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R S Stevenson

Publications and source records attributed to R S Stevenson.

4 recordsLinked to original sources
PubMed2000

The heart reinnervates after transplantation.

BACKGROUND: Whether cardiac reinnervation occurs after transplantation remains controversial. If reinnervation does occur, how sympathetic and parasympathetic efferent neurons do this remains unknown. METHODS: Power spectral analysis of heart rate variability was assessed for 1 year after cardiac autotransplantation in 9 dogs. After induction of anesthesia 13 months after transplantation, cardiac and intrinsic cardiac neuronal responses elicited by both electrical stimulation of parasympathetic or sympathetic efferent neurons and systemic or local coronary artery administration of nicotine (5 microg/kg), angiotensin II (0.75 microg/kg), and tyramine (1.2 microg/kg) were studied. The transmembrane electrical properties of intrinsic cardiac neurons were studied in vitro. Ventricular tissue catecholamine content, alpha-tubulin expression, and beta-adrenergic receptor density and affinity were studied. The presence of axons crossing suture lines was sought histologically. RESULTS: Nerves were identified crossing suture lines. Electrical or chemical (ie, nicotine or angiotensin II) activation of sympathetic efferent neurons enhanced cardiodynamics, as did tyramine. Stimulating vagal efferent preganglionic axons induced bradycardia in half of the dogs. Functional reinnervation did not correlate with specific power spectra derived from rate variability in the conscious state. Responding to nicotine and angiotensin II in situ, transplanted intrinsic cardiac neurons generated spontaneous activity. These neurons displayed nicotine-dependent synaptic inputs in vitro. Ventricular tissue had normal beta-adrenergic receptor affinity and density but reduced catecholamine and alpha-tubulin contents. CONCLUSIONS: The intrinsic cardiac nervous system receives reduced input from extracardiac sympathetic efferent neurons after transplantation and inconsistent input from parasympathetic efferent preganglionic neurons. These heterogeneous neuronal inputs are not reflected in heart rate variability or ventricular beta-adrenergic receptor function. Transplanted angiotensin II-sensitive intrinsic cardiac neurons exert greater cardiac control than do nicotine-sensitive ones. The intrinsic cardiac nervous system remodels itself after cardiac transplantation, and this indicates that direct assessment of extracardiac and intrinsic cardiac neuronal behavior is required to fully understand cardiac control after transplantation.

Animals↗
PubMed1999

Neuronally induced augmentation of cardiac output.

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.

Adrenergic beta-Agonists↗