Biochemical and physiological effects of catecholamine administration in the horse

Anderson, Marion G.; Aitken, Maureen M.

doi:10.1016/s0034-5288(18)33263-6

Cited by 27 publications

(19 citation statements)

References 14 publications

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“…Horse glands are very sensitive to its cutaneous administration, which causes a local sweating response lasting 1 h or more including gradual spreading as a clear‐cut track along superficial lymphatic vessels for long distances 30,37,129,130 . The adrenergic agonist isoprenaline also elicits sweating but sometimes after a delay 30,49,131 . The secretion caused by Ad 128 is not prevented by atropine, a parasympathetic antagonist, but is abolished by sufficiently large concentrations of dihydroergotamine, an adrenergic blocker 130 .…”

Section: Control Of Sweatingmentioning

confidence: 99%

“…They further demonstrated that heat‐induced sweating blocked by bethanidine could be restored by subsequent administration of Ad but not by NA, casting doubt on its role as the sympathetic transmitter for equine sweating. Noradrenaline infusion intramuscularly was unsatisfactory as local vasoconstriction limited absorption from the site of injection 131 . In contrast, Bullard et al 37 .…”

Section: Control Of Sweatingmentioning

confidence: 99%

“…Information from studies of perfused skin, isolated sweat glands and cultured gland cells strongly indicates that the main receptors on the equine sweat gland are β 2 adrenoceptors, 5,31,131,176,177 although horse sweat glands have been found to discharge slightly in response to α‐adrenergic stimulation 49 …”

Section: Control Of Sweatingmentioning

confidence: 99%

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Equine sweating and anhidrosis Part 1 – equine sweating

Jenkinson

Elder

Bovell

2006

Veterinary Dermatology

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Sweating has a variety of functions in mammals including pheromone action, excretion of waste products and maintenance of the skin surface ecosystem. In a small number of mammalian species, which includes humans and the Equidae, it also has an important role in thermoregulation. This review is focused specifically on the thermoregulatory role of sweat in Equidae and the causes of sweating failure (anhidrosis). The first part describes the glandular appearance, sweat composition, and output rates; and considers the latest theories on the glandular control and secretory mechanisms. It is concluded that the glands are not directly innervated but are controlled by the interplay of neural, humoral and paracrine factors. The secretory mechanism is not as simple as previously thought and is mediated by the dynamic interaction of activating pathways, including autocrine control not only of the secretory process but probably also of secretory cell reproduction, growth, and death.

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Section: Control Of Sweatingmentioning

confidence: 99%

Section: Control Of Sweatingmentioning

confidence: 99%

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Equine sweating and anhidrosis Part 1 – equine sweating

Jenkinson

Elder

Bovell

2006

Veterinary Dermatology

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“…The expelled fluid travels through the lumen of a duct into the piliary canal in the infundibulum of the hair follicle just above the sebaceous duct opening . There is convincing evidence that main receptors on the equine sweat gland are β 2 adrenoceptors, although horse sweat glands have been found to discharge in response to α 2 adrenergic stimulation . Evidence for the role of α 2 adrenergic stimulation of sweat‐induced urticaria in this horse was seen with the use of an α 2 adrenergic agonist.…”

Section: Summary Of Intradermal Test Results At 15 Minutesmentioning

confidence: 81%

Sweat Hypersensitivity‐Induced Urticaria and Sebaceous Adenitis in an American Saddlebred

Lorch

Mays

Roberts

et al. 2013

Veterinary Internal Medicne

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A 5-year-old Saddlebred gelding was presented for the evaluation of nonseasonal chronic progressive dermatitis that began at 1 year of age. The dermatitis started as a linear area of crusting and scaling on the lateral aspect of the left shoulder that would resolve in the spring and summer months. However, for the previous 3 years the lesions progressed and were present year round. Many topical and systemic treatments had been used over the 3-year period with no clinically appreciable response, including penicillin injections (dosage unknown), antifungal topical agents, iodine baths, and prednisolone (1 mg/kg PO q24h for 14 days then tapered over 30 days).For the previous 2 years, nonseasonal pruritic urticaria occurred when the horse would sweat. The pruritus was graded as 9/10 with 10 representing severe pruritus. The intensity of the pruritus limited the horse's ability to work and had increased each year. The pruritus was manifested as stomping, biting at the sides, forceful tail whipping, refusing to stand in place, extreme anxiousness, and rubbing. The urticaria subsided within 20 minutes of working, as did the pruritus. Baths with lukewarm water immediately after working controlled the pruritus. Preemptive 14-day courses of hydroxyzine pamonate (2 mg/kg q8h) and chlorpheniramine (0.5 mg/kg q12h) were ineffective.On physical examination, generalized distribution of circular to annular areas that had varying degrees of crusting and alopecia, moderate-to-severe scaling, and mild leukoderma was present. Although the lesions were generalized, the most severely affected regions included the face, neck, chest, lateral thorax, and the proximal aspect of all 4 limbs. Two smaller focal areas of thick crusts were removed, disclosing circular erosions. Focal areas of severe scale and crusting and partial alopecia were present at the junction of the pelage and mane, causing loss of the mane (Fig 1A, B). Differential diagnoses for the dermatitis included sebaceous adenitis, discoid lupus erythematosus, and sarcoidosis. Differential diagnoses for the nonseasonal urticaria included exercise-induced cholinergic urticaria (CU), as well as heat, stress-induced, or idiopathic urticaria.Initial diagnostic tests consisted of a complete blood count (CBC), serum biochemical profile, cutaneous surface cytology, superficial and deep skin scrapings, a tissue punch biopsy for fungal and bacterial cultures, and seven 6-8 mm skin punch biopsy specimens from multiple affected sites for histopathology. All tests were performed in a routine manner.1 Impression smear cytology from an erosive lesion on the dorsolumbar trunk showed many neutrophils, occasional red blood cells (RBCs) and rare extracellular cocci per oil immersion field. All superficial and deep skin scrapings were negative for parasites. All CBC and serum biochemical results were within normal limits. Bacterial and fungal tissue cultures were negative for growth of organisms. Histopathology from an alopecic and crusted lesion identified hyperplastic crusting, suppurative ly...

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“…The epinephrine tolerance test is used in other species to assess the hyperglycemic response to mobilization of glycogen from the liver as well as mobilization of fat from peripheral stores. [15][16][17] Confirmation of the importance of catecholamines in the mobilization of fat and glucose in camelids would improve our understanding of the conditions that lead to hyperglycemic or hyperlipemic disorders and perhaps allow us to develop novel, specifically directed prevention and treatment strategies. Because administration of insulin has become a focus of the medical management of fat mobilization disorders in camelids, 3 confirmation of an anticatecholamine-like role for insulin would establish administration of this hormone as the cornerstone medical intervention in the treatment of camelids with excessive fat mobilization.…”

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confidence: 99%