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The effect of adrenalectomy on the cardiac response to subacute fetal anemia. Can J Physiol Pharmacol 2011 Feb;89(2):79-88

Date

02/18/2011

Pubmed ID

21326338

Pubmed Central ID

PMC3097906

DOI

10.1139/y10-108

Scopus ID

2-s2.0-79953103129 (requires institutional sign-in at Scopus site)   9 Citations

Abstract

The mechanisms that stimulate fetal heart growth during anemia are unknown. To examine the hypothesis that adrenal hormones contribute to this process, we determined the effects of adrenalectomy (Adx) on heart growth and the activation of cardiac mitogen-activated protein kinases (MAPKs) in the presence and absence of fetal anemia. To identify mechanisms contributing to the initiation of cardiac growth, the duration of anemia was limited to a period shorter than that previously described to result in increased cardiac mass. Four groups of fetal sheep were studied (Adx-Anemic, Adx-Control, Intact-Anemic, Intact-Control). Anemia was created by daily controlled hemorrhage for 5 days; hearts were collected for analysis at 133 d gestation (term 145 d). Cardiomyocyte morphometry, immunohistochemistry for Ki-67 (proliferation marker), and Western blotting for protein levels of MAPKs and proliferating cell nuclear antigen (PCNA) were performed. Blood pressure, heart rate, heart weight-to-body weight ratio, and cardiomyocyte length and width remained similar among groups throughout the study. PCNA levels in the Adx-Anemic group were twice as high as in any other group (both ventricles, p < 0.05). Levels of phosphorylated extracellular signal-regulated kinase (ERK) were ~60% higher in the Intact-Anemic and Adx-Anemic groups, compared with the Intact-Control and Adx-Control groups (p < 0.02). These results suggest that adrenal hormones may attenuate fetal cardiomyocyte proliferation in response to anemia (as evidenced by the increased PCNA in Adx-Anemic fetuses) and that phosphorylation of myocardial ERK results from fetal anemia, irrespective of the status of the fetal adrenal gland.

Author List

Jonker SS, Scholz TD, Segar JL

Author

Jeffrey L. Segar MD Professor in the Pediatrics department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Adrenal Glands
Adrenalectomy
Anemia
Animals
Blood Pressure
Extracellular Signal-Regulated MAP Kinases
Female
Fetal Diseases
Heart
Heart Rate
Ki-67 Antigen
MAP Kinase Signaling System
Mitogen-Activated Protein Kinases
Myocytes, Cardiac
Phosphorylation
Pregnancy
Proliferating Cell Nuclear Antigen
Sheep