Neuronally induced augmentation of cardiac output

OBJECTIVE: To determine whether cardiac output can be augmented by preferen tially activating cardiac adrenergic efferent neurons. DESIGN: Elicited cardiac output responses were compared when cardiac myocyt es were directly stimulated by a beta(1)-adrenoceptor agonist versus when t hey were indirectly influenced by beta(2)-adrenergic-sensitive cardiac effe rent neurons. ANIMALS AND METHODS: The beta(1)-adrenoceptor agonist dobutamine or the sel ective beta(2)-adrenoceptor agonist terbutaline was continuously infused in dividually into the systemic circulation of 15 anesthetized pigs for 20 min s in 5 and 15 mu g/kg/min doses. Heart race, left atrial chamber pressure, regional left ventricular intramyocardial systolic pressure, left ventricul ar chamber pressure and aortic pressure were monitored. Cardiac output was determined via the thermodilution technique before and at 10 min intervals during drug infusions. Ventricular tissues were removed thereafter and imme diately frozen in liquid nitrogen for subsequent cardiac myocyte cell surfa ce beta-adrenoceptor analysis. MAIN RESULTS: Both doses of terbutaline increased heart rate (approximately +18%) and cardiac output (approximately +20%). Heart rate (+12%) and cardi ac output (+16%) increased when the high dose of dobutamine was tested. Lef t ventricular intramyocardial systolic pressure was increased by dobutamine (+15%) but not by terbutaline. Porcine ventricular cardiac myocytes primar ily possess cell surface beta(1)-, rather than beta(2)-, adrenoceptors, mak ing it unlikely that cardiac myocytes were directly affected by the doses o f terbutaline tested. CONCLUSIONS: Beta(2)-adrenoceptor agonists enhance cardiac output primarily as a result of neuronally induced increases in heart rate in the porcine m odel. Adrenergic efferent neuronal enhancement of heart rate may be an effe ctive way to increase cardiac output independently of directly augmented ve ntricular dynamics. Further study is required to determine whether the dise ased myocardium can be supported by such neurocardiological means.