Abstract
Hypercapnia in addition to hypoxia affects the mammalian cardiorespiratory system and has been suggested to exert its effects on cardiorespiratory function by slightly different mechanisms to hypoxia. In the present study, we examined cardiorespiratory changes in urethane-anesthetized rats under hypocapnic (Hypo, 10% O2), isocapnic (Iso, 10% O2 and 4% CO2), and hypercapnic (Hyper, 10% O2 and 8% CO2) hypoxia for 2 h to clarify the effects of CO2 on sustained hypoxia-induced cardiorespiratory responses. Respiratory frequency increased the most in Hypo and tidal volume in Hyper. Minute ventilation, a product of respiratory frequency and tidal volume, increased the most in the latter group. Regarding cardiovascular variables during the hypoxic exposure period, heart rate and mean blood pressure both markedly decreased in Hypo. However, decreases in these parameters were small in Iso, and both increased over the pre-exposure level in Hyper. The present results suggest that CO2 interferes with the hypoxia-activated neural pathway via another pathway under sustained exposure to hypoxia.
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