Jornal Vascular Brasileiro
https://jvascbras.org/article/doi/10.1590/S1677-54492006000400003
Jornal Vascular Brasileiro
Original Article

O processo aterosclerótico em artérias de coelhos submetidos a dieta suplementada com gema de ovo: modelo experimental de baixo custo

Atherosclerotic lesion formation in rabbits fed on egg yolk-supplemented diet: an inexpensive experimental model

Rodrigo Gibin Jaldin; Hênio Arruda Falcão Filho; Júlio Lopes Sequeira; Winston Bonetti Yoshida

http://dx.doi.org/10.1590/S1677-54492006000400003 J Vasc Bras, vol.5, n4, p.247-256, 2006
PDF
Downloads: 3
Views: 1169

Resumo

OBJETIVO: Verificar a aterogenicidade do modelo de hipercolesterolemia por suplementação alimentar com gema de ovo em coelhos e seu uso como modelo de aterosclerose experimental de baixo custo. MATERIAL E MÉTODO: Foram utilizados 14 coelhos divididos em dois grupos de sete animais: grupo controle (G1), que recebeu ração comercial ad libitum, e grupo tratado (G2), que foi alimentado com dieta suplementada com gema de ovo. Ambos os grupos foram alimentados por 90 dias. Foram realizadas dosagens do perfil lipídico dos animais nos momentos 0, 30, 60 e 90 dias. Ao término do período experimental, os animais foram submetidos a eutanásia e retirada da aorta e de seus ramos diretos para realização de estudo anatomopatológico. RESULTADOS Apenas no grupo G2 houve aumento significativo nos níveis de colesterol total e frações. Ao exame macroscópico, foram observadas estrias gordurosas no arco aórtico e aorta abdominal e, à microscopia, acúmulos lipídicos discretos na íntima da aorta abdominal, renal, carótida, transição toracoabdominal e femoral. Portanto, a dieta com gema de ovo provocou aterosclerose leve no animal de experimentação e alterações equivalentes àquelas provocadas pelo colesterol purificado comercial quando fornecido em baixa dosagem. Assim sendo, a gema de ovo pode ser utilizada como fonte de colesterol alimentar de baixo custo em modelos de aterosclerose experimental.

Palavras-chave

Aterosclerose, colesterol, aorta, coelhos, dieta, dislipidemias

Abstract

OBJECTIVE: To observe whether an inexpensive dietary-induced hypercholesterolemia model in rabbits using a chow diet supplemented with egg yolks can be used to develop atherosclerotic lesions in animals. MATERIAL AND METHOD: Fourteen rabbits were divided into two groups of seven animals: control group (G1), in which the rabbits were fed standard chow diet; and experimental group (G2), in which the rabbits were fed standard chow supplemented with egg yolks. Both groups were fed for 90 days. The lipid profile of all animals was measured at 0, 30, 60 and 90 days. At the end of the experimental period, euthanasia was performed and the aorta and its direct branches were excised to perform the histopathological examination. RESULTS: There was a significant increase in plasma total cholesterol and cholesterol fractions only in group G2. The macroscopic examination showed fatty streaks in the aortic arch and abdominal aorta. Histological analyses revealed minimal lesions consisting of macrophages foam cells in the abdominal, renal, carotid and diaphragmatic aorta and femoral arteries. Therefore, the egg yolk diet developed mild atherosclerosis in rabbits and induced the same characteristics and extent of the lesions obtained by low-dosage purified cholesterol. Thus, egg yolk can be used as an inexpensive source of cholesterol in models of experimental atherosclerosis.

Keywords

Atherosclerosis, cholesterol, aorta, rabbits, diet, dyslipidemias

References

Gebara OCE, Wajngarten M, Barreto ACP. Novos fatores de risco da doença arterial coronária. Rev Soc Cardiol Estado de São Paulo. 1997;7:340-7.

Luz PL, Uint L. Endotélio na aterosclerose: interações celulares e vasomotricidade. Endotélio e doenças cardiovasculares. 2003:131-60.

Yoshida WB. O processo aterosclerótico: da disfunção endotelial à lesão complexa. Doença aterosclerótica periférica. 2004:11-27.

Montenegro MRG. Patogenia da aterosclerose. Doenças vasculares periféricas. 2002:999-1005.

Ross R. The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature. 1993;362:801-9.

Ross R. Atherosclerosis--an inflammatory disease. N Eng J Med.. 1999;340:115-26.

Lastória S, Maffei FHA. Aterosclerose obliterante periférica: epidemiologia, fisiopatologia, quadro clínico e diagnóstico. Doenças vasculares periféricas. 2002:1007-24.

