Previous studies of reptiles and amphibians have shown that changing the body temperature consistently produces transient changes in the respiratory exchange ratio (RE) and, hence, changes in whole-body CO2 stores, and that the extracellular fluid compartment contributes to the temperature-related changes in CO2 stores. The purpose of this study was to determine whether the intracellular fluid compartment contributes to the changes in CO2 stores in undisturbed resting cane toads. Increasing body temperature from 10 to 30 degrees C temporarily elevated RE, and returning body temperature to 10 degrees C temporarily lowered RE. The estimated average change in whole-body CO2 stores associated with the transient changes in RE was 1.0 +/- 0.8 mmol kg-1 (+/- S.D., N = 6). Plasma [CO2] and, thus, extracellular fluid [CO2], were unaffected by the temperature change. Plasma calcium levels were also unaffected, so that bone CO2 stores did not contribute to changes in whole-body CO2 stores. Intracellular [CO2] was determined for the lung, oesophagus, stomach, small intestine, liver, ventricle, red blood cells, skin and 14 skeletal muscles. [CO2] was significantly lower (P < 0.05) at higher temperature in 10 of these, and seven others, although not statistically significant (P > 0.05), had mean values at least 0.5 mmol kg-1 lower at the higher temperature. The average change in intracellular [CO2] for all tissues examined was -0.165 mmol kg-1 degrees C-1. We conclude that, in cane toads, the temperature-related transients in RE result from intracellular CO2 adjustments, that different tissues have unique intracellular CO2/temperature relationships, and that a combination of respiratory and ion-exchange mechanisms is used to adjust pH as temperature changes.
Extracellular and intracellular carbon dioxide concentration as a function of temperature in the toad Bufo marinus.
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J N Stinner, D L Newlon, N Heisler; Extracellular and intracellular carbon dioxide concentration as a function of temperature in the toad Bufo marinus.. J Exp Biol 1 October 1994; 195 (1): 345–360. doi: https://doi.org/10.1242/jeb.195.1.345
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