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(Circulation Research. 2007;100:1363.)
© 2007 American Heart Association, Inc.

Integrative Physiology

Increased Ventricular Preload Is Compensated by Myocyte Proliferation in Normal and Hypoplastic Fetal Chick Left Ventricle

Angela deAlmeida, Tim McQuinn, David Sedmera

From the Department of Cell Biology and Anatomy (A.dA., T.M., D.S.); Pediatric Cardiology (T.M.), Medical University of South Carolina, Charleston; Institute of Anatomy (D.S.), First Faculty of Medicine, Charles University, Prague, Czech Republic; and Institute of Animal Physiology and Genetics (D.S.), Academy of Sciences of the Czech Republic, Prague.

Correspondence to David Sedmera, Laboratory of Cardiovascular Morphogenesis, Institute of Animal Physiology and Genetics, Videnska 1083, 142 20 Prague 4-Krc, Czech Republic. E-mail sedmera{at}iapg.cas.cz

Hemodynamics influence cardiac development, and alterations in blood flow may lead to impaired cardiac growth and malformations. The developing myocardium adapts to augmented workload by increasing cell number (hyperplasia). The aim of this study was to determine the influence of alterations in ventricular preload on fetal myocyte proliferation by manipulation of intracardiac shunting at the atrial level. We hypothesized that partial clipping of the right atrial appendage would increase the blood flow to the left ventricle and, in turn, lead to an increase in chamber volume and myocardial mass based on myocyte proliferation. Using an ex ovo culture setup, we performed partial right atrial clipping on embryonic day 8 chick embryos. Ultrasound imaging was performed before and after the surgery to assess the changes in left ventricular volume. Sampling after 24 hours was preceded by 2 hour of pulse-labeling with 5-bromodeoxyuridine. Ultrasound imaging showed that partial right atrial clipping led to a significant increase in left ventricular end-diastolic volume, demonstrating increased blood flow and preload. Anti–5-bromodeoxyuridine immunolabeling revealed a significant increase in myocyte proliferation in the left ventricle and atrium. No significant changes were found in the right heart structures. Increased left ventricular myocyte proliferation and myocardial mass after right atrial clipping was also observed in embryos with experimental left ventricular hypoplasia. These results demonstrate the ability of fetal myocardium to respond to increased preload by myocyte hyperplasia and support the rationale for prenatal surgical interventions in certain cases of congenital heart disease such as hypoplastic left heart syndrome.

Key Words: chick embryo • hemodynamics • fetal surgery • hypoplastic left heart syndrome

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Hypoplastic Left Heart Syndrome: New Insights

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