Nakazono Y, Miyamoto Y
Department of Information, Faculty of Engineering, Yamagata University, Yonezawa, Japan.
Jpn J Physiol. 1987;37(3):447-57. doi: 10.2170/jjphysiol.37.447.
To clarify the role of the carotid body in the mechanism governing exercise hyperpnea, the effect of hypoxia and hyperoxia on ventilation and cardiac output was studied in four healthy men. The VE increased 10.7% in hypoxia and decreased 10.1% in hyperoxia from normoxia as judged from the steady-state values during exercise. On the contrary, Q showed only a slight reduction of -3.2% in hyperoxia. The hypoxic hyperpnea and hyperoxic hypopnea led to a concomitant alteration in PETCO2. An overshoot following the onset of exercise was observed during the first 30s of VE response in hypoxia, which damped progressively in normoxia and hyperoxia. No remarkable difference was observed in the early transient responses of Q between hypoxia and hyperoxia. The discrepancy in the dynamics between VE and Q led to a phasic deviation in PETCO2; an isocapnic transition from the control to stimulus period in normoxia, hypocapnic in hypoxia and hypercapnic in hyperoxia. The time constant representing the kinetics of VE and that for VCO2 prolonged significantly in hyperoxia. These results support the cardiodynamic consequence of exercise hyperpnea, i.e., the carotid body is the first to respond to the increase in CO2 flow into the lungs.
为阐明颈动脉体在运动性呼吸增强调节机制中的作用，对4名健康男性进行了低氧和高氧对通气及心输出量影响的研究。根据运动期间的稳态值判断，与常氧相比，低氧时每分钟通气量（VE）增加10.7%，高氧时降低10.1%。相反，高氧时心输出量（Q）仅轻微降低3.2%。低氧性呼吸增强和高氧性呼吸减弱导致呼气末二氧化碳分压（PETCO2）随之改变。在低氧时，VE反应的前30秒观察到运动开始后的过冲现象，在常氧和高氧时逐渐衰减。低氧和高氧时Q的早期瞬态反应未观察到明显差异。VE和Q动态变化的差异导致PETCO2出现阶段性偏差；常氧时从对照期到刺激期为等碳酸过渡，低氧时为低碳酸，高氧时为高碳酸。代表VE动力学的时间常数和代表二氧化碳排出量（VCO2）的时间常数在高氧时显著延长。这些结果支持运动性呼吸增强的心脏动力学后果，即颈动脉体是对进入肺部的二氧化碳流量增加最先做出反应的部位。
