Journal of Comparative Pathology

1998

DOI: 10.1016/s0021-9975(05)80126-4

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Systemic atherosclerosis in dogs: Histopathological and immunohistochemical studies of atherosclerotic lesions

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Endothelial Damage2

Suitable Preclinical Models For Dyslipidemia With Elevated P1

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Cited by 31 publications

(30 citation statements)

References 14 publications

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“…Although not studied here, it has been shown that the histology of lesion development in mouse models is similar to that in humans; however, the major limitation of mouse models is that the most-common complications of plaque rupture and superimposed thrombosis (and subsequent acute myocardial infarction and ischemic stroke) rarely occur in mouse models ( 59 ). Recently, NHPs, pigs, dogs, and hamsters on atherogenic diets have been used as models of human atherosclerosis (60)(61)(62). The hamster model is questioned because no consistent lesion development has been observed in several hamster strains ( 63 ).…”

Section: Suitable Preclinical Models For Dyslipidemia With Elevated Pmentioning

confidence: 94%

Plasma lipid profiling across species for the identification of optimal animal models of human dyslipidemia

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et al. 2012

Journal of Lipid Research

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Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide ( 1 ). Dyslipidemia has been shown to be one of the most potent risk factors for coronary heart disease (CHD) ( 2, 3 ). Dyslipidemia is characterized by elevated plasma cholesterol, especially low density lipoprotein cholesterol (LDL-c) levels. Management of dyslipidemia is considered throughout the primary and secondary prevention of CHD ( 4 ). For the past 20 years, the statin (3-hydroxy-3-methylglutaryl CoA reductase inhibitors) class of cholesterol-lowering drugs has been used for the treatment of hypercholesterolemia, either alone or in combination with other classes of lipid-lowering drugs Abstract In an attempt to understand the applicability of various animal models to dyslipidemia in humans and to identify improved preclinical models for target discovery and validation for dyslipidemia, we measured comprehensive plasma lipid profi les in 24 models. These included fi ve mouse strains, six other nonprimate species, and four nonhuman primate (NHP) species, and both healthy animals and animals with metabolic disorders. Dyslipidemic humans were assessed by the same measures. Plasma lipoprotein profi les, eight major plasma lipid fractions, and FA compositions within these lipid fractions were compared both qualitatively and quantitatively across the species. Given the importance of statins in decreasing plasma low-density lipoprotein cholesterol for treatment of dyslipidemia in humans, the responses of these measures to simvastatin treatment were also assessed for each species and compared with dyslipidemic humans. NHPs, followed by dog, were the models that demonstrated closest overall match to dyslipidemic humans. For the subset of the dyslipidemic population with high plasma triglyceride levels, the data also pointed to hamster and db/db mouse as representative models for practical use in target validation. Most traditional models, including rabbit, Zucker diabetic fatty rat, and the majority of mouse models, did not demonstrate overall similarity to dyslipidemic humans in this study . -

“…Although not studied here, it has been shown that the histology of lesion development in mouse models is similar to that in humans; however, the major limitation of mouse models is that the most-common complications of plaque rupture and superimposed thrombosis (and subsequent acute myocardial infarction and ischemic stroke) rarely occur in mouse models ( 59 ). Recently, NHPs, pigs, dogs, and hamsters on atherogenic diets have been used as models of human atherosclerosis (60)(61)(62). The hamster model is questioned because no consistent lesion development has been observed in several hamster strains ( 63 ).…”

Section: Suitable Preclinical Models For Dyslipidemia With Elevated Pmentioning

confidence: 94%

Plasma lipid profiling across species for the identification of optimal animal models of human dyslipidemia

¹

,

²

,

³

et al. 2012

Journal of Lipid Research

View full text Add to dashboard Cite

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide ( 1 ). Dyslipidemia has been shown to be one of the most potent risk factors for coronary heart disease (CHD) ( 2, 3 ). Dyslipidemia is characterized by elevated plasma cholesterol, especially low density lipoprotein cholesterol (LDL-c) levels. Management of dyslipidemia is considered throughout the primary and secondary prevention of CHD ( 4 ). For the past 20 years, the statin (3-hydroxy-3-methylglutaryl CoA reductase inhibitors) class of cholesterol-lowering drugs has been used for the treatment of hypercholesterolemia, either alone or in combination with other classes of lipid-lowering drugs Abstract In an attempt to understand the applicability of various animal models to dyslipidemia in humans and to identify improved preclinical models for target discovery and validation for dyslipidemia, we measured comprehensive plasma lipid profi les in 24 models. These included fi ve mouse strains, six other nonprimate species, and four nonhuman primate (NHP) species, and both healthy animals and animals with metabolic disorders. Dyslipidemic humans were assessed by the same measures. Plasma lipoprotein profi les, eight major plasma lipid fractions, and FA compositions within these lipid fractions were compared both qualitatively and quantitatively across the species. Given the importance of statins in decreasing plasma low-density lipoprotein cholesterol for treatment of dyslipidemia in humans, the responses of these measures to simvastatin treatment were also assessed for each species and compared with dyslipidemic humans. NHPs, followed by dog, were the models that demonstrated closest overall match to dyslipidemic humans. For the subset of the dyslipidemic population with high plasma triglyceride levels, the data also pointed to hamster and db/db mouse as representative models for practical use in target validation. Most traditional models, including rabbit, Zucker diabetic fatty rat, and the majority of mouse models, did not demonstrate overall similarity to dyslipidemic humans in this study . -

