Huang M H, Hull S S, Foreman R D, Lazzara R, Wolf S
University of Oklahoma Health Sciences Center.
Integr Physiol Behav Sci. 1992 Jan-Mar;27(1):6-12. doi: 10.1007/BF02691087.
The shortening of the QT interval of the electrocardiogram coincident with acceleration of heart rate and vice versa has been accepted for many years as evidence that the action potential duration and hence QT are necessarily dependent on heart rate. Exceptions to this rule have been attributed to the intervention of counteracting autonomic effects. In order to test this assumption, 26 conscious dogs divided into three groups were tested during baroreceptor stimulation by a bolus injection of phenylephrine. Seventeen dogs had been used in earlier studies in which they had undergone an experimental anterior myocardial infarction with apparent full recovery. A group of those dogs underwent beta-adrenergic blockade by intravenous atenolol 30 min prior to the baroreceptor activation. To test the intactness of the baroreceptor responses in the previously infarcted dogs, a third group of nine dogs that had had no prior myocardial infarction was included. All dogs were adapted to the laboratory environment and were not sedated during experiments. Simultaneous recordings of RR, QT interval, and phasic arterial pressure were made in all dogs before and during baroreceptor stimulation. In the normal group, and the previously infarcted group that received no atenolol, baroreceptor stimulation elicited a small (8/msec), but significant prolongation of the QT associated with a nearly 50% reduction in heart rate. The QT interval of the atenolol-treated dogs, although significantly more prolonged before stimulation, remained unchanged during the reflex. The data indicate that withdrawal of ventricular sympathetic tone may prolong the QT interval, thereby confirming the role of sympathetic innervation in the control of QT.(ABSTRACT TRUNCATED AT 250 WORDS)
心电图QT间期缩短与心率加快同时出现,反之亦然,多年来一直被视为动作电位持续时间以及QT必然依赖于心率的证据。该规律的例外情况被归因于自主神经拮抗作用的干预。为了验证这一假设,将26只清醒犬分为三组,通过静脉推注去氧肾上腺素进行压力感受器刺激试验。17只犬曾用于早期研究,在这些研究中它们经历了实验性前壁心肌梗死且明显完全恢复。其中一组犬在压力感受器激活前30分钟通过静脉注射阿替洛尔进行β-肾上腺素能阻滞。为了测试先前梗死犬的压力感受器反应是否完整,纳入了第三组9只未曾发生过心肌梗死的犬。所有犬均适应实验室环境,实验期间未使用镇静剂。在压力感受器刺激前后,对所有犬同时记录RR、QT间期和动脉相压力。在正常组以及未接受阿替洛尔治疗的先前梗死组中,压力感受器刺激引起QT轻度(8/毫秒)但显著延长,同时心率降低近50%。阿替洛尔治疗的犬的QT间期,尽管在刺激前显著延长,但在反射过程中保持不变。数据表明,心室交感神经张力的降低可能延长QT间期,从而证实了交感神经支配在QT控制中的作用。(摘要截选至250字)