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1.
Article | IMSEAR | ID: sea-215940

ABSTRACT

Aim:Ibuprofen is analgesic, antipyretic and anti-inflammatory drug, which is widely used as a cheap over-the counter drug(OTC); however, this drug accompanies anti coagulation/anti platelets effects which sometimes might illicit adverse effects. In this study, we investigated effect of ibuprofen on prothrombin time (PT), activated partial thromboplastin time (aPTT) and platelet count using wistar albino rats.Methods:A total of 21 rats grouped into 3(control, acute and chronic exposure groups, with all consisting of 7rats each) was used. The acute and chronic exposure group were given 0.7mg of ibuprofen orally for 1 and 21 days, respectively. Blood sample was collected via cardiac puncture thenanalyzed.Results:PT was significantly higher in both group 2 and 3 (acute and chronic exposure, respectively)than that of the control. Acute exposure group showed the highest PT rise.A PTT was not significantly different between group 2 and 3 versus the control group. Platelet count was significantly lower in both group 2 and 3than that in the control group (p<0.05). Group 3 (chronic exposure) showed the lowest platelet count.Conclusion:Oral administration of ibuprofen affected coagulation parameters and a longer exposure reduce platelets count. A strictly prescription for this drug may be needed to prevent its indiscriminate use

2.
Article | IMSEAR | ID: sea-200754

ABSTRACT

Diclofenac sodium is a nonsteroidal anti-inflammatory drug often obtainable as a prescription drug or over the counter. It is very effective in the control of inflammation and pain due to arthritis or pains arising following many disease conditions becauseof its antipyretic, anti inflammatory and analgesic potentials. Despite the beneficial effects of diclofenac sodium, it has been implicated in some adverse effects. In this study, we examined the effect of acute and chronic administration of diclofenac sodium on some hematological (PCV, WBC differentials) and coagulation (prothrombin time, activated partial prothrombin time and platelets count) parameters of albino Wister rats using the standard methods. Twenty four Albino Wister rats were divided intothree groups of 8 rats and grouped as control, acute study and chronic study. The rats were administered 0.2 mg of diclofenac sodium for 24 hours for acute and 3 weeks for chronic studies respectively. The rats were sacrificed and blood collected for analysis of PCV, WBC differentials, prothrombin time, activated partial prothrombin time and platelets count using the standard methods. Results show that acute administration of diclofenac sodium at 0.2 mg has no effect on hematological and coagulation parameters, but chronic administration could instigate significant reduction in PCV, platelets count, neutrophils and monocytes (p<0.001), whilethere is a significant increase in PT, INR, lymphocytes (p<0.001). Considering these alterations, it is advisable that this drug should be made a strictly prescription drug in order to prevent indiscriminate use of this medication and to prevent attendant anemia and coagulopathy that may follow chronic use.

3.
Article | IMSEAR | ID: sea-200679

ABSTRACT

Cardiac arrhythmia affects ~ 6% in those over 65 years of age (old), but with 0.2% occurrence in those of 45 years and below (young). Arrhythmia can result from dysregulation of the cardiac impulse generation and its conduction. Connexin proteins are responsible for cardiac impulse conduction, and phosphorylation of connexin 43 determines its functional ability. In this study, Phosphorylated connexin 43, density and expression were assessed in ventricular tissues from young (6 months old) and old (24 monthsold) Wister rats, using the techniques of western blot and immunohistochemistry. Results show that phosphorylated Cx43 in the left ventricle of 24 months old rats significantly declined (P=0.04 & 0.01) by method of western blot and immunohistochemistry respectively, but did not differ in the right ventricle. The left ventricle is known to be responsible for cardiac output. This data suggest an age-associated decline in the expression of phosphorylated connexin 43 in the left ventricle, which may play a significant role in the development of cardiac arrhythmia in the elderly.

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