DEXAMETHASONE INDUCES A TRANSIENT RELATIVE CARDIOMEGALY IN NEONATAL RATS

Effects of s.c. administration of dexamethasone (1-25-mu-g/rat pup/d) during the first 5 d postpartum on survival rates, body weight, heart weight, heart-to-body weight ratios, and heart dimensions were determi ned. Dexamethasone decreased survival, body weight, and heart weight, but increased heart-to-body weight ratios and myocardial percentage of dry weight (0.44 to 0.52-1.06 and 20 to 23%, respectively; p < 0.05) by 7 d postpartum. By 21 d postpartum, differences in absolute body we ight and heart weight between control and experimental animals were re duced; however, myocardial percentage of dry weight and heart-to-body weight ratios were indistinguishable. Microscopic analysis of 7-d-old hearts disclosed that interventricular septum, left ventricular free w all thicknesses, and left ventricle chamber diameter were reduced (0.9 3 to 0.76-0.85 mm, 1.19-1.34 to 0.92-1.07 mm, and 1.35-1.40 to 0.89-1. 23 mm, respectively; p < 0.05), whereas right ventricular free wall th ickness was unaffected and right ventricle chamber diameter was increa sed (0.29-0.31 to 0.42-0.46 mm) by dexamethasone. Thus, dexamethasone reduced survival and retarded growth of neonatal rats. Retardation of heart growth was less severe, producing a transient relative cardiomeg aly characterized by 1) increased myocardial percentage of dry weight, 2) increased left ventricular free wall-to-chamber ratio, and 3) rete ntion of absolute right ventricular free wall thickness. This relative cardiomegaly appeared to be resolved by 21 d postpartum, as reflected in myocardial percentage of dry weight and heart-to-body weight ratio s. These data suggest that this system might be a useful model for elu cidating cellular and molecular mechanisms through which ventricular h ypertrophy might arise in infants receiving dexamethasone therapy for bronchopulmonary dysplasia.