The effect of cortisone on experimentally produced myocardial infarcts.

Administration of a moderately large or large dose of cortisone to dogs having acute myocardial infarctions inhibited slightly the rate of removal of necrotic muscle fibers in these animals as compared with untreated animals. Delay was appreciable at four and six days after production of the infarct in animals receiving 2.5 mg. of cortisone per kilogram of body weight and at 4, 6, 12 and 21 days in animals receiving 10 mg. per kilogram. At all other periods up to essentially complete healing of the infarcts as defined at 60 days, no appreciable differences existed between treated and untreated animals. ITH the general availability of cor-tisone, the study of its influeniice on such fundamental body reactions as inflammation, connective tissue growth, and immunologic responses has been possible. That administration of cortisone does materially alter these reactions in many animals under certain conditions is now well known. The lack of inlformation concerning the effect of cortisone on the healing of myocardial in-farcts prompted the investigation of this problem in dogs. During the formulation of this problem, two reports on the results of investigations along these lines appeared in the literature.1' 2 The fact that strikingly different results were obtained by two groups of investigators (Johnson and associates; Chapman and associates) made the problem all the more inviting to pursue. Johnson and associates1' 3 reported on the effects of cortisone on experimentally produced myocardial infarcts ill dogs. When they gave the animals 25 to 40 mg. of cortisone daily beginning at the time of ligation of the anterior descending corollary artery, they found that the resulting myocardial infarcts were strikingly smaller than were the infarcts in the From the iaIyo Clinic and the Mayo Foundation, 742 animals of the control group, which underwent the same operation but did not receive cor-tisone. They also found fewer adhesions in the surgical area, less postoperative morbidity, a lower mortality rate, and a marked decrease in fibroblastic proliferation in the animals treated with cortisone. Increased vascularity of the infarcts in the treated animals was also noted. Chapman and co-workers'2 gave 7 mg. of cortisone per kilogram of body weight daily to a group of dogs and ligated the anterior descending coronary artery in its proximal third. Control animals were similarly operated on but did not receive cortisone. Examination of the infarcts in 10 and 30 days disclosed 0lo gross differences between the animals receiving cor-tisone and …