THE CIRCULATORY EFFECTS OF CATECHOLAMINES AND OUABAIN IN GLUCOCORTICOID-DEFICIENT ANIMALS

¹ Department of Pharmacology, Division of Basic Health Sciences, Emory University, Atlanta, Georgia

Glucocorticoid deficiency produced in dogs by chronic administration of dichloro-diphenyl-dichloroethane (o,p'-DDD) was demonstrated by decreased plasma 17-OH-corticosteroids (17-OHCS), abolition of ACTH-induced increase of 17-OHCS and ACTH-induced decrease of eosinophils. Plasma Na⁺, K⁺ and volume and blood pressure and heart rate were unaltered. After 2 weeks of treatment with DDD the dogs were anesthetized for experimentation. Blood pressure and heart contractile force and rate responses to graded doses of epinephrine and norepinephrine were determined in one series of treated dogs and were compared to those in untreated dogs. As a final test, cardiac contractile force response to ouabain was determined in most dogs. Cardioaccelerator and vasopressor responses to the amines and cardiac contractile force responses to ouabain were similar in treated and untreated dogs. However, the positive inotropic effect of high doses of amines was depressed in treated dogs. Administration of prednisolone for 3 days reversed these effects of DDD. DDD-induced glucocorticoid deficiency produced little apparent direct circulatory effect but diminished the animals' ability to withstand stressful procedures, such as thoracotomy and multiple injections of vasopressor amines. Blood pressure and blood volume declined progressively during the course of experiments in DDD-treated dogs but not in untreated dogs. Similar hypovolemic shock was produced in anesthetized dogs by repeated i.v. injections of epinephrine and norepinephrine but not by isoproterenol, a vasodepressor amine. The mechanism of the loss of blood volume is not known. It is not due to histamine release. Prednisolone prevented the development of hypovolemic shock in DDD-treated dogs.

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