The mechanism of adrenergic effects on ventricular vulnerability, appearing in the form of a decrease in the ventricular fibrillation threshold, reduction of the electrical diastolic threshold, shortening of the refractory period as well as an increased asynchrony of recovery of excitability, was analysed in dogs under chloralose-urethane anesthesia. All these alterations of the electrophysiological parameters of the heart seem to be closely related to stimulation of the adrenergic beta receptors; this was shown by the fact that the selective beta receptor blocking agent 1-INPEA which is without any notable quinidine-like action effectively prevented these changes whereas the alpha-receptor blocking agent phenoxybenzamine did not. This was so irrespective of whether ventricular vulnerability was increased by direct stimulation of the cardiac sympathetic nerve (stellate ganglia) or by reflex sympathetic stimulation (by means of temporary bilateral carotid occlusion) or by infusions of adrenaline or noradrenaline.
- Asynchrony of recovery of excitability
- Carotid occlusion
- Ganglion stellate stimulation
- Ventricular refractoriness
- Ventricular vulnerability
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