Senges J, Mizutani T, Pelzer D, Brachmann J, Sonnhof U, Kübler W
Circ Res. 1979 Jun;44(6):856-63. doi: 10.1161/01.res.44.6.856.
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.
我们使用细胞内微电极研究缺氧对兔心脏离体、灌流的窦房（SA）结、心房和房室（AV）结的影响。缺氧通过降低舒张期去极化斜率降低了SA结纤维的自发冲动起始速率。随着Po2逐渐降低，窦性心率降低；同时，快速心房刺激后的校正窦房结恢复时间受影响较小，仅在严重缺氧条件下才显示出明显延长。缺氧降低了SA结和AV结的动作电位幅度，但未降低心房的动作电位幅度。缺氧使SA和AV结传导减慢；心房内传导未受到明显影响。AV结传导阻滞在较低心房率时发生，且AV结的有效不应期延长。在缺氧情况下，常观察到SA和AV结冲动传播的不均匀性。这与两个结区内的隐匿性折返有关。用离子敏感微电极测量心房组织的细胞外K+浓度。即使在长时间严重缺氧后，[K+]o仍保持不变。这些结果与急性缺氧主要抑制慢反应活动但对快速内向钠电流影响很小的假设一致。
