Modification of the baroreceptor control of atrio-ventricular conduction induced by digitalis in man

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Abstract
Several studies in animals and in man have suggested that the inhibitory influence of baroreceptors on heart rate and peripheral circulation is enhanced by digitalis. Because the atrio-ventricular node represents a key site for the clinical action of digitalis we studied how baroreceptor control of atrio-ventricular conduction is modified by digitalis at therapeutical doses. In eight subjects heart rate was kept constant by atrial pacing to assess neural influences on atrio-ventricular conduction rate without the modifications caused by simultaneous changes in cardiac cycle length. Arterial baroreceptors were stimulated by increasing or reducing blood pressure (intra-arterial recording), via an iv bolus of phenylephrine or nitroglycerine. The baroreflex sensitivity was assessed in ms·mmHg−1 as the slope of the linear regressions relating the rise or fall in systolic blood pressure to the lengthening or shortening in St- (atrial stimulus artifact) Q interval (ECG recording). The study was performed before and 45 min after iv administration of digitalis (0.8 mg of Lanatoside C®). Baroreflex sensitivity during baroreceptor stimulation was 2.9±1.1 ms·mmHg−1(mean ±SE) before digitalis, whereas after digitalis a significantly and markedly greater value of 5.6±1.5 ms·mmHg−1 was found. Baroreflex sensitivity during baroreceptor deactivation was 0.9±0.1 ms·mmHg−1 before digitalis, and was not significantly affected by the drug. Thus in man the baroreceptor control of atrio-ventricular conduction is strikingly potentiated by digitalis although this potentiation is only evident in the upper portion of the stimulus-response curve of the reflex. This phenomenon may be one of the mechanisms that account for the beneficial slowing in atrioventricular conduction rate that is produced by digitalis in several clinical conditions.