Pickar J G
Department of Anatomy and Physiology, College of Veterinary Medicine, Kansas State University, Manhattan, Kansas 66506, USA.
J Appl Physiol (1985). 1997 Jul;83(1):113-9. doi: 10.1152/jappl.1997.83.1.113.
The purpose of the present investigation was to determine whether chemical stimulation of cardiac receptors is sufficient to inhibit locomotion. Decerebrate, unanesthetized cats were induced to walk on a treadmill by electrically stimulating the mesencephalic locomotor region (MLR). Cardiac receptors were stimulated by injecting nicotine (62.3 +/- 8.6 microg/kg, mean +/- SE) into the pericardial sac. Cardiac nerve activity was reversibly blocked by injecting procaine (2%) into the pericardial sac. Locomotion was monitored by using bipolar needle electrodes inserted into the lateral gastrocnemius (LG) and tibialis anterior (TA) muscles. Integrated electromyographic (iEMG) activity from each muscle was quantified on a step-by-step basis. Intrapericardial (ipc) nicotine inhibited locomotion and evoked the coronary chemoreflex. Blood pressure and heart rate decreased significantly by 45.6 +/- 7.1 mmHg and 59.3 +/- 12.3 beats/min, respectively. Nicotine ipc significantly reduced iEMG activity by 24-28% in the LG muscles. The TA muscles were not affected consistently by ipc nicotine. The locomotor inhibition and the depressor reflex paralleled each other and occurred within 5 s of nicotine injection. Procaine ipc blocked the nicotine-induced locomotor inhibition and depressor reflex. The effects of procaine were largely reversible, because ipc nicotine reduced iEMG activity in the LG (25-46%) but not in the TA muscles after washing procaine from the pericardial sac. These results demonstrate that cardiac receptors sensitive to nicotine inhibit MLR-induced locomotion in the decerebrate cat. These findings indicate the presence of a neural pathway from the heart whereby endogenous stimuli could reflexly alter motor control.
本研究的目的是确定对心脏感受器的化学刺激是否足以抑制运动。通过电刺激中脑运动区（MLR），诱导去大脑、未麻醉的猫在跑步机上行走。通过向心包腔内注射尼古丁（62.3±8.6微克/千克，平均值±标准误）来刺激心脏感受器。通过向心包腔内注射2%的普鲁卡因可逆性地阻断心脏神经活动。使用插入外侧腓肠肌（LG）和胫骨前肌（TA）的双极针电极监测运动。对每块肌肉的肌电图（iEMG）综合活动进行逐步骤量化。心包内（ipc）尼古丁抑制运动并诱发冠状动脉化学反射。血压和心率分别显著下降45.6±7.1毫米汞柱和59.3±12.3次/分钟。ipc尼古丁使LG肌肉的iEMG活动显著降低24% - 28%。TA肌肉未受到ipc尼古丁的一致影响。运动抑制和降压反射相互平行，且在注射尼古丁后5秒内出现。ipc普鲁卡因阻断了尼古丁诱导的运动抑制和降压反射。普鲁卡因的作用在很大程度上是可逆的，因为在心包腔内冲洗掉普鲁卡因后，ipc尼古丁降低了LG肌肉（25% - 46%）而非TA肌肉的iEMG活动。这些结果表明，对尼古丁敏感的心脏感受器抑制去大脑猫中MLR诱导的运动。这些发现表明存在一条从心脏发出的神经通路，内源性刺激可通过该通路反射性地改变运动控制。