Törnwall ME, Virtamo J, Haukka JK, Albanes D, Huttunen JK. Life-style factors and risk for abdominal aortic aneurysm in a cohort of Finnish male smokers. Epidemiology. 2001;12:94-100.

Kritchevsky D, Tepper SA, Davidson LM, Fisher EA, Klurfeld DM. Experimental atherosclerosis in rabbits fed cholesterol-free diets. Atherosclerosis. 1989;75:123-7.

Kritchevsky D. Diet and atherosclerosis. J Nutr Health Aging.. 2001;5:155-9.

Ramos Morales EL. La aterosclerosis: algunas consideraciones acerca de su estudio experimental; revisión bibliográfica. Rev Cuba Med.. 1987;26:965-70.

Kolodgie FD, Petrov A, Virmani R. Targeting of apoptotic macrophages and experimental atheroma with radiolabeled annexin V: a technique with potential for noninvasive imaging of vulnerable plaque. Circulation. 2003;108:3134-9.

Asai K, Kuzuya M, Naito M, Funaki C, Kuzuya F. Effects of splenectomy on serum lipids and experimental atherosclerosis. Angiology. 1988;39:497-504.

Alfonso Valiente MA, Almeida Carralero G, Quintela Pena AM, Simón Carballo R. Evaluación de un posible modelo experimental de aterosclerosis carotídea en conejos hipercolesterolémicos. Rev Cubana Invest Biomed.. 2001;20:192-6.

Bocan TM, Mueller SB, Mazur MJ, Uhlendorf PD, Brown EQ, Kieft KA. The relationship between the degree of dietary-induced hypercholesterolemia in the rabbit and atherosclerotic lesion formation. Atherosclerosis. 1993;102:9-22.

Fernandes AAH, Alves MJQF, Boteon EM, Rosa GJM, Novelli ELB. Avaliação do colesterol plasmático em coelhos com hipercolesterolemia induzida e tratados com extrato etanólico de própolis. Rev Bras Plantas Medicinais. 2002;4:1-5.

Tabela de Composição Química dos Alimentos. .

Bachorik PS, Rifkind BM, Kwiterovich PO. Lipídios e deslipoproteinemias. Diagnósticos clínicos e tratamento por métodos laboratoriais. 1999:208-36.

Holman RL, Mcgill HC Jr., Strong JP, Geer JC. Technics for studying atherosclerotic lesions. Lab Invest.. 1958;7:42-7.

Duff GL, McMillan GC. The effect of alloxan diabetes on experimental atherosclerosis in rabbit. J Exper Med.. 1949;89:611-30.

Kritchevsky D, Tepper SA, Wright S, Czarnecki SK. Influence of graded level of conjugated linoleic acid (CLA) on experimental atherosclerosis in rabbits. Nutr Res.. 2002;22:1275-9.

Stary HC. The histological classification of the atherosclerotic lesions in human coronary arteries. Atherosclerosis and coronary artery disease. 1996:463-74.

Kritchevsky D. Dietary protein, cholesterol and atherosclerosis: a review of the early history. J Nutr.. 1995;125:589S-93S.

Ross R. The pathogenesis of atherosclerosis--an update. N Engl J Med.. 1986;314:488-500.

Aikawa M, Sugiyama S, Hill CC. Lipid lowering reduces oxidative stress and endothelial cell activation in rabbit atheroma. Circulation. 2002;116:1390-6.

Stahlke Jr. HS, França LHG, Stahlke PH, Stahlke PS. Hiper-homocisteinemia causando aterogênese na aorta de coelhos: modelo experimental. J Vasc Br.. 2004;3:20-30.

Aikawa M, Rabkin E, Okada Y. Lipid lowering by diet reduces matrix metalloproteinase activity and increases collagen content of rabbit atheroma: a potential mechanism of lesion stabilization. Circulation. 1998;97:2433-44.

Nicholls SJ, Cutri B, Worthley SG. Impact of short-term administration of high-density lipoproteins and atorvastatin on atherosclerosis in rabbits. Arterioscler Thromb Vasc Biol.. 2005;25:2416-21.

Sociedade Brasileira de Angiologia e Cirurgia Vascular (SBACV)"> Sociedade Brasileira de Angiologia e Cirurgia Vascular (SBACV)">
5de95ae40e88252165e31d41 jvb Articles
Links & Downloads
1677-7301 (Electronic)
J Vasc Bras ©2024 All rights reserved.

J Vasc Bras

Share this page
Page Sections