Acute myocardial infarction induces bilateral stellate ganglia neural remodeling in rabbits

Bich Lien Nguyen, Hongmei Li, Michael C. Fishbein, Shien-Fong Lin, Carlo Gaudio, Peng-Sheng Chen, Lan Chen

Research output: Contribution to journalArticle

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Abstract

Introduction: Myocardial infarction (MI) results in cardiac nerve sprouting in the myocardium. Whether or not similar neural remodeling occurs in the stellate ganglia (SGs) is unknown. We aimed to test the hypothesis that MI induces bilateral SG nerve sprouting. Methods: Acute MI was created by coronary artery ligation in rabbits (n=12). Serum nerve growth factor (NGF) level was measured by enzyme-linked immunosorbent assay. The hearts and bilateral SGs were harvested for immunohistochemistry after 1 week in six rabbits and after 1 month in six rabbits. Immunostaining for tyrosine hydroxylase (TH), growth-associated protein 43 (GAP43), choline acetyltransferase (ChAT), and synaptophysin (SYN) was performed to determine the magnitude of nerve sprouting. Tissues from six normal rabbits were used as controls. Nerve density was determined by computerized morphometry. Results: Myocardial infarction results in increased serum NGF levels at 1 week (1519.8±632.2 ng/ml) that persist up to 1 month (1361.2±176.3 ng/ml) as compared to controls (89.6±34.9 ng/ml) (P=.0002 and P=.0001, respectively). Immunostaining demonstrated nerve sprouting and hyperinnervation in both SGs after MI. The nerve densities (μm 2/ganglion cell) in SG 1 week after MI and 1 month after MI and those in control groups, respectively, were as follows: GAP43: 278±96, 225±39, and 149±57 (P=.01); SYN: 244±152, 268±115, and 102±60 (P=.02); TH: 233±71, 180±50, and 135±68 (P=.047); ChAT: 244±100, 208±46, and 130±41 μm 2/cell (P=.01). Conclusions: Myocardial infarction increases serum NGF levels and induces nerve sprouting and hyperinnervation in bilateral SGs for at least 1 month after MI. The hyperinnervation includes both adrenergic axons and cholinergic axons in the SG.

Original languageEnglish
Pages (from-to)143-148
Number of pages6
JournalCardiovascular Pathology
Volume21
Issue number3
DOIs
StatePublished - May 2012

Fingerprint

Stellate Ganglion
Myocardial Infarction
Rabbits
Nerve Growth Factor
GAP-43 Protein
Synaptophysin
Choline O-Acetyltransferase
Tyrosine 3-Monooxygenase
Axons
Serum
Ganglia
Adrenergic Agents
Cholinergic Agents
Ligation
Coronary Vessels
Myocardium
Enzyme-Linked Immunosorbent Assay
Immunohistochemistry
Control Groups

Keywords

  • Autonomic nervous system
  • Myocardial infarction
  • Nerve sprouting
  • Stellate ganglion
  • Sudden cardiac death
  • Ventricular arrhythmia

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pathology and Forensic Medicine

Cite this

Acute myocardial infarction induces bilateral stellate ganglia neural remodeling in rabbits. / Nguyen, Bich Lien; Li, Hongmei; Fishbein, Michael C.; Lin, Shien-Fong; Gaudio, Carlo; Chen, Peng-Sheng; Chen, Lan.

In: Cardiovascular Pathology, Vol. 21, No. 3, 05.2012, p. 143-148.

Research output: Contribution to journalArticle

Nguyen, Bich Lien ; Li, Hongmei ; Fishbein, Michael C. ; Lin, Shien-Fong ; Gaudio, Carlo ; Chen, Peng-Sheng ; Chen, Lan. / Acute myocardial infarction induces bilateral stellate ganglia neural remodeling in rabbits. In: Cardiovascular Pathology. 2012 ; Vol. 21, No. 3. pp. 143-148.
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abstract = "Introduction: Myocardial infarction (MI) results in cardiac nerve sprouting in the myocardium. Whether or not similar neural remodeling occurs in the stellate ganglia (SGs) is unknown. We aimed to test the hypothesis that MI induces bilateral SG nerve sprouting. Methods: Acute MI was created by coronary artery ligation in rabbits (n=12). Serum nerve growth factor (NGF) level was measured by enzyme-linked immunosorbent assay. The hearts and bilateral SGs were harvested for immunohistochemistry after 1 week in six rabbits and after 1 month in six rabbits. Immunostaining for tyrosine hydroxylase (TH), growth-associated protein 43 (GAP43), choline acetyltransferase (ChAT), and synaptophysin (SYN) was performed to determine the magnitude of nerve sprouting. Tissues from six normal rabbits were used as controls. Nerve density was determined by computerized morphometry. Results: Myocardial infarction results in increased serum NGF levels at 1 week (1519.8±632.2 ng/ml) that persist up to 1 month (1361.2±176.3 ng/ml) as compared to controls (89.6±34.9 ng/ml) (P=.0002 and P=.0001, respectively). Immunostaining demonstrated nerve sprouting and hyperinnervation in both SGs after MI. The nerve densities (μm 2/ganglion cell) in SG 1 week after MI and 1 month after MI and those in control groups, respectively, were as follows: GAP43: 278±96, 225±39, and 149±57 (P=.01); SYN: 244±152, 268±115, and 102±60 (P=.02); TH: 233±71, 180±50, and 135±68 (P=.047); ChAT: 244±100, 208±46, and 130±41 μm 2/cell (P=.01). Conclusions: Myocardial infarction increases serum NGF levels and induces nerve sprouting and hyperinnervation in bilateral SGs for at least 1 month after MI. The hyperinnervation includes both adrenergic axons and cholinergic axons in the SG.",
keywords = "Autonomic nervous system, Myocardial infarction, Nerve sprouting, Stellate ganglion, Sudden cardiac death, Ventricular arrhythmia",
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T1 - Acute myocardial infarction induces bilateral stellate ganglia neural remodeling in rabbits

