Effect of hypoxia on the sinoatrial node, atrium, and atrioventricular node in the rabbit heart.
We used intracellular microelectrodes to study the effects of hypoxia on the isolated, superfused sinoatrial (SA) node, atrium, and atrioventricular (AV) node of the rabbit heart. Hypoxia decreased the rate of spontaneous impulse initiation in SA nodal fibers by decreasing the slope of diastolic depolarization. With gradually decreasing Po2, the sinus rate was reduced; concomitantly, the corrected sinus node recovery time after rapid atrial stimulation was much less affected demonstrating marked prolongation only under severe anoxic conditions. Hypoxia decreased the amplitude of action potentials of the SA node and of the AV node but not of the atrium. SA and AV nodal conduction were slowed by hypoxia; intraatrial conduction was not significantly affected. AV nodal conduction block occurred at lower atrial rates, and the effective refractory period of the AV node was prolonged. Inhomogeneity of SA and AV nodal impulse propagation often was observed in the presence of hypoxia. This was associated with concealed reentry within both nodal areas. The extracellular K+ concentration of the atrial tissue was measured with ion-sensitive microelectrodes. [K+]o remained unchanged even after prolonged periods of severe hypoxia. These results are consistent with the hypothesis that acute hypoxia predominantly inhibits slow response activity but has only little effect on the fast inward sodium current.
D000200:Action Potentials; D000818:Animals; D001283:Atrioventricular Node / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial; D004562:Electrocardiography; D006325:Heart Atria; D006329:Heart Conduction System / Q000503:physiopathology*; D000860:Hypoxia / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D011817:Rabbits; D012849:Sinoatrial Node / Q000503:physiopathology*
D011188:Potassium