Effect of low doses of cosyntropin on serum cortisol concentrations in clinically normal dogs

Linda G. Martin Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman, WA 99164-6610

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Ellen N. Behrend Department of Clinical Sciences, College of Veterinary Medicine, Auburn University, Auburn, AL 36849-5523

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Katrina L. Mealey Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman, WA 99164-6610

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D. Mark Carpenter Department of Mathematics and Statistics, College of Sciences and Mathematics, Auburn University, Auburn, AL 36849-5310

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Kathy C. Hickey Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman, WA 99164-6610

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Abstract

Objective—To determine the lowest of 5 doses of cosyntropin (1.0, 0.5, 0.1, 0.05, or 0.01 μg/kg) administered IV that stimulates maximal cortisol secretion in clinically normal dogs.

Animals—10 clinically normal dogs.

Procedures—5 dose-response experiments were performed in each of the dogs. Each dog received 5 doses of cosyntropin (1.0, 0.5, 0.1, 0.05, and 0.01 μg/kg) IV in random order (2-week interval between each dose). Serum samples for determination of cortisol concentrations were obtained before (baseline) and at 10, 20, 30, 40, 50, 60, 120, and 240 minutes after cosyntropin administration.

Results—Compared with baseline values, mean serum cortisol concentration in the study dogs increased significantly after administration of each of the 5 cosyntropin doses. Mean peak serum cortisol concentration was significantly lower after administration of 0.01, 0.05, and 0.1 μg of cosyntropin/kg, compared with findings after administration of 0.5 and 1.0 μg of cosyntropin/kg. After administration of 0.5 and 1.0 μg of cosyntropin/kg, mean peak serum cortisol concentration did not differ significantly; higher doses of cosyntropin resulted in more sustained increases in serum cortisol concentration, and peak response developed after a longer interval.

Conclusions and Clinical Relevance—Administration of cosyntropin IV at a dose of 0.5 μg/kg induced maximal cortisol secretion in healthy dogs. Serum cortisol concentration was reliably increased in all dogs after the administration of each of the 5 doses of cosyntropin. These data should be useful in subsequent studies to evaluate the hypothalamic-pituitary-adrenal axis in healthy and critically ill dogs.

Abstract

Objective—To determine the lowest of 5 doses of cosyntropin (1.0, 0.5, 0.1, 0.05, or 0.01 μg/kg) administered IV that stimulates maximal cortisol secretion in clinically normal dogs.

Animals—10 clinically normal dogs.

Procedures—5 dose-response experiments were performed in each of the dogs. Each dog received 5 doses of cosyntropin (1.0, 0.5, 0.1, 0.05, and 0.01 μg/kg) IV in random order (2-week interval between each dose). Serum samples for determination of cortisol concentrations were obtained before (baseline) and at 10, 20, 30, 40, 50, 60, 120, and 240 minutes after cosyntropin administration.

Results—Compared with baseline values, mean serum cortisol concentration in the study dogs increased significantly after administration of each of the 5 cosyntropin doses. Mean peak serum cortisol concentration was significantly lower after administration of 0.01, 0.05, and 0.1 μg of cosyntropin/kg, compared with findings after administration of 0.5 and 1.0 μg of cosyntropin/kg. After administration of 0.5 and 1.0 μg of cosyntropin/kg, mean peak serum cortisol concentration did not differ significantly; higher doses of cosyntropin resulted in more sustained increases in serum cortisol concentration, and peak response developed after a longer interval.

Conclusions and Clinical Relevance—Administration of cosyntropin IV at a dose of 0.5 μg/kg induced maximal cortisol secretion in healthy dogs. Serum cortisol concentration was reliably increased in all dogs after the administration of each of the 5 doses of cosyntropin. These data should be useful in subsequent studies to evaluate the hypothalamic-pituitary-adrenal axis in healthy and critically ill dogs.

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