“…Distribution of canine apoB-100 (CapoB-100) immunopositive signals in atherosclerotic lesions has been reported previously 7,8 . Immunopositive reactions against anti-CapoB-100 polyclonal antibody 12 were seen in endothelial cells and foamy cytoplasm of macrophages (Fig.…”

mentioning

confidence: 82%

“…The distribution of plasma lipids and lipoproteins in dogs is quite unlike that in humans, with dogs having approximately five to six times as much HDL as LDL. 10 Although a few reports referred to the distribution of apoB in canine atherosclerotic lesions, 7,8 there is no information about the distribution of apoA-I. In this study, using immunohistochemical techniques, we attempt to determine and compare localization of apoA-I and apoB-100 in normal and atherosclerotic lesions of canine aortas, coronary arteries, and peripheral arteries.…”

mentioning

confidence: 98%

Immunohistochemical Detection of Apolipoprotein A-I and B-100 in Canine Atherosclerotic Lesions

Sako¹,

et al. 2003

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Abstract. We attempt to determine and compare the localization of apolipoproteins (apo) apoA-I and B-100 in atherosclerotic lesions of canine aortas, coronary arteries, and the peripheral arteries, using immunohistochemical techniques. Histopathologically, atherosclerotic lesions were characterized by deposition of lipids and infiltration of lipid-laden foamy cells in the tunica intima and tunica media, sometimes forming fibrofatty plaques containing abundant sudanophilic and mineralized material. Canine apoA (CapoA)-I and canine apoB (CapoB)-100 immunopositive signals were simultaneously observed in mild and severe atherosclerotic lesions of the aorta, coronary arteries, splenic arteries, and renal arteries in the double-immunolabeled sections. Both CapoA-I and CapoB-100 positive signals were seen in the cytoplasm of endothelial cells, smooth muscle cells, and macrophages. The subendothelial space and extracellular matrix in the tunica intima and media were also positive. Neither CapoA-I nor CapoB-100 positive signals were seen in normal arteries. These findings closely resemble those of the localization of apoA-I and apoB-100 in human atherosclerotic lesions.

“…Atherosclerosis leads primarily to thickening of the arterial wall in dogs, secondary to depositions of lipid and cholesterol that cause disruption of the tunica intima with extension to the tunica media and tunica adventitia (Kagawa et al 1998). Lesions can be found in the aorta and muscular arteries in many organs, i.e.…”

Section: Endothelial Damagementioning

confidence: 99%

“…heart, eyes, spleen, kidneys, lungs, pancreas, alimentary tract, urogenital organs, prostate and urinary bladder. Direct immunohistochemistry staining identified lipids containing low density lipoprotein (Kagawa et al 1998). Three dog breeds, Miniature schnauzer, Doberman pinscher, and Labrador retriever, were identified as most frequently affected (Liu et al 1986).…”

Section: Endothelial Damagementioning

confidence: 99%

Thromboembolic Conditions, Aetiology Diagnosis and Treatment in Dogs and Cats

2010

Acta Vet. Brno

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In veterinary medicine, thrombo-embolism (TE) is an under-appreciated medical condition that requires immediate recognition. Since TE is multifactorial and its mode of presentation may vary, veterinarians face great difficulties in making a definitive diagnosis in a timely manner. In addition, most of the underlying conditions that give rise to TE are life-threatening and an aggressive diagnostic and therapeutic approach is required. Not only does the diagnosis and treatment of this condition require the collaboration of many specialties, the costs of therapy can be excessive with a high risk of recurrence. As such, owners have to be thoroughly informed before the therapy commences. While TE has been well-characterized in humans and is associated with significant morbidity and mortality, little information of similar quality is available in veterinary medicine. In addition, TE in animals is distinct from its human counterpart and we cannot simply adapt what is known from human clinical trials. With the promise of improvements in imaging modalities that improve our diagnostic capabilities, the window of opportunity to treat TE increases. This article focuses on aetiology, clinical presentation, diagnosis, and treatment of dogs and cats affected by TE. Prothrombotic conditions, non-pulsatile blood flow, endothelial damage, hypercoagulability, clinical presentationThrombo-embolism (TE) in animal patients (canine and feline) can occur at various anatomical locations, including pulmonary vessels, portal vein, vena cava, aortic trifurcation, heart, renal and cerebral arteries, intestinal and mesenteric vessels, spleen, iliac, femoral, coronary and brachial arteries, femoral vein, and vessels of the microcirculation (Butler 1971;Liu et al. 1986; Klein et al. 1989;LaRue and Murtaugh 1990;Laste et al. 1992;Van Winkle and Bruce 1993;Rawlings et al. 1993;Sottiaux and Franck 1998;Palmer et al. 1998;Driehuys et al. 1998;Sottiaux and Franck 1999; Diaz Espineira 1999;Bateman et al. 1999;Norris et al. 1999;Boswood et al. 2000; Tsujino et al. 2005; Gonçalves et al. 2008). The clinical effects of thrombo-embolism depend mainly on the size and site of the final destination of the thrombus/embolus.It is commonly accepted that arterial thrombi are composed predominantly of platelets as compared to fibrin. This is in contrast to vein thrombi, where platelets are scarce and there are larger amounts of cross-linked fibrin. Arterial clots are also generally firmly attached to the underlying vessel wall. In this setting, clot dislodgement will sometimes occur, causing re-canalization of the vessel with relief of the obstruction, but the threat of embolism distally remains. In contrast, venous thrombi are mainly associated with lower limb deep vein thrombosis (DVT) in humans. DVT, however, is not common in veterinary patients. This is thought to be due to the differences in the epigenetics, platelet structure, vascular anatomy and physiological non-bipedal circulation. In fact, venous thrombi tend to be occlusive with resulting ...

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