Department of Physiology, Graduate School of Health Sciences, Hiroshima University, Japan.
Am J Physiol Heart Circ Physiol. 2011 Apr;300(4):H1373-85. doi: 10.1152/ajpheart.01296.2010. Epub 2011 Feb 4.
To examine whether withdrawal of cardiac vagal efferent nerve activity (CVNA) predominantly controls the tachycardia at the start of exercise, the responses of CVNA and cardiac sympathetic efferent nerve activity (CSNA) were directly assessed during fictive motor activity that occurred spontaneously in unanesthetized, decerebrate cats. CSNA abruptly increased by 71 ± 12% at the onset of the motor activity, preceding the tachycardia response. The increase in CSNA lasted for 4-5 s and returned to the baseline, even though the motor activity was not ended. The increase of 6 ± 1 beats/min in heart rate appeared with the same time course of the increase in CSNA. In contrast, CVNA never decreased but increased throughout the motor activity, in parallel with a rise in mean arterial blood pressure (MAP). The peak increase in CVNA was 37 ± 9% at 5 s after the motor onset. The rise in MAP gradually developed to 21 ± 2 mmHg and was sustained throughout the spontaneous motor activity. Partial sinoaortic denervation (SAD) blunted the baroreflex sensitivity of the MAP-CSNA and MAP-CVNA relationship to 22-33% of the control. Although partial SAD blunted the initial increase in CSNA to 53% of the control, the increase in CSNA was sustained throughout the motor activity. In contrast, partial SAD almost abolished the increase in CVNA during the motor activity, despite the augmented elevation of 31 ± 1 mmHg in MAP. Because afferent inputs from both muscle receptors and arterial baroreceptors were absent or greatly attenuated in the partial SAD condition, only central command was operating during spontaneous fictive motor activity in decerebrate cats. Therefore, it is likely that central command causes activation of cardiac sympathetic outflow but does not produce withdrawal of cardiac parasympathetic outflow during spontaneous motor activity.
为了检验心脏迷走传出神经活动（CVNA）的撤回是否主要控制运动起始时的心动过速，在未麻醉去大脑猫的自发性模拟运动期间，直接评估了 CVNA 和心脏交感传出神经活动（CSNA）的反应。CSNA 在运动活动开始时突然增加了 71±12%，先于心动过速反应。CSNA 的增加持续了 4-5 秒，尽管运动活动没有结束，但仍回到基线。心率增加了 6±1 次/分钟，与 CSNA 增加的时间进程相同。相比之下，CVNA 从未减少，而是在整个运动活动中与平均动脉血压（MAP）的升高平行增加。CVNA 的峰值增加发生在运动开始后 5 秒，为 37±9%。MAP 的升高逐渐发展到 21±2mmHg，并在整个自发性运动活动中持续。部分主动脉弓切断术（SAD）使 MAP-CSNA 和 MAP-CVNA 关系的压力反射敏感性降低至对照的 22-33%。尽管部分 SAD 将 CSNA 的初始增加减弱至对照的 53%，但 CSNA 在整个运动活动中持续增加。相比之下，尽管 MAP 升高了 31±1mmHg，但部分 SAD 几乎消除了运动过程中 CVNA 的增加。由于在部分 SAD 条件下，肌肉感受器和动脉压力感受器的传入输入缺失或大大减弱，只有中枢命令在去大脑猫的自发性模拟运动中起作用。因此，在自发性运动活动期间，中枢命令可能导致心脏交感传出激活，但不会产生心脏副交感传出的撤回。
