Bauer R M, Iwamoto G A, Waldrop T G
Department of Physiology and Biophysics, University of Illinois, Urbana 61801.
Am J Physiol. 1989 Nov;257(5 Pt 2):R1154-61. doi: 10.1152/ajpregu.1989.257.5.R1154.
Cardiorespiratory alterations during exercise are mediated through feedback from contracting muscles and descending drive from rostral brain sites such as the posterior hypothalamus. The role of medullary sites, which process this information, was examined in this study. In anesthetized cats, muscular contraction elicited by stimulation of L7 and S1 ventral roots and electrical stimulation of sites in the posterior hypothalamus both evoked increases in arterial pressure, heart rate, and minute ventilation. The reflex increase in arterial pressure produced by muscular contraction was attenuated significantly 15-20 min after bilateral microinjections of an excitatory amino acid (EAA) receptor antagonist, kynurenic acid (KYN), into the ventrolateral medulla (VLM). The reflex increase in arterial pressure evoked by muscular contraction returned to control levels 90 min after VLM microinjections of KYN. Microinjection of KYN into the VLM had no effect on the cardiorespiratory responses to posterior hypothalamic stimulation. These findings suggest that neurons in the VLM modulate the reflex pressor response evoked by muscular contraction. This reflex may be mediated through an interaction with EAA receptors on neurons in the VLM.
运动期间的心肺变化是通过收缩肌肉的反馈以及来自诸如下丘脑后部等脑前部区域的下行驱动来介导的。本研究考察了处理该信息的延髓部位的作用。在麻醉的猫中,刺激L7和S1腹侧神经根引起的肌肉收缩以及下丘脑后部部位的电刺激均引起动脉压、心率和每分通气量增加。在双侧向延髓腹外侧(VLM)微量注射兴奋性氨基酸(EAA)受体拮抗剂犬尿氨酸(KYN)15 - 20分钟后,肌肉收缩引起的动脉压反射性增加显著减弱。在VLM微量注射KYN 90分钟后,肌肉收缩引起的动脉压反射性增加恢复到对照水平。向VLM微量注射KYN对下丘脑后部刺激引起的心肺反应没有影响。这些发现表明,VLM中的神经元调节肌肉收缩引起的反射性升压反应。该反射可能是通过与VLM中神经元上的EAA受体相互作用来介导的。