Effect of cardamom oil on gastric secretions, gastric mucosa and induced contractions in rat stomach fundus

The aim of this work was to demonstrate the effect of cardamom oil on gastric secretions, gastric mucosa and induced contractionsin rat stomach fundus. This study was carried out on 40 rats divided into five groups each of 8 rats: Group 1: Control group. Group 2: Received a single dose of cardamom oil [5 ul Kg orally] Group 3: Received a single dose of cardamom oil [50 ul Kg orally] Group 4: Pretreated with cimetidine before cardamom administration. Group 5: Pretreated with atropine before cardamom oil. In all groups the gastric secretion was collected by pyloric ligation, for estimation of HCL concentration, mucin content and peptic activity. Furthermore. isolated stomach fundus strips were used for demonstration of cardamom oil effect on induced gastric contractions. The oil produced a dose dependent increase in both free and total gastric acidity as well as peptic activity. It also produced a slight increase in gastric mucin content. The oil at a dose of 5 ul/kg produced gastric hyperemia in 50% of rats, while a dose of 50 ul/kg produced mild gastric erosinos in 75% of the tested rats. Pretreatment with cimetidine [50 mg/kg] before administration of cardamom oil resulted in a significant reduction in both free and total gastric acidity as compared to that of the untreated animals. Moreover, pretreatment with atropine [1 mg/kg] before administration of cardamom Oil also produced a significant reduction in free and total gastric acidity as compared to that of the untreated animals. Additionally, the oil inhibited the histamine induced stomach fundus contractions on one hand and enhanced that induced by acetylcholine on the other. Cardamom oil has a stimulatory effect on gastric secretion

Effect of the tetracyclic antidepressant maprotiline ongastric secretion and ethanol induced ulcer in rats

The effect of maprotiline [a tetracyclic antidepressant] in a dose of 5 mg/kg, orally for 21 days on gastric secretions and ethanol induced gastric ulcer was tested in rats. Maprotiline decreased the volume, free and total HCI acid concentration and peptic activity. While it produced an increase in mucin content as compared with the control group. Moreover, Maprotiline pretreatment [5 mg/kg, daily for 21 days orally] decreased the ulcer index of ethanol induced ulcer by 59.2%. The data suggest that Maprotiline in the tested dose had acid-pepsin antisecretory effect and ulcer protective activity against ethanol induced ulcer. These effects may be mediated through anticholinergic, antihistaminergic and the possible antidopaminergic effects of Maprotiline