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Exogenous ghrelin suppresses cardiac sympathetic tone following acute myocardial infarct in rats
Author(s) -
Schwenke Daryl Owen,
Tokudome Takeshi,
Kishimoto Ichiro,
Cragg Patricia,
Kangawa Kenji
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.750.4
Subject(s) - ghrelin , medicine , myocardial infarction , cardiology , ligation , cardiac function curve , endocrinology , infarction , cardiac output , heart failure , saline , hormone , blood pressure
Acute myocardial infarction (MI) initiates an increase in cardiac sympathetic nerve activity (SNA), which exacerbates ventricular remodelling and cardiac dysfunction. Ghrelin, a growth hormone‐releasing peptide, is an effective treatment for improving cardiac function in chronic heart failure. Ghrelin may also have important therapeutic benefits during the early stages of MI, since studies have shown that ghrelin reduces sympathetic tone. In this study we hypothesised that ghrelin would prevent the increase in cardiac SNA that normally occurs following MI. Cardiac SNA was continuously recorded in urethane‐anaesthetized rats for five hours following ligation of the left anterior descending coronary artery. Rats received either saline or ghrelin (150 μg/kg, s.c.) one minute, or two hours, after infarction. SNA remained stable in sham rats. Myocardial infarction induced a maximal 110% increase in SNA, which was completely prevented in those rats that also immediately received an injection of ghrelin. When ghrelin was injected two hours after the MI (when SNA had increased by ∼85%), SNA significantly fell to pre‐MI activity. These results show that ghrelin acutely prevents the increase in cardiac SNA following MI. Further studies are now essential to determine whether this prophylactic benefit of ghrelin will aid in attenuating subsequent cardiac dysfunction. A Departmental Grant supported this research.