Mechanisms of bradycardia induced by digitalis substances

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Abstract
In cats anesthetized with chloralose-urethan, intravenous injection of acetylstrophanthidin, 18.7-56 [mu]g/kg, caused varying degrees of bradycardia and slight hypotension. These responses were markedly reduced after interruption of the blood supply to the nodose ganglia and/or section of the carotid sinus nerves. When the dose was reduced to 6-14 [mu]g/kg, intravenous injection induced no cardiovascular changes and intravertebral injection induced slight bradycardia, whereas intracarotid injection induced marked bradycardia and hypotension, appearing in two distinct phases. In the initial phase the responses appeared immediately after completion of the injection and were eliminated after sectioning of the carotid sinus nerve on the same side. In the late phase the responses appeared after an interval of 1-5 min. They were of greater magnitude and were eliminated when the blood supply to the nodose ganglion was interrupted. Vagotomy on the same side markedly reduced the bradycardic responses in both phases, but did not modify the hypotension. Injection of acetylstrophanthidin, 2-10 [mu]g, into the fourth ventricle induced moderate bradycardia. Responses to electrical stimulation of the peripheral end of the cut vagus nerve were markedly potentiated after intravenous injections of acetylstrophanthidin, 30 [mu]g/kg, or digoxigenin, 15 [mu]g/kg. The data suggest that these digitalis substances induced sinus bradycardia by acting predominantly on the receptors in the nodose ganglion and in the efferent vagal pathways and, to a lesser extent, on the carotid sinus receptors and the central vagal nucleus.