Cardiac receptors evoke ventilatory response with increased venous PCO2 at constant arterial PCO2

The effects of elevated venous PCO2 and denervation of the cardiac ventricles on ventilation were studied in 20 anesthetized open-chest unidirectionally ventilated White Leghorn cockerels. Venous PCO2 was increased by insufflating the gut with high CO2 while recording changes in the amplitude of the sternal movements. Arterial blood gases were held constant by unidirectionally ventilating the lungs with gas flows approximately five times the animal's resting minute volume. Insufflating the gut with 90% N2-10% O2 did not change the level of ventilation, whereas with 90% CO2-10% O2 the amplitude of sternal movement increased 500% above that with no gut gas flow. Exchange of N2 for the CO2 was followed by a rapid reduction of ventilatory movements to control levels. Arterial blood gases remained constant during gut gas insufflation, whereas mixed venous PCO2 increased and mixed venous pH decreased when high CO2 was given to the gut. Cutting the middle cardiac nerves, which primarily innervate the ventricles of the heart, reduced the ventilatory response to CO2 gut insufflation by 67%. Sympathetic denervation of the thoracic viscera did not change the responses. It appears that, in the chicken, increasing the mixed venous PCO2 while holding the arterial blood gases constant alters ventilation by an afferent system located in the venous circulation or in the right ventricle which is sensitive to changes in PCO2.     

Time-dependent variations of transcutaneous PCO2 level in normal subjects

Transcutaneous PCO2 (PtcCO2), which is linearly related to arterial PCO2, was continuously recorded in healthy, adult, normal volunteers for 8-h periods. Recording this variable with the apparatus employed permits measurement of changes in the level of ventilation while subjects are freely ambulant and unencumbered by invasive and flow-resistive respiratory apparatus. The time series obtained exhibited marked periodicities. The frequencies and amplitudes varied between subjects. Peak-to-peak variation was 10-20% of mean values. There was no apparent association between fluctuations in PCO2 and activity other than formal exercise. Visual inspection of the time series and preliminary statistical analysis of digitally converted data suggested that the time-dependent changes of PtcCO2 were normally distributed. However, more rigorous statistical examination revealed that in no case was PtcCO2 actually normally distributed.     

Fixed breathing frequency decreases end-tidal PCO2 in humans.

We tested the effect of a fixed breathing frequency on the partial pressure of CO2 in the end-tidal air (PETCO2) in resting healthy subjects. In the first experiment, three different rates of breathing were dictated: the same frequency of breathing as the subject's control one (1f), a double frequency (2f), and half of the control frequency (0.5f). 10 min dictate of 1f and 2f induced a decrease of PETCO2. The dictate of 0.5f had no significant effect on PETCO2. In the second experiment, 1f was dictated for 30 min, inducing a decrease of PETCO2 throughout the duration of the dictate. These results demonstrate that fixing the breathing frequency by the dictate affects the chemostatic control of ventilation.