metricas
covid
Buscar en
Clínica e Investigación en Arteriosclerosis
Toda la web
Inicio Clínica e Investigación en Arteriosclerosis Efecto antiaterogénico de la atorvastatina en pollos alimentados con una dieta ...
Journal Information
Vol. 14. Issue 5.
Pages 225-229 (January 2002)
Share
Share
Download PDF
More article options
Vol. 14. Issue 5.
Pages 225-229 (January 2002)
Full text access
Efecto antiaterogénico de la atorvastatina en pollos alimentados con una dieta rica en colesterol
Antiatherogenic effect of atorvastatin on chickens fed with a cholesterol enriched diet
Visits
3733
J.V. Ortegaa,
Corresponding author
juanvicente.lia@terra.es

Correspondencia: Hospital Los Arcos.Pº de Colón, 54. Santiago de la Ribera.30720 San Javier. Murcia
, B. García-Pérezb, J. Fernández-Pardoc, M.T. Castellsd, S. Escobare, M. Valdésb
a Hospital Los Arcos. Santiago de la Ribera
b Hospital Universitario Virgen de la Arrixaca. Murcia
c Hospital General Universitario.Murcia
d Universidad de Murcia
e Veterinario avícola
This item has received
Article information
Fundamento

El modelo animal de aves para el estudio experimental de la aterosclerosis ha sido poco utilizado

Objetivo

Demostrar el efecto antiaterogénico de la atorvastatina a dosis de 3 mg/kg/día en pollos alimentados con una dieta rica en colesterol

Métodos

Se han utilizado 18 pollos de raza Leghorn, de 15 días de edad, separados al azar en tres grupos: a) grupo control, alimentado con dieta normal; b) grupo aterogénico, con dieta rica en huevos, y c) grupo aterogénico tratado con atorvastatina. Transcurridas 8 semanas, se procedió al sacrificio de los animales, previa extracción de muestras sanguíneas para realizar distintas determinaciones. Se disecó la aorta torácica y abdominal para, tras tinción con Sudán III, cuantificar por planimetría la extensión y desarrollo de las placas arteroscleróticas, comparando los resultados de cada grupo

Resultados

En el grupo tratado con atorvastatina, las concentraciones (media ± desviación estándar) de colesterol LDL fueron significativamente más bajas que en el grupo aterogénico control (159,6 ± 69,5 frente a 291,0 ± 144,1 mg/dl; p < 0,05). Similares diferencias se observaron en las concentraciones de colesterol no HDL (163,8 ± 70,1 frente a 295,2 ± 144,5 mg/dl; p < 0,05) y en el porcentaje del área aórtica afectada por la placa arteriosclerótica (6,0 ± 4,9% frente al 18,7 ± 3,2%; p < 0,01). Los restantes parámetros analizados no presentaron diferencias significativas entre los distintos grupos

Conclusiones

En el presente modelo experimental, la atorvastatina disminuyó significativamente las concentraciones de cLDL y no HDL en un 45%, y redujo el desarrollo de arteriosclerosis aórtica en un 67%

Palabras clave:
Pollos
Modelos animales
Colesterol
Aterosclerosis
Inhibidores de la hidroximetilglutaril-CoA reductasa
Atorvastatina
Background

Experimental model of chickens for atherosclerosis has been poorly used

Objective

To demonstrate the antiatherogenic effect of atorvastatin (3 mg/kg/day) on an experimental model of chickens fed with a cholesterol-rich diet

Methods

Eighteen white 15 days-old Leghorn chickens were randomly allocated to one of three groups: a) control group, fed with a normal diet; b) atherogenic control group, fed with an egg rich diet, and c) atherogenic group treated with 3 mg/kg/day of atorvastatin. Eight weeks after, all the animals were sacrificed, blood samples being previously drawn to perform biological analysis. The thoracic and abdominal aorta was dissected to quantify by planimetry, after staining it with Sudan III, the extension and development of the atherosclerotic plaque, comparing the results of each group

Results

In the group treated with atorvastatin, the levels (mean ± standard deviation) of LDL cholesterol were significantly lower than in the atherogenic control group (159.6 ± 69.5 vs. 291.0 ± 144.1 mg/dl; p < 0.05). Similar differences were observed in the levels of non-HDL cholesterol (163.8 ± 70.1 vs. 295.2 ± 144.5 mg/dl; p < 0.05) and in the percentage of the aortic area affected by the plaque (6.0 ± 4.9% vs. 18.7 ± 3.2%; p < 0.01). The remainder parameters did not show significant differences among the groups

Conclusions

In the present experimental model, atorvastatin significantly decreased the concentrations of LDL and non-HDL cholesterol about 45% and reduced the development of aortic arteriosclerosis by 67%

