Pressure-Induced Cardiac Enlargement in Neonatal and Adult Rats Left Ventricular Functional Characteristics and Evidence of Cardiac Muscle Cell Proliferation in the Neonate

Pressure-induced cardiac enlargement was created in neonatal (21 days of age) and adult (250-275 g) rats by abdominal aortic constriction. Sham-operated and aorta-constricted neonates were studied 2, 3, 4, and 5 weeks after surgery. Left ventricular weight was elevated by approximately 50% at all times studied. Radioautography demonstrated a marked elevation in H-thymidine-labeled nuclei in cardiac muscle and nonmusde cells in aortaconstricted neonates. Other experiments examined the functional characteristics of hearts subjected to pressure overload while in either the neonatal or the adult state. Five weeks after surgery, left ventricular pressure and left ventricular weight were elevated to nearly identical degrees in both groups of experimental rat*. Under control conditions, heart rate and the maximum rate of left ventricular pressure development were not altered significantly in either neonatal or adult rats with aortic constriction. Aortic peak flow velocity, cardiac index, and stroke index also were within normal limits in neonates with aortic constriction; however, these measurements were reduced significantly in adults with aortic constriction. Stroke volume augmentation in response to saline infusion and inotropic responsiveness to isoproterenol were unaltered in aorta-constricted neonates but were markedly attenuated in aorta-constricted adults. The maintenance of normal heart functional characteristics represents a major point of distinction between pressure-induced cardiac enlargement in neonatal and aduh rats which correlates with the presence or absence of cardiac muscle ceD proliferation during adaptive heart growth.