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Heart Research Center (G.D.G., S.L., S.J., J.S., K.L.T.) and Departments of Medicine (Cardiovascular Medicine) (G.D.G., K.L.T.), Physiology and Pharmacology (G.D.G., S.J., K.L.T.), and Surgery (Cardiothoracic) (J.S.), Oregon Health & Science University, and Portland Veterans Affairs Medical Center (G.D.G.), Portland, Oregon 97239-3098
Address all correspondence and requests for reprints to: Kent L. Thornburg, Heart Research Center, L464, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97239-3098. E-mail: thornbur{at}ohsu.edu.
The role of cortisol in regulating cardiac myocyte growth in the near-term fetal sheep is unknown. We hypothesized that cortisol would suppress cardiomyocyte proliferation and stimulate cardiomyocyte binucleation and enlargement, signs of terminal differentiation. Cardiomyocyte dimensions and percent binucleation were determined in isolated cardiac myocytes from seven cortisol-treated and seven control fetuses; percentage of myocytes positive for Ki-67 was determined in an additional four cortisol-treated and four control hearts. Cortisol was infused into the circumflex coronary artery at subpressor rates (0.5 µg/kg·min, 7 d). Cortisol infusion had no hemodynamic effects, compared with controls or pretreatment conditions. Cortisol treatment increased heart weight (44.0 ± 8.7 g vs. control, 34.9 ± 9.1 g, P < 0.05). Heart to body weight ratio was greater in treated hearts, compared with controls (10.3 ± 1.9 vs. 7.7 ± 0.9 g/kg, P < 0.01). Ventricular myocyte length, width, and percent binucleation were not different between groups. The proportion of treated myocytes in the cell cycle staining for Ki-67 was higher in the left ventricle (5.5 ± 0.1 vs. 2.7 ± 0.4%, P < 0.005) and right ventricle (4.4 ± 0.4 vs. 3.7 ± 0.7%, P < 0.05), compared with controls. Wet weight to dry weight ratios from cortisol-treated and control hearts were not different. In conclusion, whereas cortisol infused into the fetal sheep heart has no effect on cardiomyocyte size or maturational state, it stimulates entry of cardiomyocytes in the cell cycle. Thus, increases in fetal heart mass associated with subpressor doses of cortisol are due to cardiomyocyte proliferation and not hypertrophic growth.
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