Interaction between CO2 production and ventilation in the hypoxic kitten.

We hypothesized that in the hypoxic newborn the drop in metabolic rate, and particularly in CO2 production (VCO2), contributes to the magnitude of the ventilatory response. Experiments were performed on unanesthetized newborn kittens in a warm [28-30 degrees C ambient temperature (Ta)] or cold (20 degrees C) environment. Breathing pattern and gaseous metabolism were measured by the barometric technique and the inflow-outflow O2 and CO2 difference, respectively. At 30 degrees C, hypoxia (10% O2) decreased VCO2 and induced rapid and shallow breathing, with little effect on minute ventilation (VE). Normoxic exposure to 20 degrees C determined a parallel increase in VE and metabolism; at this Ta, hypoxia decreased VCO2 more than at the higher Ta, and the drop in tidal volume (VT) was also proportionally larger; hence, at 20 degrees C, hypoxic VE was markedly below the normoxic values. Despite these changes in breathing pattern, at neither Ta during hypoxia did arterial PCO2 increase above the normoxic value; in fact, arterial PCO2 at 20 degrees C was slightly decreased because of the important drop in VCO2. Exposure to hypoxia with a CO2 load (inspired CO2 = 1, 3, or 5%) did not abolish the hypometabolic response; the hypoxic depressant effect on VT was either unchanged (by 1% CO2), completely offset (by 3% CO2), or reversed (by 5% CO2), with parallel effects on VE. The results are consistent with the hypothesis that in the newborn the level of CO2, by controlling VT, could represent a link between the metabolic and ventilatory responses to acute hypoxia.