Objective: The oxidative process in atherogenesis generated by proinflammatory
induction and response to antioxidants vitamins in an experimental model were analyzed.
Methods: Male rats were used: (A)Control, (B)Control+vitamin E plus C, (C)Hyperfibrinogenemia
and (D)Hyperfibrinogenemia+vitamins E plus C. Hyperfibrinogenemia induced by
daily injection of adrenaline (0.1mg/day/rat) for 120 days. Treatment: 3.42 mg/kg of vitamin
E plus 2.14 mg/kg of vitamin C, fifteen days after induction. Vascular histology analyzed
by optical microscopy. Fibrinogen, nitrites and superoxide dismutase analyzed by
spectrophotometry. Statistics: MANOVA, Hotelling test for post testing, significance level
Results: (C) group showed higher fibrinogen than (A) and (B)(p<0.001). Compared to (C)
group, (D) showed a decrease of fibrinogen (p<0.001). A marked increase in nitrites was
found in (C) versus (A), (B) and (D) groups (p<0.001). Superoxide dismutase activity increased
in (C) group compared to groups (A) and (B) (p<0.001). In the group (D) an increase
of the activity of this enzyme was observed in comparison to groups (C)(p<0.001),
(A) and (B) (p<0.0001 in both). The (C) group shown endothelial denudation, thickening of
the vascular intima and extracellular matrix enlargement with foam cells(p<0.001).
Conclusion: These results strongly suggest that vitamins E plus C produce regression of inflammatory
and oxidative stress processes in this experimental model.