Abstract

Cardiac enlargement that develops during pregnancy is an important yet under‐studied adaptation to physiologic stress. In light of recent evidence of resident stem cell pools in the heart, we tested the hypothesis that pregnancy‐induced cardiac enlargement may involve both myocyte hypertrophy and new myocyte formation. 6 nonpregenant age matched controls (C) and 6 mice in late pregnancy (LP, 17–19 days) were studied. Hearts were formalin fixed and 5μ sections were examined. Laminin staining was used to identify cell perimeter and determine myocyte cross‐sectional area (MCSA). Wet weights of LP hearts were 23% greater than C (240±9 vs 195±13mg). Increases in MCSA were not proportional to increases in heart mass. MCSA of LP (262±3μ2, n=225) was 11% greater than of C (236± 3μ2, n=225). Analysis of sections from different regions of the heart showed different degrees of MCSA hypertrophy. Apex, mid and basal sections were analyzed from all hearts. No difference in MCSA among sections was found in C. MCSA of all sections were greater in LP than C, but MCSA of the mid‐heart in LP (275 ±4μ2, n=75) were greater than MCSA of apex (252± 5μ2, n=75) and base (259 ±4μ2, n=75). Myocyte hypertrophy during pregnancy is not sufficient to account for the whole‐heart enlargement suggesting that new myocytes are generated during pregnancy. Hypertrophy is not evenly distributed during pregnancy suggesting an unequal distribution of wall stress.

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