AU - Nguyen, Bich Lien

AU - Li, Hongmei

AU - Fishbein, Michael C.

AU - Lin, Shien-Fong

AU - Gaudio, Carlo

AU - Chen, Peng-Sheng

AU - Chen, Lan

PY - 2012/5

Y1 - 2012/5

N2 - Introduction: Myocardial infarction (MI) results in cardiac nerve sprouting in the myocardium. Whether or not similar neural remodeling occurs in the stellate ganglia (SGs) is unknown. We aimed to test the hypothesis that MI induces bilateral SG nerve sprouting. Methods: Acute MI was created by coronary artery ligation in rabbits (n=12). Serum nerve growth factor (NGF) level was measured by enzyme-linked immunosorbent assay. The hearts and bilateral SGs were harvested for immunohistochemistry after 1 week in six rabbits and after 1 month in six rabbits. Immunostaining for tyrosine hydroxylase (TH), growth-associated protein 43 (GAP43), choline acetyltransferase (ChAT), and synaptophysin (SYN) was performed to determine the magnitude of nerve sprouting. Tissues from six normal rabbits were used as controls. Nerve density was determined by computerized morphometry. Results: Myocardial infarction results in increased serum NGF levels at 1 week (1519.8±632.2 ng/ml) that persist up to 1 month (1361.2±176.3 ng/ml) as compared to controls (89.6±34.9 ng/ml) (P=.0002 and P=.0001, respectively). Immunostaining demonstrated nerve sprouting and hyperinnervation in both SGs after MI. The nerve densities (μm 2/ganglion cell) in SG 1 week after MI and 1 month after MI and those in control groups, respectively, were as follows: GAP43: 278±96, 225±39, and 149±57 (P=.01); SYN: 244±152, 268±115, and 102±60 (P=.02); TH: 233±71, 180±50, and 135±68 (P=.047); ChAT: 244±100, 208±46, and 130±41 μm 2/cell (P=.01). Conclusions: Myocardial infarction increases serum NGF levels and induces nerve sprouting and hyperinnervation in bilateral SGs for at least 1 month after MI. The hyperinnervation includes both adrenergic axons and cholinergic axons in the SG.

AB - Introduction: Myocardial infarction (MI) results in cardiac nerve sprouting in the myocardium. Whether or not similar neural remodeling occurs in the stellate ganglia (SGs) is unknown. We aimed to test the hypothesis that MI induces bilateral SG nerve sprouting. Methods: Acute MI was created by coronary artery ligation in rabbits (n=12). Serum nerve growth factor (NGF) level was measured by enzyme-linked immunosorbent assay. The hearts and bilateral SGs were harvested for immunohistochemistry after 1 week in six rabbits and after 1 month in six rabbits. Immunostaining for tyrosine hydroxylase (TH), growth-associated protein 43 (GAP43), choline acetyltransferase (ChAT), and synaptophysin (SYN) was performed to determine the magnitude of nerve sprouting. Tissues from six normal rabbits were used as controls. Nerve density was determined by computerized morphometry. Results: Myocardial infarction results in increased serum NGF levels at 1 week (1519.8±632.2 ng/ml) that persist up to 1 month (1361.2±176.3 ng/ml) as compared to controls (89.6±34.9 ng/ml) (P=.0002 and P=.0001, respectively). Immunostaining demonstrated nerve sprouting and hyperinnervation in both SGs after MI. The nerve densities (μm 2/ganglion cell) in SG 1 week after MI and 1 month after MI and those in control groups, respectively, were as follows: GAP43: 278±96, 225±39, and 149±57 (P=.01); SYN: 244±152, 268±115, and 102±60 (P=.02); TH: 233±71, 180±50, and 135±68 (P=.047); ChAT: 244±100, 208±46, and 130±41 μm 2/cell (P=.01). Conclusions: Myocardial infarction increases serum NGF levels and induces nerve sprouting and hyperinnervation in bilateral SGs for at least 1 month after MI. The hyperinnervation includes both adrenergic axons and cholinergic axons in the SG.

KW - Autonomic nervous system

KW - Myocardial infarction

KW - Nerve sprouting

KW - Stellate ganglion

KW - Sudden cardiac death

KW - Ventricular arrhythmia

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