Autoregulation of cardiac cycle length: role of catecholamines

The mechanism of autoregulation of cardiac cycle length during phasic alterations in perfusion via the sinus node artery is unclear. Inasmuch as transient catecholamine release has been documented during sinus node artery injections, we sought to determine whether autoregulation of cycle length might be related to a beta receptor-mediated process. We used chloralose-anesthetized mongrel dogs. A right thoracotomy was performed, the vagi and sympathetic inputs to the heart were cut and electrograms were recorded from the sinoatrial (SA) node, right atrium, right ventricle and His bundle. The SA node artery was catheterized and distribution verified. Perfusion of normal Tyrode's solution via the SA node artery at 3 ml/min resulted in significant cycle length slowing which was maximal immediately after onset of perfusion. Plots of the derivative of cycle length with respect to time indicated either a monophasic or biphasic pattern of response. Administration of propranolol (2 mg/kg i.v.) resulted in a significant prolongation of control cycle length. Perfusion of normal Tyrode's solution after propranolol resulted in significantly greater degrees of cycle length prolongation (as judged by integration of area under cycle length curves) as well as only monophasic response patterns. These results suggest that infusions of normal Tyrode's solution, via the SA node artery, at physiologic flow rates are accompanied by concurrent catecholamine release throughout the infusion. This catecholamine release may contribute to the homeostatic regulation of cardiac cycle length.