Serial changes in CO₂ storage in tissues

Attempts to use the steady state CO₂ storage capacity of tissues to predict the rate of blood P_CO2 rise during acute exposure to CO₂ have been unsuccessful. This discrepancy might be explained by the failure of some or all of the body tissues to exert their full capacity to store CO₂ during brief exposures to hypercapnia. This hypothesis was tested in 29 dogs and 10 goats by determining the in vivo CO₂ dissociation slope (Δtissue CO₂ concentratipn/Δvenous P_CO2) in three different tissues, brain, spleen and muscle, during transient states of CO₂ retention produced by apneic oxygenation or ventilation with 3% CO₂. By six minutes of apneic oxygenation, the CO₂ dissociation slope of the brain was 3.8 ml/kg/mm Pv_CO2; and that of the spleen, 4.2; while this value for muscle was much less, only 1.0 and was unchanged by alteration in the total level of muscle perfusion. Studies with 3% CO₂ indicated that the CO₂ dissociation of brain and spleen was nearly constant from 5 to 20 min of CO₂ exposure but that of muscle gradually increased. These results indicate that factors other than perfusion limit CO₂ storage in muscle, and this reduced ability of muscle to store CO₂ largely accounts for the low storage capacity of the body during brief periods of exposure to CO₂.