Fukuda Y, Sato A, Suzuki A, Trzebski A
Department of Physiology, Tokyo Metropolitan Institute of Gerontology, Japan.
J Auton Nerv Syst. 1989 Oct;28(1):61-74. doi: 10.1016/0165-1838(89)90008-8.
Contribution of autonomic nervous system activity to the heart rate and blood pressure responses during chemoreceptor excitations by systemic hypoxia and hypercapnia and to hyperoxia and hypocapnia was analyzed in the urethane-anesthetized, artificially ventilated rats. Systemic hypoxia induced a co-activation of two antagonistic nerves: an increase in cardiac sympathetic and in cardiac vagal efferent nerve discharges. Increased heart rate was due to predominance of the cardiac sympathetic over the cardiac vagal activation. In spite of a marked reflex increase in the renal and cardiac sympathetic nerve activities, the local vasodilator effect of hypoxia prevented consistent changes in arterial blood pressure. Bilateral section of the carotid sinus nerves (CSN) mostly abolished autonomic nerve responses and produced a profound decreases in the blood pressure during hypoxia. Hyperoxia elicited a pressor response due to peripheral vasoconstriction with no significant change in the autonomic nerve activities except for a decrease in the cardiac sympathetic nerve discharges. Hypercapnia significantly increased blood pressure and renal nerve sympathetic activity. In contrast to hypoxia, hypercapnia excited cardiac sympathetic and inhibited cardiac vagal activity. This reciprocal effect did not elicit neurogenic cardioacceleration, because it was masked by the local inhibitory action of CO2 on the heart rate. The increase in sympathetic activities and in blood pressure during hypercapnia persisted after bilateral CSN section indicating that the responses were mediated by central rather than by peripheral chemoreceptors. Hypocapnia produced a significant increase in cardiac vagal discharges yet a cardioacceleratory response occurred due to the local effect upon heart rate. The present results indicate that in the rat, autonomic nervous responses differ depending on the type, i.e. hypoxic or hypercapnic, chemoreceptor stimuli. Reflex heart rate and blood pressure responses do not follow the autonomic nerve activities exactly. Circulatory responses are greatly modified by local peripheral effects of hypoxic, hyperoxic, hypocapnic or CO2 stimuli on the cardiovascular system. Species differences characterizing the autonomic nerve responsiveness to chemical stimuli in the rat are described.
在氨基甲酸乙酯麻醉、人工通气的大鼠中，分析了自主神经系统活动对全身低氧和高碳酸血症以及高氧和低碳酸血症引起的化学感受器兴奋期间心率和血压反应的贡献。全身低氧诱导了两条拮抗神经的共同激活：心脏交感神经和心脏迷走传出神经放电增加。心率增加是由于心脏交感神经激活超过心脏迷走神经激活。尽管肾和心脏交感神经活动有明显的反射性增加，但低氧的局部血管舒张作用阻止了动脉血压的持续变化。双侧切断颈动脉窦神经（CSN）大多消除了自主神经反应，并在低氧期间使血压大幅下降。高氧由于外周血管收缩引起升压反应，除心脏交感神经放电减少外，自主神经活动无明显变化。高碳酸血症显著升高血压和肾神经交感神经活动。与低氧不同，高碳酸血症兴奋心脏交感神经并抑制心脏迷走神经活动。这种相互作用并未引发神经源性心动加速，因为它被二氧化碳对心率的局部抑制作用所掩盖。双侧切断CSN后，高碳酸血症期间交感神经活动和血压的增加仍然存在，表明这些反应是由中枢而非外周化学感受器介导的。低碳酸血症使心脏迷走神经放电显著增加，但由于对心率的局部作用仍出现心动加速反应。目前的结果表明，在大鼠中，自主神经反应因化学感受器刺激的类型（即低氧或高碳酸血症）而异。反射性心率和血压反应并不完全跟随自主神经活动。循环反应受到低氧、高氧、低碳酸血症或二氧化碳刺激对心血管系统的局部外周作用的极大影响。描述了大鼠自主神经对化学刺激反应性的种属差异。
