Cortisone-induced hypertension and cardiovascular lesions in mice


  • Supported by grants from the National Institute of Health, U.S.P.H.S., HE 04052.


Daily subcutaneous injections of cortisone acetate (0.5, 1.5 or 2.5 mg) were given to three groups of mice for seven consecutive days. Daily systolic blood pressures of the anesthetized mice were obtained by adapting the method of Friedman and Freed ('49). The maximal arterial pressure increase for the 0.5, 1.5 and 2.5 mg groups was 22%, 31% and 41% respectively. This supports the conclusion that cortisone produces hypertension in mice when administered in large doses. Mural hyalinization, vacuolization and cellular proliferation of coronary arteries were greatest in the 0.5 mg group. The highest incidence of myocardial necrosis, 56%, was in the group receiving 2.5 mg of cortisone daily. The frequency and severity of myocardial and renal cortical necrosis were directly related to the size of the cortisone dose. Adrenal medullary vacuolization and lipid infiltration of the liver were common in all experimental groups.