ABSTRACT
Objective: To compare the chronotropic action of citalopram, fluoxetine and paroxetine on frog heart
Study Design: Experimental animal study
Place and Duration of Study: This study was conducted at Yusra Medical and Dental College, Islamabad from October 2015 to February 2016
Materials and Methods: Stunning and pithing of the frog was done following which the heart was exposed. The apex was attached to a force transducer. Heart rate readings were recorded on Power lab. Three groups were designed. In every set of experiments basal readings [without drug] were initially recorded that served as the control and then the tissue was treated with one antidepressant. In Group I we documented the effects of citalopram. In Group II we observed the effects of fluoxetine and in Group III we noted the effect of paroxetine. Statistical analysis was done using SPSS version 22. A p value of less than or equal to 0.05 was considered statistically significant
Results: The isolated heart tissue sample was exposed to 0.5ml of drug. Citalopram at a concentration of 1.54mM reduced the heart rate from 30 to 19 beats/min. Fluoxetine at a concentration 1.6mM brought down the heart rate from 23 to 20 beats/min. Whereas, paroxetine at a concentration of 1.3mM increased the heart rate from 21 to 23 beats/min
Conclusion: Citalopram out of the three chosen drugs caused the most marked reduction n in heart rate. Fluoxetine caused a subtle reduction in heart rate. Paroxetine on the other hand caused a mild increase in heart rate
ABSTRACT
Objective: To compare the inhibitory effects of Glibenclamide and Repaglinide on loperamide induced relaxation of isolated ileum of Rabbit. Study Design: Comparative controlled in-vitro experimental Study. Place and Duration of Study: This study was conducted at Department of Pharmacology, Yusra Medical and Dental College Islamabad from February to April 2014. Materials and Methods: Isolated pieces of small intestine of rabbits placed in freshly prepared Tyrode nutritional solution. Six groups were designed. In group I, effect of Acetylcholine on the intestine was observed. In group I1 ileum was exposed to serial dilutions of acetyl choline in the presence of fixed concentration of loperamide dose response curve was plotted. In group 111 fixed dose of Glibenclamide 1u6 was given and dose response curve was plotted with Acetylcholine. In group IV fixed dose of Repaglinide was given and dose response curve was lotted with Acetylcholine. Group V was given Loperamidffilibenclamide and dose responce curve was plotted with Acetylcholine, while group VI was given Loperamide+Repaglinide and dose response curve was plotted with Acetylcholine. The effects were observed and recorded on Power lab. Results: Acetyl choline has produced dose dependent increase in force of contraction from 4.9 to 7.2 mN. In the presence of glibenclamide the force of intestinal smooth muscle contraction increase from 6.4 to 7.8mN and in the presence of loperamide the force decreased from 4.8 to 3.03mN. In the end effect observed with acetyl choline in the presence of loperamide and glibenclamide is 6.5 to 7.7mN. Similarly with repaglinide alone the force of contraction increased from 5.4 to 9.6mN and with repaglindie + loperamide from 4.3 to 21.5 mN. On statistical analysis 't' test as applied and P value was found to be significant that is PK0.05. The dose response curve of acetylcholine on intestinal smooth muscle of rabbit shifted towards left side with glibenclarnide and rapaglinide alone. In the presence of Loperamide the curve shifted towards right side. Glibenclamide and repaglinide when given together with loperamide respectively lead to leftwards shift of the dose response curve. Conclusion: Hence sulfonylurea glibenclamide and repaglinide, the oral anti-diabetics effectively reversed the relaxation of intestinal smooth muscle by loperamide
ABSTRACT
The use of beta blockers is limited by their ability to produce bronchospasm in asthmatics. Third generation beta-blockers like Nebivolol may show better tolerability because they may augment the release of nitric oxide [NO] from endothelial cells. However the involvement of NO in the respiratory effect of Nebivolol remains controversial. The present study, carried out on isolated tracheal muscle strips of guinea pigs, was designed to explore this controversy. Varying concentration of histamine ranging from 10[-7] M to 10[-3] M were used to plot a concentration response curve on the isolated tracheal muscle strips of guinea pig and was used as a control. The same concentration response curve was plotted in presence of a fixed concentration of Nebivolol 10[-6] M and then again in presence of a fixed concentration of L-Nitro Arginine Methyl Ester [L-NAME] 10[-4] M and Nebivolol 10[-6] M together in a series of experiments using six sets of isolated tracheal muscle strips in each case. Nebivolol did not produce any significant shift in the concentration response curve while in the presence of L-NAME, Nebivolol shifted the histamine concentration response curve upwards and to the left. Nebivolol does not augment the histamine induced contraction of respiratory smooth muscle of guinea pig but in the presence of Nitric Oxide inhibitor L-NAME a significant augmentation of the same curve occurs, indicating a role of NO in the sparing of respiratory smooth muscle by Nebivolol