Volumen: 17 # Number : 1
Publication Date : Enero - Abril Year: 2013
Authors: Baez MC1, 2, Tarán M1, Culasso JM1, 3, Balceda A1, 4,
Scribano MP1, Moya M1, 4
Abstract: Hiperfibrinogenemia (HF) was considered that reflects the inflammatory and prooxidative process associated at subclinical atherosclerosis mediated by cytokines, oxidized
LDL and oxygen free radicals. We studied in an experimental model of atherogenesis induced by HF the probable lesions on endothelial level and the mitochondrial
morphology. Three groups of male rats were used: A) Control, B) HFx30ds and C) HFx60ds. HF was induced by subcutaneous injection of adrenaline (0.1 ml/rat/day) and its concentration was studied by spectrophotometry. Histopathology was analyzed by optical microscopy (OM) and mitochondrial morphology by electron microscopy (EM). Statistics: ANOVA and Chi-square, significance level p<0.05. In groups (B) and (C) plasma fibrinogen concentration increased compared with (A) (p <0.001). The MO group (B) showed 81.66% to 88.88% endothelial denudation and intimal thickening in (C), 95% presented denudation and 99% intimal thickening (p<0.01 for both groups). In groups (B) and (C) the total, mean number and mitochondrial crests reduced significantly, the intermembranous
matrix increased and swelling was observed with respect to (A) (p<0.01). Persistent HF would generate the progression of lesions to endothelial level causing changes in its structure and would impact directly at the mitochondrial morphology perpetuating the atherogenic process.
Key words: Fibrinogen, atherogenesis, endothelial dysfunction, mitochondria
Pages : 21-25
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