Electrophysiological Effects of α‐Adrenergic Stimulation

Publisher Website
Google Scholar
Abstract
Autonomic blockade for in vivo electrophysiological studies generally involves atropine and beta blockers, ignoring the potential role of α‐adrenergic activity, To evaluate the importance, if any, of α‐adrenergic tone, the electrophysiological effects of incremental doses of phenylephrine were examined in eight chloralose‐anesthetized dogs. In order to study direct effects, all dogs were both beta blocked (with nadolol) and vagally blocked (with the combination of vagotomy and atropine). Results were also obtained after normalization of Wood pressure with nitroprusside or the α‐blocker, prazosin, Phenylephrine caused dose‐dependent increases in systolic and diustolic Wood pressure. This was accompanied by consistent but modest decreases in sinus cycle length (control RR interval 492 ± 34 msec vs 459 ± 29 msec after dose 1 of phenylephrine, P < 0.05, 516 ± 41 vs 484 ± 34 msec control versus dose 2. P < 0.05). These increases in automaticity were not prevented after normalization of arterial pressure by nitroprusside, but were reversed when concomitant α‐recepfor blockade was achieved with prazosin, suggesting that sinus node acceleration resulted directly from α‐receptor stimulation. No effects on atrial, AV nodal or His‐Purkinje conduction were noted. In addition, phenylephrine did not affect atrial, AV nodal, or ventricular refractoriness. In conclusion, conduction and refractoriness of normal cardiac tissue (other than the sinus node) are unaffected by direct α‐receptor stimulation. This justifies the use of combined beta and muscarinic blockers to achieve autonomic blockade under most circumstances.