• T Sudo and Y Fukuda.
• Department of Physiology II, School of Medicine, Chiba University, Chuoh-ku, Chiba, 260 Japan.
• Jpn. J. Physiol. 1997 Dec 1;47(6):531-6.

AbstractThe ventilatory response to acute systemic hypoxia has been thought to be determined by the balance between hypoxic stimulation via peripheral chemoreceptors and hypoxic inhibition of the respiratory neurons. In moderate-severe hypoxia, the latter predominates the former resulting in ventilatory "depression" (HVD). However, ventilation relative to metabolic rate (V.O2) during HVD is "not depressed" but remains increased because of associated reduction in O2 uptake (V.O2). The experiment presented here was conducted to elucidate the changes in CO2 output (V.CO2) and acid-base status during hypoxia and their role in ventilatory regulation. Ventilation, metabolic rate (V.O2, V.CO2), acid-base status and blood lactate concentration were measured during and after inhalation of hypoxic gases in halothane-anesthetized and spontaneously breathing rats. The HVD occurred at FIO2 0.08 with increased blood lactate concentration, increased venous PCO2 and a large drop in venous pH without significant changes in arterial pH and PCO2. Furthermore, the amount of reduction in V.CO2 during HVD was much smaller than that of V.O2 and the V.CO2/V.O2 ratio increased. These findings suggest that CO2 output becomes relatively higher than O2 consumption in moderate-severe hypoxia. The possible origin of CO2 accumulation in the venous blood, such as the buffering of lactic acid by bicarbonate, and its role in ventilatory stimulation are discussed. Since there was no large increase in V.E and metabolic rate in the post-hypoxic period, "O2 debt" during HVD was small.

23 keywords...

hide…