The effect of adrenalectomy on the cardiac response to subacute fetal anemia

Sonnet Jonker, Thomas D. Scholz, Jeffrey L. Segar

Research output: Contribution to journalArticle

7 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)79-88
Number of pages10
JournalCanadian Journal of Physiology and Pharmacology
Volume89
Issue number2
DOIs
StatePublished - Feb 2011
Externally publishedYes

Fingerprint

Adrenalectomy
Anemia
Proliferating Cell Nuclear Antigen
Cardiac Myocytes
Extracellular Signal-Regulated MAP Kinases
Mitogen-Activated Protein Kinases
Control Groups
Hormones
Fetal Heart
Adrenal Glands
Growth
Fetal Development
Sheep
Fetus
Heart Rate
Western Blotting
Immunohistochemistry
Body Weight
Phosphorylation
Hemorrhage

Keywords

  • Cardiomyocyte
  • Cortisol
  • Fetus
  • Heart
  • Hyperplasia
  • Mapk
  • Sheep

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)
  • Pharmacology

Cite this

The effect of adrenalectomy on the cardiac response to subacute fetal anemia. / Jonker, Sonnet; Scholz, Thomas D.; Segar, Jeffrey L.

In: Canadian Journal of Physiology and Pharmacology, Vol. 89, No. 2, 02.2011, p. 79-88.

Research output: Contribution to journalArticle

@article{9c5e8ef6a64f42198a5044723693f4b1,
title = "The effect of adrenalectomy on the cardiac response to subacute fetal anemia",
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.",
keywords = "Cardiomyocyte, Cortisol, Fetus, Heart, Hyperplasia, Mapk, Sheep",
author = "Sonnet Jonker and Scholz, {Thomas D.} and Segar, {Jeffrey L.}",
year = "2011",
month = "2",
doi = "10.1139/Y10-108",
language = "English (US)",
volume = "89",
pages = "79--88",
journal = "Canadian Journal of Physiology and Pharmacology",
issn = "0008-4212",
publisher = "National Research Council of Canada",
number = "2",

}

TY - JOUR

T1 - The effect of adrenalectomy on the cardiac response to subacute fetal anemia

AU - Jonker, Sonnet

AU - Scholz, Thomas D.

AU - Segar, Jeffrey L.

PY - 2011/2

Y1 - 2011/2

N2 - 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.

AB - 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.

KW - Cardiomyocyte

KW - Cortisol

KW - Fetus

KW - Heart

KW - Hyperplasia

KW - Mapk

KW - Sheep

UR - http://www.scopus.com/inward/record.url?scp=79953103129&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79953103129&partnerID=8YFLogxK

U2 - 10.1139/Y10-108

DO - 10.1139/Y10-108

M3 - Article

C2 - 21326338

AN - SCOPUS:79953103129

VL - 89

SP - 79

EP - 88

JO - Canadian Journal of Physiology and Pharmacology

JF - Canadian Journal of Physiology and Pharmacology

SN - 0008-4212

IS - 2

ER -