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Document Details :

Title: Simvastatin: pharmacological response in experimental hyperfibrinogenaemias
Author(s): MOYA, Mónica , CAMPANA, Vilma , GAVOTTO, Antonio , SPITALE, Luis , SIMES, Juan , PALMA, José
Journal: Acta Cardiologica
Volume: 60    Issue: 2   Date: April 2005   
Pages: 159-164
DOI: 10.2143/AC.60.2.2005026

Abstract :
Through a disorder in the endothelial haemostatic balance, hyperfibrinogenaemia could generate endothelial dysfunction. Statins would have antiinflammatory effects on injured endothelium.

Objective — Simvastatin pharmacological response in rats with hyperfibrinogenaemias induced by laparotomies was studied.

Methods and results — Rats were subjected to multiple injuries (MI) for 30 days (1 laparotomy/week) and for 60 days (1 laparotomy/2 weeks). Simvastatin (0.035 mg/kg) was administered orally to the 30-day multiple injuries group after the third injury for a period of 10 days. A similar dose was administered to the 60-day multiple injuries group after the second injury for a period of 45 days. Blood samples of all the groups were obtained 72 hours after the last injury. In the 30 and 60-day multiple injuries groups, a statistically significant fibrinogen increase was observed (336.6 ± 7.5 and 358.7 ± 9.9, respectively) compared with the control group (207.0 ± 3.0) (p < 0.001). There were no significant differences in the plasmatic fibrinogen (PF) levels between the control and simvastatin treated groups (224.9 ± 1.4 and 216.3 ± 4.3, respectively). There were significant differences between the 30 or 60-day MI untreated groups compared with the 30 or 60-day multiple injuries + simvastatin treated group (p < 0.001). Endothelial denudation and intima widening were observed in the untreated injured groups, whereas in the 60 day multiple injuries group + simvastatin, a regression of histopathological lesions was observed.

Conclusions — the decrease of the inflammatory component that would accompany early atherogenesis processes and the regression of the histopathological lesions after treatment could be attributed to the decreased plasmatic fibrinogen.