BACKGROUND: The purpose of this study was to investigate the effectiveness of atrial natriuretic peptide on ischemic myocardium through the induction of heat-shock protein 72. METHODS: 30 isolated rabbit hearts perfused on isolated heart apparatus were randomly assigned to receive either warm Krebs-Henseleit solution with 1 µmol L(-1) atrial natriuretic peptide (n = 15) or warm Krebs-Henseleit solution without atrial natriuretic peptide (n = 15) in preischemic, ischemic, and postischemic conditions. In all rabbit hearts, global ischemia was produced by clamping the aortic and atrial inflow lines. Concentrations of atrial natriuretic peptide were measured in hearts with left ventricular dysfunction following ischemia, and correlated with the hypertrophic growth sustained by overexpression of heat-shock protein 72 microRNA-133. RESULTS: The levels of atrial natriuretic peptide were markedly higher in the group that received atrial natriuretic peptide, and strongly correlated with both band lengths of heat-shock protein 72 and overexpression of microRNA-133 in the hypertrophic myocyte. CONCLUSIONS: Perfusion levels of atrial natriuretic peptide induce increased expression of heat-shock protein 72 microRNA-133 in dysfunctional left ventricle.
BACKGROUND: The purpose of this study was to investigate the effectiveness of atrial natriuretic peptide on ischemic myocardium through the induction of heat-shock protein 72. METHODS: 30 isolated rabbit hearts perfused on isolated heart apparatus were randomly assigned to receive either warm Krebs-Henseleit solution with 1 µmol L(-1) atrial natriuretic peptide (n = 15) or warm Krebs-Henseleit solution without atrial natriuretic peptide (n = 15) in preischemic, ischemic, and postischemic conditions. In all rabbit hearts, global ischemia was produced by clamping the aortic and atrial inflow lines. Concentrations of atrial natriuretic peptide were measured in hearts with left ventricular dysfunction following ischemia, and correlated with the hypertrophic growth sustained by overexpression of heat-shock protein 72 microRNA-133. RESULTS: The levels of atrial natriuretic peptide were markedly higher in the group that received atrial natriuretic peptide, and strongly correlated with both band lengths of heat-shock protein 72 and overexpression of microRNA-133 in the hypertrophic myocyte. CONCLUSIONS: Perfusion levels of atrial natriuretic peptide induce increased expression of heat-shock protein 72 microRNA-133 in dysfunctional left ventricle.