Homeostasis of carbon dioxide during intravenous infusion of carbon dioxide

Abstract

When rats are infused intravenously continuously with blood enriched in an extracorporeal system with 100% CO2, they are found to excrete the infused CO2 quantitatively. The excretion is accomplished by increasing ventilation in proportion to the infusion rate. Neither mean arterial pH nor Pco2 shows a statistically significant change. This constancy of composition is observed at CO2 infusion rates ranging from zero to an amount equal to six times the resting metabolic CO2 production. Similarity of this hyperpnea to the chief characteristics of the hyperpnea of exercise is notable. Increased oxygen uptake during this procedure is about 3.5 ml/l. of ventilation, a reasonable value for the oxygen cost of ventilation. Since, during this process the animal is quiescent and shows no other metabolic changes it is suggested that the effective signal for the regulation of arterial Pco2 is CO2 itself. The ability of the experimental animal to respond successfully to high rates of loading seems to be limited by failure to make appropriate circulatory adjustments. Removing CO2 by equilibrating blood with 100% o2 in the extracorporeal circuit decreases ventilation, but readily leads to an uncontrolled alkalosis. Submitted on April 13, 1960

Role of metabolic CO2 production in ventilatory response to steady-state exercise.

“…2), and is therefore unlikely to be the critical stimulus. An alternate possibility to account for the isocapnic hyperpnea is that of oscillation of Paco2 about its mean value, as first suggested by Yamamoto and Edwards (17). It has been well documented that under normal conditions, Paco2 and arterial pH oscillate during each respiratory cycle about their mean values (33,34).…”

“…The second hypothesis maintains that the hyperpnea of exercise is completely attributable to the increased delivery of CO2 to the lungs (16); but because arterial hypercapnia is absent, the precise C02-related stimulus linking ventilation and pulmonary CO2 excretion, and its site of detection have not been specified. Support for this hypothesis has been derived from a number of studies in which CO2 was infused into the venous blood of experimental animals (venous CO2 loading), resulting in an increase in ventilation, but no measurable increase in Paco2 (i.e., isocapnic hyperpnea) (17)(18)(19)(20). The demonstration of isocapnic hyperpnea in response to venous CO2 loading has been extrapolated to imply that the isocapnic hyperpnea of exercise may also be attributable solely to the associated increase in Vco2.…”

Carbon dioxide and venous return and their interaction as stimuli to ventilation in the cat

“…First, we have searched for unusual forms of the C02 signal in arterial blood which might provide an additional stimulus to respiration when C02 is perfused such as has been suggested by Yamamoto & Edwards (1960) and by Linton (1976Linton ( , 1977. We have found none.…”

A respiratory drive in addition to the increase in CO2 production at raised body temperature in rats

“…2e of Cunningham et al 1986). This is also the case when minute ventilation is measured at the start of exercise (Wasserman et al 1986;Duffin & McAvoy, 1988), when temperature has not yet risen detectably, and is also the case when attempts are made to simulate the increase in COµ production with venous COµ loading at constant temperature in rats (Yamamoto & Edwards, 1960), dogs (Stremel et al 1978) and sheep (Phillipson et al 1981). Thus the line shifts upwards but in parallel on the ventilation axis and the intercept on the Pa,COµ axis (the apnoeic threshold) falls to a lower Pa,COµ level.…”