Spontaneous Disseminated Panarteritis in Laboratory Beagle Dogs in a Toxicity Study: A Possible Genetic Predilection

Ruben, Zadok; Deslex, Paul; Nash, G.; Redmond, Ninfa I.; Poncet, Michel; Dodd, D. C.

doi:10.1177/019262338901700111

Cited by 33 publications

(28 citation statements)

References 8 publications

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“…These reports provide the most relevant information on cases with a close resemblance to what we have observed but a number of other reports on arteritis in the dog (3,(12)(13)(14)(16)(17)(18) and in humans (19,20) give valuable information in this subject area. An interesting report on necrotizing vasculitis complicating a toxicity study has been published (21).…”

Section: Discussionsupporting

confidence: 67%

An Idiopathic Febrile Necrotizing Arteritis Syndrome in the Dog: Beagle Pain Syndrome,

1989

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The clinical, laboratory, and pathologic features ofa syndrome in dogs characterized by intermittent pain, fever, neutrophilia, and necrotizing arteritis are described to alert others involved in toxicity testing to the existence of this disorder. It is considered that this idiopathic syndrome is a latent condition, the expression of which can be precipitated in predisposed dogs by experimental treatment, and thus, its occurrence could complicate interpretation of toxicity studies. We have observed the disorder in 14 beagle dogs. The syndrome is rare and most cases for study were supplied by the breeder. Typical clinical signs observed included evidence of pain when the mouth was opened, grunting when lifted, and standing with an arched back and lowered head. Appetite was usually reduced. Body temperature was elevated (e.g., 104-106°F). There was progressive, bilateral atrophy of temporal and cervical musculature. Such signs have been observed to persist unremittingly or, more commonly, with periods of expression and remission. Neutrophilic leukocytosis and thrombocytosis were present. Hemoglobin and hematocrit were usually slightly decreased. Serum total protein was usually normal but albumin was reduced and alpha-2 globulins were markedly increased. Rheumatoid factor was elevated in several dogs. Arteritis was observed histologically and was characterized by necrosis, intimal proliferation, neutrophil and mononuclear cell infiltration in the media and periarterial tissues, and hemorrhage. Amyloidosis was observed in several dogs. The cause of this disorder is unknown. Knowledge of the distinct features of this syndrome should obviate complication of interpretation of results in toxicity studies and hopefully will lead to studies ofthis syndrome to provide an understanding ofits etiopathogenesis.

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Section: Discussionsupporting

confidence: 67%

An Idiopathic Febrile Necrotizing Arteritis Syndrome in the Dog: Beagle Pain Syndrome,

1989

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“…Although the coronary arterial lesions in dogs treated with minoxidil were qualitatively similar to those induced by other vasodilators and cardiostimulatory/vasodilator drugs (10,11,21,22,31,38) or even some of the spontaneous cases (17,33), there were some significant quantitative differences. Unlike spontaneous cases (25) and dogs treated with nicorandil (Mesfin, unpublished data) the extramural coronary arteries were not involved in dogs treated with minoxidil.…”

Section: Mechanism Ofright Atrial Lesions In Dogs Treated With Toxic mentioning

confidence: 80%

Pathogenesis of Cardiovascular Alterations in Dogs Treated with Minoxidil

et al. 1989

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Minoxidil and other potent vasodilators cause coronary arterial injury, right atrial hemorrhagic lesions, and subendocardial necrosis in dogs, This paper discusses the pathogenesis of coronary arterial and right atrial lesions associated with minoxidil in the dog, Acute coronary vascular injury characterized by segmental medial hemorrhage and necrosis and perivascular inflammation occurred only during the first few days of treatment, after which tolerance to further acute injury developed, At 30 d or more of treatment, coronary vascular injury was characterized by perivascular fibrosis rarely attended by medial distortion or hyperplasia and subintimal thickening, changes consistent with responses to previous injury, Right atrial hemorrhagic lesions, unlike coronary vascular injury, often became progressively more extensive with continued treatment. At 3 d, atrial hemorrhage and inflammation were confined to the subepicardium ofthe right atrium, evidently around affected subepicardial branches of the right coronary artery, At 30 d, fibrovascular proliferative right atrial lesions (granulation tissue with evidence of continual hemorrhage) extended from the epicardium to the myocardium, with eventual replacement ofthe atrial wall by mature connective tissue at I yr of treatment. Minoxidil-induced cardiovascular lesions were not prevented by treatment with a l3-blocker (propranolol), or an a-blocker (dibenzylene), or by sympathetic neural activity suppression (surgical sympathectomy or constant carotid sinus nerve stimulation), suggesting that the sympathetic response to the pharmacologic activity of minoxidil was not responsible for the induction of the cardiovascular lesions. Minoxidil-related vascular lesions were confined to the most pharmacologically responsive segment of the arterial system, the coronary arteries, suggesting that medial injury may have been associated with tensile changes in the arterial wall.

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“…The picture is confounded by the observation that similar vascular lesions are reported to occur spontaneously in beagle dogs (9,20,47), although it is of note that the lesions occurring with PD 156707 were not seen in control animals. In all cases, such arterial lesions were characterized by medial hemorrhage and/or fibrinoid necrosis with associated mediaVadventitia1 accumulation of inflammatory cells.…”

Section: Discussionmentioning

confidence: 99%