Atherosclerosis

1993

DOI: 10.1016/0021-9150(93)90057-2

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The distribution of fibro-fatty atherosclerotic lesions in the aortae of casein- and cholesterol-fed rabbits

Ralph G. Kratky

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Difference Hap -(Cholesterol -Casein)1

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Cited by 22 publications

(13 citation statements)

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“…48 It also supports our view that the abdominal aorta is involved in substantial atherosclerotic lesion formation in the low-level cholesterol-fed rabbit. Despite the fact that lesion extent was reduced in the abdominal aorta compared with the thoracic aorta, there is still a greater than 40% probability of lesion formation in the proximal two thirds of the abdominal aorta.…”

Section: Difference Hap -(Cholesterol -Casein)supporting

confidence: 84%

Cholesterol-fed and casein-fed rabbit models of atherosclerosis. Part 1: Differing lesion area and volume despite equal plasma cholesterol levels.

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et al. 1994

Arterioscler Thromb

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One-month-old male New Zealand White rabbits were fed either a cholesterol-free casein diet (CAS; n=10); low-level cholesterol-supplemented (0.125% to 0.5% by weight) chow (CH; n=10); or standard laboratory rabbit chow (n=3) for 24 weeks, during which total plasma cholesterol (TPC) levels were matched for the two experimental groups (TPC CAS =475±39 mg/dL; TPCCH=515±70 mg/dL 2 demonstrated that the atherogenic component of the diet was cholesterol. Their pioneering experiment, in which dietary cholesterol was used to induce hyperlipidemia that resulted in atherosclerotic lesions, established the rabbit as an experimental model of atherosclerosis that is still used today. More recently, it has been discovered 3 that a cholesterol-free, casein-enriched diet induces an endogenous hypercholesterolemia that also results in atherosclerotic lesion formation.Induction of hypercholesterolemia in the rabbit with dietary cholesterol results in a very-low-density lipoprotein (VLDL) hypercholesterolemia in which the VLDL particles, enriched in cholesterol, 4 migrate as ^-lipoproteins on agarose gel electrophoresis and are thus often referred to as /J-VLDL. "7 In contrast, induction of hypercholesterolemia in the rabbit by using a semipurified diet enriched in casein results in a low-density lipoprotein (LDL) hypercholesterolemia similar to that seen in humans. 8 For this reason, the casein-fed rabbit has been used extensively in biochemical studies of lipoprotein metabolism. Only a few groups have characterized different rabbit models of atherosclerosis by using both extensive biochemical analyses and detailed morphological examinations of lesion formation.1417 However, extensive morphological evaluation including lesion area, volume, and topographic distribution has not been performed. In 1978, Ross et al 18 examined the characteristics of the casein-fed and the cholesterol-fed rabbit models to compare the effects of different lipoprotein profiles on atherosclerotic lesion formation. When animals were matched for total plasma cholesterol (TPC), the caseinfed and cholesterol-fed rabbits, although differing in lipoprotein profile, had the same extent of lesion formation. In an attempt to fully characterize the caseinfed and the cholesterol-fed rabbit models of atherosclerosis, in the present study we examined the lipoprotein profiles and the atherosclerotic lesions in the entire aorta of rabbits fed a semisynthetic diet enriched in casein and in rabbits fed a cholesterol-supplemented diet. Because the two groups were matched for TPC, we were able to examine the effect of the different lipoprotein profiles in these animals on the extent, volume, and topographic distribution of lesion formation. The relation of the lipoprotein profiles of these animals to the microscopic morphology and site specificity of lesion type is presented in the accompanying article.

“…48 It also supports our view that the abdominal aorta is involved in substantial atherosclerotic lesion formation in the low-level cholesterol-fed rabbit. Despite the fact that lesion extent was reduced in the abdominal aorta compared with the thoracic aorta, there is still a greater than 40% probability of lesion formation in the proximal two thirds of the abdominal aorta.…”

Section: Difference Hap -(Cholesterol -Casein)supporting

confidence: 84%

Cholesterol-fed and casein-fed rabbit models of atherosclerosis. Part 1: Differing lesion area and volume despite equal plasma cholesterol levels.

