhibitory effect persisted up to the end of experiments.Oral administration of E.A. extraction in pylorus ligated conscious rats showed that the drug significantly stimulated gastric acid secretion and juice volume at a dose 1300 mg/kg within 1 hour, but there was no effect at lower doses. These results suggest that E.A. fruit has an anti-secretory action on cholinergic stimulated acid secretion by oral administration. This effect is less than the intragastric administration of the drug [% 81 +/- 4 inhibition]. It is likely that the inhibitory effect is mediated by cholinergic nervous system and/or non-neuronal membranes. We also suggest that the oral E.A. extract has no effect on basal acid secretion at lower doses