Marcadores de estrés oxidativo en aterogénesis inducida por hiperfibrinogenemia / Oxidative stress markers in atherogenesis induced by hyperfibrinogenemia
Arch. cardiol. Méx
; 79(2): 85-90, abr.-jun. 2009. graf, tab, ilus
Article
en Es
| LILACS
| ID: lil-565727
Biblioteca responsable:
BR1.1
ABSTRACT
INTRODUCTION:
We studied plasmatic TNF-alpha, nitric oxide (NO) and citrulline behaviors and probable morphological mitochondrial alterations in aortic smooth muscle cells, in rats with atherogenesis induced by hyperfibrinogenemia in A) control, B) multiple injured for 30 days and C) multiple injured for 60 days. MATERIAL ANDMETHODS:
Hyperfibrinogenemia induction adrenaline injection (0,1 mg/rat/day). TNF-alpha (pg/dL) was determined by Elisa and NO (microM) and citrulline (mM) by spectrophotometry. Morphological mitochondrial alterations were studied by electronic microscopy. Variables were analized ANOVA, r coefficient and chi2 test.RESULTS:
We observed a significant increment of TNF-alpha in multiple injured for 30 days (B) (50.05 +/- 2.29) as well as in multiple injured for 60 days (C) (74.99 +/- 2.82) related to control (A) (33.01 +/- 1.49) (p<0.001 in both groups). Citrulline presented a significant increased in (B) (5.56 +/- 0.20) and (C) (6.84 +/- 0.13) when compared to (A) (4.41 +/- 0.23) (p<0.001 in both situations). Mean while NO biodisponibility diminished significantly in (B) (8.97 +/- 0.70) and in (C) (5.32 +/- 0.68) when compared to (A) (21.65 +/- 1.74) (p<0.001 in both situations).CONCLUSIONS:
Hyperfibrinogenemia could modify the NO physiopathological pathway and produced morphological mitochondrial alterations in aortic smooth muscle cells, probably producing ischemic lesions in the vascular wall and altering the vasodilatation response.
Texto completo:
1
Colección:
01-internacional
Base de datos:
LILACS
Asunto principal:
Fibrinógeno
/
Factor de Necrosis Tumoral alfa
/
Citrulina
/
Estrés Oxidativo
/
Aterosclerosis
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Enfermedades Metabólicas
/
Óxido Nítrico
Límite:
Animals
Idioma:
Es
Revista:
Arch. cardiol. Méx
Asunto de la revista:
CARDIOLOGIA
Año:
2009
Tipo del documento:
Article
País de afiliación:
Argentina