¹

,

²

,

³

et al. 1994

Arterioscler Thromb

View full text Add to dashboard Cite

One-month-old male New Zealand White rabbits were fed either a cholesterol-free casein diet (CAS; n=10); low-level cholesterol-supplemented (0.125% to 0.5% by weight) chow (CH; n=10); or standard laboratory rabbit chow (n=3) for 24 weeks, during which total plasma cholesterol (TPC) levels were matched for the two experimental groups (TPC CAS =475±39 mg/dL; TPCCH=515±70 mg/dL 2 demonstrated that the atherogenic component of the diet was cholesterol. Their pioneering experiment, in which dietary cholesterol was used to induce hyperlipidemia that resulted in atherosclerotic lesions, established the rabbit as an experimental model of atherosclerosis that is still used today. More recently, it has been discovered 3 that a cholesterol-free, casein-enriched diet induces an endogenous hypercholesterolemia that also results in atherosclerotic lesion formation.Induction of hypercholesterolemia in the rabbit with dietary cholesterol results in a very-low-density lipoprotein (VLDL) hypercholesterolemia in which the VLDL particles, enriched in cholesterol, 4 migrate as ^-lipoproteins on agarose gel electrophoresis and are thus often referred to as /J-VLDL. "7 In contrast, induction of hypercholesterolemia in the rabbit by using a semipurified diet enriched in casein results in a low-density lipoprotein (LDL) hypercholesterolemia similar to that seen in humans. 8 For this reason, the casein-fed rabbit has been used extensively in biochemical studies of lipoprotein metabolism. Only a few groups have characterized different rabbit models of atherosclerosis by using both extensive biochemical analyses and detailed morphological examinations of lesion formation.1417 However, extensive morphological evaluation including lesion area, volume, and topographic distribution has not been performed. In 1978, Ross et al 18 examined the characteristics of the casein-fed and the cholesterol-fed rabbit models to compare the effects of different lipoprotein profiles on atherosclerotic lesion formation. When animals were matched for total plasma cholesterol (TPC), the caseinfed and cholesterol-fed rabbits, although differing in lipoprotein profile, had the same extent of lesion formation. In an attempt to fully characterize the caseinfed and the cholesterol-fed rabbit models of atherosclerosis, in the present study we examined the lipoprotein profiles and the atherosclerotic lesions in the entire aorta of rabbits fed a semisynthetic diet enriched in casein and in rabbits fed a cholesterol-supplemented diet. Because the two groups were matched for TPC, we were able to examine the effect of the different lipoprotein profiles in these animals on the extent, volume, and topographic distribution of lesion formation. The relation of the lipoprotein profiles of these animals to the microscopic morphology and site specificity of lesion type is presented in the accompanying article.

“…At the celiac branch, lesions developed along the lateral edge of the flow divider 15 within 7 days of the start of cholesterol feeding. For longer-term feeding, lesion length was largest on either the lateral 1535 or distal 36 portion of the branches. Barakat et al 4 have observed a significant correlation between the frequency of sites with increased HRP permeability and lesion length 15 around intercostal arteries but have not observed any correlation for areas around the celiac artery or other abdominal branches.…”

mentioning

confidence: 98%

“…The distribution of lesions around intercostal and celiac branches in rabbits fed a cholesterol 1535 or casein 36 diet was determined by the polar-mapping method. Around intercostal branches, lesions appeared lateral to the orifice after 15 days of cholesterol feeding.…”

mentioning

confidence: 99%

“…Around intercostal branches, lesions appeared lateral to the orifice after 15 days of cholesterol feeding. 15 For longer periods of a high-cholesterol 1535 or casein 36 diet, the longest lesions were distal to the branch site. At the celiac branch, lesions developed along the lateral edge of the flow divider 15 within 7 days of the start of cholesterol feeding.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Characterization of sites with elevated LDL permeability at intercostal, celiac, and iliac branches of the normal rabbit aorta.

