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1 Pediatrics (Neonatology), University of Iowa, Iowa City, Iowa, United States
2 Heart Research Center, OHSU, Portland, Oregon, United States; Physiology and Pharmacology, OHSU, Portland, Oregon, United States
3 Heart Research Center, OHSU, Portland, Oregon, United States; Physiology and Pharmacology, OHSU, Portland, Oregon, United States; Cardiovascular Medicine (School of Medicine), OHSU, Portland, Oregon, United States
4 Heart Research Center, Oregon Health Sciences University, Portland, Oregon, United States
5 Heart Research Center, OHSU, Portland, Oregon, United States; Physiology and Pharmacology, OHSU, Portland, Oregon, United States; Cardiovascular Medicine (School of Medicine), OHSU, Portland, Oregon, United States; Portland VA Medical Center, Portland, Oregon, United States
* To whom correspondence should be addressed. E-mail: ssj{at}efn.org.
While the fetal heart grows by myocyte enlargement and proliferation, myocytes lose their capacity for proliferation in the perinatal period after terminal differentiation. The relationship between myocyte enlargement, proliferation and terminal differentiation has not been studied under conditions of combined arterial and venous hypertension, as occurs in some clinical conditions. HYPOTHESIS: Fetal arterial and venous hypertension initially leads to cardiomyocyte proliferation, followed by myocyte enlargement. METHODS: Two groups of fetal sheep received intravascular plasma infusions for 4 or 8 days (from 130 days gestation) to increase vascular pressures. Fetal hearts were arrested in diastole and dissociated. Myocyte size, terminal differentiation (%binucleation), and cell cycle activity (Ki-67[+] cells as a percent of mononucleated myocytes) were measured. RESULTS: Chronic plasma infusion greatly increased venous and arterial pressures. Heart (but not body) weights were ~30% greater in hypertensive fetuses than controls. The incidence of cell cycle activity doubled in hypertensive fetuses compared to controls. After 4 days of hypertension, myocytes were (~11%) longer, but only after 8 days were they wider (~12%). After 8 days, %binucleation was ~50% greater in hypertensive fetuses. CONCLUSIONS: We observed two phases of cardiomyocyte growth and maturation in response to fetal arterial and venous hypertension. In the early phase, the incidence of cell cycle activity increased and myocytes elongated. In the later phase, the incidence of cell cycle activity remained elevated, %binucleation increased and cross-sections were greater. This study highlights unique fetal adaptations of the myocardium, and the importance of experimental duration when interpreting fetal cardiac growth data.
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