Key words:
Chickens
Animal models
Cholesterol
Atherosclerosis
Hydroxymethylglutaryl-CoA reductase inhibitors
Atorvastatin
Full text is only aviable in PDF
Bibliografía
[1.]
D. Waters, L. Higginson, P. Gladstone, B. Kimball, M. Le May, S.J. Boccuzzi, et al.
Effects of monotherapy with an HMG CoA reductase inhibitor on the progression of coronary atherosclerosis as assessed by serial quantitative arteriography: the Canadian Coronary Atherosclerosis Intervention trial.
Circulation, 89 (1994), pp. 959-968
[2.]
J.W. Jukema, A.V. Bruschke, A.J. van Boven, J.H. Reiber, E.T. Bal, A.H. Zwinderman, et al.
Effects of lipid lowering by pravastatin on progression and regression of coronary artery disease in symptomatic men with normal to moderately elevated serum cholesterol levels in Regression Growth Evaluation Statin Study (REGRESS.
Circulation, 91 (1995), pp. 2528-2540
[3.]
Scandinavian Simvastatin Survival Study Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S).
Lancet, 344 (1994), pp. 1383-1389
[4.]
Lipid Research Clinics Program. The Lipid Research Clinics Coronary Primary Prevention trial results. The relationship of reduction in incidence of coronary heart disease to cholesterol lowering.
JAMA, 251 (1984), pp. 365-374
[5.]
J. Shepherd, S.M. Cobbe, I. Ford, C.G. Isles, A.R. Lorimer, P.W. MacFarlane, et al.
for the West of Scotland Coronary Prevention Study Group. Prevention of coronary heart disease with pravastatin in men with hypercholesterolaemia.
N Engl J Med, 333 (1995), pp. 1301-1307
[6.]
G. Brown, J.J. Albers, L.D. Fisher, S.M. Schaefer, J.T. Lin, C. Kaplan, et al.
Regression of coronary disease as a result of intensive lipid-lowering therapy in men with levels of apolipoprotein B.
N Engl J Med, 323 (1990), pp. 1289-1298
[7.]
A.E. La Ville, A.M. Seddon, M. Shaikh, P.M. Rowles, N. Woolf, B. Lewis.
Primary prevention of atherosclerosis by lovastatin in a genetically hyperlipidaemic rabbit strain.
Atherosclerosis, 78 (1989), pp. 205-210
[8.]
García Pérez B. Efecto del nifedipino, verapamilo y diltiazem sobre la placa arteriosclerosa inducida experimentalmente en pollos alimentados con huevos [tesis doctoral]. Universidad de Murcia, 1992
[9.]
D.V. Dauber, L.N. Katz.
Experimental atherosclerosis in the chick.
Arch Path, 36 (1948), pp. 473-492
[10.]
R.W. St Clair.
The contribution of avian models to our understanding of atherosclerosis and their promise for the future.
Lab Anim Sci, 48 (1998), pp. 565-568
[11.]
T.M. Bocan, M.J. Mazur, S.B. Mueller, E.Q. Brown, D.R. Sliskovic, P.M. O´Brien, et al.
Antiatherosclerotic activity of inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase in cholesterol-fed rabbits: a biochemical and morphological evaluation.
Atherosclerosis, 111 (1994), pp. 127-142
[12.]
B.J. Auerbach, B.R. Krause, C.L. Bisgaier, R.S. Newton.
Comparative effects of HMG-CoA reductase inhibitors on apo B production in the casein-fed rabbit: atorvastatin versus lovastatin.
Atherosclerosis, 115 (1995), pp. 173-180
[13.]
B.R. Krause, R.S. Newton.
Lipid-lowering activity of atorvastatin and lovastatin in rodent species: triglyceride-lowering in rats correlates with efficacy in LDL animal models.
Atherosclerosis, 117 (1995), pp. 237-244
[14.]
J. Alfon, C. Pueyo, T. Royo, L. Badimon.
Effects of statins in thrombosis and aortic lesion development in a dyslipemic rabbit model.
Thromb Haemost, 81 (1999), pp. 822-827
[15.]
E. Donetti, T. Piliego, G. Raule, R. Newton, M. Calore, R. Paoletti, et al.
Pharmacological modulation of neointimal hyperplasia in hyper and normo-cholesterolemic rabbits: a comparison among different HMG-CoA reductase inhibitors.
Atherosclerosis, 134 (1997), pp. 97
[16.]
T.M.A. Bocan, S.B. Mueller, E.Q. Brown, P. Lee, M.J. Bocan, T. Rea, et al.
HMG-CoA reductase and ACAT inhibitors act synergistically to lower plasma cholesterol and limit atherosclerotic lesion development en the cholesterol-fed rabbit.
Atherosclerosis, 139 (1998), pp. 21-30
[17.]
R. Maeso, P. Aragoncillo, J. Navarro-Cid, L.M. Ruilope, C. Diaz, G. Hernandez, et al.
