Neuronally induced augmentation of cardiac output.

Article Details

Citation

Copy to clipboard

Stevenson RS, Thompson GW, Wilkinson M, Murphy DA, Armour JA

Neuronally induced augmentation of cardiac output.

Can J Cardiol. 1999 Dec;15(12):1361-6.

PubMed ID

10620742 [ View in PubMed

]

Abstract

OBJECTIVE: To determine whether cardiac output can be augmented by preferentially activating cardiac adrenergic efferent neurons. DESIGN: Elicited cardiac output responses were compared when cardiac myocytes were directly stimulated by a beta1-adrenoceptor agonist versus when they were indirectly influenced by beta2- adrenergic-sensitive cardiac efferent neurons. ANIMALS AND METHODS: The beta1-adrenoceptor agonist dobutamine or the selective beta2-adrenoceptor agonist terbutaline was continuously infused individually into the systemic circulation of 15 anesthetized pigs for 20 mins in 5 and 15 microgram/kg/min doses. Heart rate, left atrial chamber pressure, regional left ventricular intramyocardial systolic pressure, left ventricular 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 immediately frozen in liquid nitrogen for subsequent cardiac myocyte cell surface beta-adrenoceptor analysis. MAIN RESULTS: Both doses of terbutaline increased heart rate (approximately +18%) and cardiac output (approximately +20%). Heart rate (+12%) and cardiac output (+16%) increased when the high dose of dobutamine was tested. Left ventricular intramyocardial systolic pressure was increased by dobutamine (+15%) but not by terbutaline. Porcine ventricular cardiac myocytes primarily possess cell surface beta1-, rather than beta2-, adrenoceptors, making it unlikely that cardiac myocytes were directly affected by the doses of terbutaline tested. CONCLUSIONS: Beta2-adrenoceptor agonists enhance cardiac output primarily as a result of neuronally induced increases in heart rate in the porcine model. Adrenergic efferent neuronal enhancement of heart rate may be an effective way to increase cardiac output independently of directly augmented ventricular dynamics. Further study is required to determine whether the diseased myocardium can be supported by such neurocardiological means.

DrugBank Data that Cites this Article

Drug Targets

Drug	Target	Kind	Organism	Pharmacological Action	Actions
Terbutaline	Beta-2 adrenergic receptor	Protein	Humans	Yes	Agonist	Details