Author/Authors :
Mohamed, Fatma A Ain Shams University - Faculty of Medicine - Physiology Department, Egypt , Youssef, Magda HM Ain Shams University - Faculty of Medicine - Physiology Department, Egypt , EI-Salamony, Gehan I Ain Shams University - Faculty of Medicine - Physiology Department, Egypt , El Hamdy, Faiza AM Ain Shams University - Faculty of Medicine - Physiology Department, Egypt
Abstract :
The present work was planned to investigate the effect of hyperuricemia, a suggested cardiovascular risk factor, on the different cellular blood elements, in order to throw more light on the role of elevat-ed uric acid levels in the development and progress of cardiovascular diseases. Experimental hyperuricemia was induced in rats, by using oxonic/uric acid regimen, for 5-days, 2-weeks and 4-weeks. Control normouricemic rats received the solvent, methylcellulose, for matching durations. In all groups, plasma uric acid level, erythrocyte count, hemoglobin content, packed cell volume, blood indices [Mean corpuscular volume, mean corpuscular hemoglobin and mean corpuscular hemoglobin concentration], erythrocyte osmotic fragility, total and differential leucocytic counts, platelet count and indices [Mean platelet volume and platelet distribution width], as well as ADP-induced platelet aggregation were determined. Also, C-reactive protein (CRP) and plasma nitrate levels were estimated. The studied erythrocyte parameters were non-significantly changed. The neutrophil % was significantly increased and the lymphocyte % was significantly decreased in all hyperuricemic groups. The ADP-induced platelet aggregation was significantly enhanced in the 3 hyperuricemic groups. Further, CRP was increased in the 2-and 4-weeks hyperuricemic groups, while plasma nitrate level showed an initial increase, in the 5-days hyperuricemic group, followed by a progressive decrease that was statistically significant in the 4-weeks hyperuricemic group in comparison with the 5-days hyperuricemic group. The encountered effects could possibly be attributed to the pro-inflammatory and free radical-inducing influence of elevated uric acid. The observed neutrophil and platelet activation, known predisposing factors to thrombosis, together with the increased level of the inflammatory marker CRP as well as the reduced NO production, with prolonged exposure to hyperuricemia, might share in causing the hyperuricemia-associated endothelial dysfunction and atherosclerotic plaque formation, thereby contributing to cardiovascular ailment.
