In a rat model, elevated CO2 causes rapid reversible depolarization in liver cells and delayed depolarization in skeletal muscle cells.
Hypothesizes tissue-specific CO2 effects on rat membrane potentials; leaves open translation to human physiology or clinical hypercapnia.
The effects of increasing the inspired CO(2) concentration on the transmembrane resting potential (RP), intracellular electrolytes, and cell pH of rat liver and muscle were studied.2. Elevation of CO(2) produced a rapid reversible fall in hepatic RP. This effect is mediated by a decrease in plasma pH and is in part due to hypoxia.3. The decrease in hepatic RP could not be accounted for by shifts in electrolytes, and an effect on membrane permeability is suggested.4. The hepatic RP was also found to be decreased by hypoxia and increased by hyperoxia.5. Muscle RP showed no immediate change in response to CO(2) but after 60 min there was significant depolarization. This effect could be accounted for on the basis of electrolyte shifts between cells and plasma, by use of the Goldman equation.6. Cell pH data showed that liver is buffered approximately threefold more than skeletal muscle.7. While intracellular pH fell in response to CO(2) the H(+) gradient remained constant in muscle and increased in liver.
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Williams et al. (1971) studied this question.
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