Abstract

Using contrast-enhanced computed tomography, the effects of hyperosmolar mannitol and methylprednisolone on experimentally produced myocardial infarcts were evaluated serially over the course of approximately 1 month. Infarct size, initial perfusion defect (jeopardized segment) and noninfarcted muscle mass were determined in three groups of conditioned mongrel dogs. Group 1 (n = 11) served as the control group, groups 2 and 3 were pretreated with mannitol (375 mg/kg, n = 10) or methylprednisolone (7.5 mg/kg, n = 11). Each animal in the treatment groups was treated with identical doses of the originally administered agent twice daily for 7 days after coronary occlusion. Each group developed increases in the noninfarcted muscle mass of the left ventricle (compensatory hypertrophy). The mean increase averaged more than 20% over 30 days when all groups were included together. Infarct size was smaller in both of the treatment groups. However, at 4 days after infarction, mannitol-treated dogs had a mean infarct size that was 68 +/- 8% (+/- standard error of the mean) of the size of control infarcts (p less than 0.01) and methylprednisolone-treated dogs had a mean infarct size that was 77 +/- 6% of the size of control infarcts (p less than 0.01) (referenced to the initial perfusion defect). At 30 days, these differences were less substantial (though still significant), 88 +/- 4% and 85 +/- 5%, respectively. Pharmacologic interventions can be shown to alter the size of an acute myocardial infarction, particularly when examined over the time course of infarct healing.(ABSTRACT TRUNCATED AT 250 WORDS)

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