Abstract
This study was undertaken to more fully examine the characteristics of vagally induced tachycardia (VIT). Anesthetized dogs were prepared for electrical stimulation of the right vagosympathetic trunk and the right ansa subclavia. After atropine, vagosympathetic trunk stimulation elicited a 41±7% increase in heart rate. This response was characterized by a short latency and long recovery time. Ansa subclavia Stimulation elicited a 61±5% increase in heart rate and was characterized by a short latency and a short recovery time. The VIT consists of a ‘fast’ component accounting for the short latency and a ‘slow’ component accounting for the prolonged recovery time. Practolol virtually eliminated the ansa subclavia response and the ‘fast’ component of VIT. The ‘slow’ component of VIT persisted but with a long latency. It was concluded that vagal cardioaccelerator pathways may not depend on activation of β-adrenergic receptors.
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