Atorvastatin reduces endothelium-dependent constrictor factors in dyslipemic rabitts.
Gen Pharmacol, 34 (2000), pp. 263-272
[18.]
C. Bustos, M.A. Hernández-Presa, M. Ortego, J. Tuñón, L. Ortega, F. Pérez, et al.
HMG-CoA reductase inhibition by atorvastatin reduces neointimal inflammation in a rabbit model of atherosclerosis.
J Am Coll Cardiol, 32 (1998), pp. 2057-2064
[19.]
J.R. Burnett, L.J. Wilcox, D.E. Telford, S.J. Kleinstiver, P. Hugh, P. Barrett, et al.
Inhibition of HMG-CoA reductase by atorvastatin decreases both VLDL and LDL apolipoprotein B production in miniature pigs.
Arterioscler Thromb Vasc Biol, 17 (1997), pp. 2589-2600
[20.]
M. Shiomi, T. Ito, T. Tsukada, T. Yata, Y. Watanabe, Y. Tsujita, et al.
Reduction of serum cholesterol levels alters lesional composition of atherosclerotic plaques. Effect of pravastatin sodium on atherosclerosis in mature WHHL rabbits.
Arterioscler Thromb Vasc Biol, 15 (1995), pp. 1938-1944
[21.]
A.K. Khachadurian, T. Shimamura, S.J. Rozovski, R. Ananthakrishnan, B. Armenian, E. Coly, et al.
Pravastatin decreases serum lipids and vascular cholesterol deposition in Watanabe heritable hyperlipidemic (WHHL) rabbits.
Jpn Heart J, 32 (1991), pp. 675-685
[22.]
M. Shiomi, T. Ito, T. Tsukada, M. Shiraishi, T. Yata.
Effect of fluvastatin sodium on the smooth muscle cells in atherosclerotic plaques. In vivo study using low-density lipoprotein receptor deficient Watanabe heritable hyperlipidemic (WHHL) rabbits.
Arzeimittelforschung, 48 (1998), pp. 680-685
[23.]
F. Poernama, R. Subramaniam, M.E. Cook, A.D. Attie.
High density lipoprotein deficiency syndrome in chickens in not associated with an increased susceptibility to atherosclerosis.
Arterioscler Thromb, 12 (1992), pp. 601-607
[24.]
W. Koenig, M. Sund, M. Frohlich, H.G. Fischer, H. Lowel, A. Doring, et al.
C-Reactive protein, a sensitive marker of inflammation, predicts future risk of coronary heart disease in initially healthy middle-aged men: results from the MONICA (Monitoring Trends and Determinants in Cardiovascular Disease) Augsburg Cohort Study, 1984 to 1992.
Circulation, 99 (1999), pp. 237-242
[25.]
P.M. Ridker, N. Rifai, M.A. Pfeffer, F. Sacks, E. Braunwald.
Long-term effects of pravastatin on plasma concentration of C-reactive protein. The Cholesterol and Recurrent Events (CARE) Investigators.
Circulation, 100 (1999), pp. 230-235
[26.]
P.M. Ridker, N. Rifai, M.J. Stampfer, C.H. Hennekens.
Plasma concentration of interleukin-6 and the risk of future myocardial infarction among apparently healthy men.
Circulation, 101 (2000), pp. 1767-1772
[27.]
R.S. Rosenson, C. Tangney.
Beneficial effect of statin.
[28.]
A.D. Marais, J.C. Firth, M.E. Bateman, P. Byrnes, C. Martens, J. Mountney.
Atorvastatin: an effective lipid-modifying agent in familial hypercholesterolemia.
Arterioscler Thromb Vasc Biol, 17 (1997), pp. 1527-1531
[29.]
A.S. Wierzbicki, P.J. Lamb, Y.K. Semra, M.A. Crook.
Effect of atorvastatin on plasma fibrinogen.
Lancet, 351 (1998), pp. 569-570
[30.]
M. Davidson, J. McKenney, E. Stein.
Comparison of one-year efficacy and safety of atorvastatin versus lovastatin in primary hypercholesterolemia.
Am J Cardiol, 79 (1997), pp. 1475-1481
[31.]
P. Lesnik, A. Vonica, M. Guerin, M. Moreau, M.J. Chapman.
Anticoagulant activity of tissue factor pathway inhibitor in human is preferentially associated with dense subspecies of LDL and HDL and with Lp (a).
Arterioscler Thromb, 13 (1993), pp. 1066-1075
[32.]
P.M. Sandset, H. Lund, J. Norseth, U. Abildgaard, L. Ose.
Treatment with hydroxymethylglutaryl-coenzyme A reductase inhibitors in hypercholesterolemia induces changes in the components of the extrinsic coagulation system.
Arterioscler Thromb, 11 (1991), pp. 138-145
Copyright © 2002. Sociedad Española de Arteriosclerosis y Elsevier España, S.L.
Download PDF
Article options
es en pt

¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?

Você é um profissional de saúde habilitado a prescrever ou dispensar medicamentos