possible role for gastroprotectives on aspirin-induced gastric ulcer in rats

Gastric ulcer is a discontinuity in the gastric mucosa that occurs due to imbalance between gastric mucosal protective factors and aggressive factors. The Aim of the present work was to test and compare the protective effects of an antisecretory H2 receptor blocker; ranitidine and other recently suggested gastroprotective drugs: L-arginine; a precursor of NO, zinc sulfate; an anti-inflammatory antioxidant agent and pioglitazone; a PPAR-gamma agonist, on a rat model of aspirin induced gastric ulcer. Acute gastric lesion was induced in rats by a single oral dose of aspirin 300mg/ kg body weight. L-arginine 200mg / kg b. wt, zinc sulfate 80 mg/ kg b. wt, and pioglitazone 10 mg / kg b. wt. were given alone and in combination with ranitidine 50 mg / kg b. wt for 3 days before induction of gastric lesion. Aspirin induced a significant increase in gastric mucosal lesion score and free and total gastric hydrochloric acid with a significant decrease in gastric nitric oxide and mucin levels as compared to normal group. A significant increase in gastric malondialdhyde and decrease in reduced glutathione as compared to normal group. L-arginine, zinc sulfate, and pioglitazone produced improvement of most of the measured parameters as compared to non-treated group. Combination of L-arginine and ranitidine was superior in prophylaxis against aspirin-induced gastric ulcer when compared to the effects of each drug used individually, and the other studied combinations. The role of HCl and NO seems more important in the pathogenesis of aspirin induced gastric ulcer, as evidenced by the better protective effects of combination of ranitidine and L-arginine in comparison to the ranitidine with either zinc sulfate or pioglitazone

Effect of the anti-oestrogen tamoxifen on some bile constituents in the dog

The effect of oral administration of tamoxifen in a dose of 0.3 mg/kg daily for 3 months was investigated on some constituents of hepatic bile, gallbladder bile and serum of mongrel dogs. Tamoxifen caused significant increase in the level of total cholesterol, triglycerides, alkaline phosphatase and bilirubin in bile and serum. Total protein concentration did not change significantly in both bile and serum. Also, serum albumin did not alter, while albumin/globulin ratio significantly decreased. Osmolality and sodium increased in bile while potassium level decreased. No changes were observed in serum osmolality, sodium or potassium levels. These results support the concept that tamoxifen has some estrogen-like effects

Comparative study between the effects of digitoxin versus digoxin on ferrokinetics

Nineteen male rabbits were included in the present study and classified into three groups to study the effect of repeated oral daily administration of digitoxin [10 mug/kg body wt.] or digoxin [50 mug/kg body wt.] for four weeks on some liver functions [SGPT, SGOT, total serum bilirubin, total serum proteins, serum alkaline phosphatase and prothrombin activity], ferrokinetic parameters [basal plasma iron, post absorption plasma iron tolerance curve, TIBC, UIBC and percent saturation of transferrin], hematological parameters [red cell count, hemoglobin concentration, hematocrit value and red cell indices] and histochemical parameters [iron contents and peroxidase enzyme activity in both the liver and kidney]. The results showed that digoxin produced significant decrease of basal plasma iron, post absorption curve and percentage of saturation of transferrin with significant increase of UIBC. Digoxin produced also mild reduction of iron contents and peroxidase enzyme activity in both the liver and kidney. Digitoxin produced insignificant changes in all the studied parameters. The findings of the present study may suggest that oral administration of digoxin interferes with some ferrokinetics, mainly the intestinal absorption of iron. The effect of digoxin on ferrokinetics seems to affect the cellular iron containing enzymes. The addition of iron therapy was recommended, whenever possible, to patients receiving digoxin for a long time

Atherogenic effect of cigarette smoke exposure and high salt intare using the rabbit as an experimental model

The effect of cigarette smoke exposure and high salt intake, either singly or in combination, were assessed on some atherogenic factors. Significant increases in total cholesterol were found in all treated groups. When combined cigarette smoke exposure and high salt intake had an additive effect. This was combined with a lack of effect on HDL cholesterol. Cigarette smoke exposure resulted in a 28% increase in serum triglycerides. Although high salt intake alone was without effect on this parameter, it had a synergistic effect when combined with cigarette smoke exposure. Platelet aggregation was significantly increased after cigarette smoke exposure, high salt diet intake and their combination. Significant decrease of prothrombin time and partial thromboplastin time were recorded after high salt intake and its combination with cigarette smoke exposure, which may denote increase tendency for thrombus formation. Results were fully discussed

Propranolol versus prazosin on some aspects of lipid metabolism in rats exposed to cigarette smoke: a biochemical, histological and histochemical study

The effects of prazosin and propranolol monotherapy on serum lipids were compared in rats exposed to cigarette smoke. Cigarette smoke exposure for two weeks resulted in a significant increase in serum triglycerides and LDL-cholesterol. Changes in total cholesterol / LDL-cholesterol ratio were not statistically significant. Prazosin monotherapy [0.5 mg/kg/day p.o. for two weeks] resulted in a decrease [insignificant] in serum triglycerides, total and LDL-cholesterol concentrations and total cholesterol/LDL-cholesterol ratio. Propranolol monotherapy [70 mg/kg/day p.o. for two weeks] resulted in a significant increase in serum triglycrides, total cholesterol and LDL-cholesterol, while the total cholesterol/LDL-cholesterol ratio. Propranolol monotherapy [70 mg/kg/day p.o. for two weeks] resulted in a significant increase in serum triglycerides, total cholesterol and LDL-cholesterol, while the total cholesterol/LDL-cholesterol ratio showed a significant drop. Cigarette smoke exposure in rats treated by prazosin resulted in attenuation of the deleterious effects of smoke on triglycerides and LDL-cholesterol. However, potentiation of the effects of exposure to cigarette smoke was noted in the propranolol treated group. Histological study of the liver in the different groups by H and E, and both the enzymatic [succinic dehydrogenase, non-specific esterase, alkaline and acid phosphatases] and the non-enzymatic histochemical [Sudan black B, OTAN and Schultz reactions] findings sustantiate thebiochemical data obtained. It is suggested that the effects of prazosin on serum lipids may be mediated, at least in part, by blocking an action of either the sympathetic nervous system or sirculating catecholamines that normally modulate lipoprotein metabolism and might mediate the lipid alterations induced by smoking. Furthermore, the data suggest that propranolol may induce significant, potentially atherogenic changes in lipid metabolism, whereas prazosin may represent an advantageous alternative as an antihypertensive agent, especially in smoking subjects with an already atherogenic lipoprotein profile