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1994

Arterioscler Thromb

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En face autoradiography of the endothelium was used to quantify the distribution, area, and permeability of sites with enhanced permeability to !25 I-low-density lipoprotein ( 125 I-LDL) around the intercostal and celiac arteries and at the iliac bifurcation of normal rabbit aortas. The density of such sites was highest in the upper thoracic aorta and around the celiac and superior mesenteric branches and was lowest in the lower abdominal aorta. Permeable sites occurred more frequently distal to the intercostal branch orifices and both lateral and distal to the orifice at the celiac branch. At the intercostal branch orifices, these sites were larger, with a lower permeability and higher frequency than those away from the branch. At the celiac flow divider, sites of elevated autoradiographic grain density were more permeable and larger than at other locations in the abdominal aorta. Mean regional permeabilities were obtained by weighted area averages of low-and high-permeability sites. Mean regional permeabilities around the intercostal branches were 1.5 times higher than values away from the intercostal branches. Within 0.25 and 1 mm away from the celiac flow divider, mean regional permeability was 3.1 and 1.3 times higher, respectively, than those away from the flow divider. Few sites of elevated permeability were found distal to the aortoiliac bifurcation, and the permeabilities at the medial and lateral walls of the iliac arteries were not different. Mitotic cells were associated with 13 ±8% of all sites with elevated permeability to 125 I-LDL. The frequency of mitotic endothelial cells was not increased at branch sites, suggesting that mechanisms other than cell replication were responsible for increased LDL permeability in the rabbit. These results suggest that the permeability and frequency of occurrence of sites with elevated permeability around the celiac and intercostal branches may influence the distribution and severity of early lesions in rabbits fed a hypercholesterolemic diet. 4 Correspondingly, sites of increased concentrations of radioiodinated albumin and cholesterol in pig and dog aortas correlated with regions prone to subsequent lesion formation.5 ' 6 Radiolabeled LDL concentrations and degradation rates at lesionprone sites around arterial branches in normocholesterolemic rabbits and pigeons are greater than at lesionresistant sites away from branches.7 ' 8 However, with cholesterol feeding, radiolabeled LDL concentrations at lesion-prone sites increased further 9 without significant changes in permeability. 2The mechanisms responsible for altered endothelial permeability to macromolecules are poorly understood, although sites with elevated LDL and albumin permeability in the rat aorta are associated with mitotic and dying cells. 1011 the absence of significant cellular metabolism and matrix binding, the steady-state concentration of LDL can double if only 0.2% to 1% of the endothelium exhibits increased permeability.12 ' 13 Since long-term accumulation of LDL within arteries is s...

“…[2][3][4][5] In rabbits fed a cholesterol-enhanced diet, however, there is no evidence for a reversal with age: the juvenile pattern of sudanophilia is observed even in animals maintained on the diet well into maturity. [6][7][8] These distributions may be related to variations in the net uptake of plasma macromolecules by the arterial wall. In immature rabbits, uptake of circulating albumin is greater downstream of aortic branches than upstream, 9 but the opposite pattern is seen after the age of sexual maturity.…”

mentioning

confidence: 99%

Contrasting Patterns of Spontaneous Aortic Disease in Young and Old Rabbits

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1998

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Abstract-The pattern of spontaneous lipid deposition around aortic branch ostia was mapped in New Zealand White rabbits aged 1 month or 2 to 6 years. The young rabbits were studied within 1 day of weaning, and the older rabbits had been maintained on a low-protein, low-fat diet. Plasma concentrations of total cholesterol for the two groups averaged 75 and 18 mg/dL, respectively. Aortas were fixed in situ at a pressure of 90 to 100 cm H 2 O, stained with oil red O, and photographed en face under an epifluorescence microscope. Areas of staining contrasted in color with the fixativestimulated autofluorescence of nondiseased tissue and were mapped by placing grids over the photomicrographs. Disease around intercostal ostia was rare, but two distributions were established by combining data from many branches. In weanlings, staining was seen within a triangular area downstream of the branch. In old animals, this area had the lowest frequency of disease; lesions tended to occur downstream of the spared region, along axes lying to either side of it, and at the lateral and upstream margins of the ostium. Disease was less rare at celiac branches. It occurred mainly downstream of the ostium in weanlings, whereas upstream sites were most affected in old animals, although significant disease remained at the juvenile locations. Earlier reports have described similar age-related distributions of disease in human aortas, consistent with a common underlying mechanism. The distributions also correlate with the spatial variations in arterial transport properties established in previous studies, and may be determined by them. (Arterioscler Thromb Vasc Biol. 1998;18:300-308.)

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