Why the study?
Does myocardial hypertrophy alter intracellular pH regulation during hypercapnia in rats?
Does myocardial hypertrophy alter intracellular pH regulation during hypercapnia in rats?
Hypertrophic rat myocardium shows an increased ability to regulate intracellular pH during hypercapnia, likely due to enhanced bicarbonate uptake rather than increased nonbicarbonate buffers.
May indicate better pH regulation in hypertrophied myocardium; leaves open translation to human cardiac acidosis or hypertrophy.
The myocardial cell pH (pHi) observed during breathing of 0, 7.5, or 10% CO2 in air for 3 h was studied in rats with myocardial hypertrophy due to aortic stenosis and in sham-operated rats. The change in pHi during hypercapnia was significantly smaller in the rats with myocardial hypertrophy, with the apparent nonbicarbonate buffer value (delta [HCO3-]i/delta pHi) being almost three times that of the sham-operated rats. In vitro CO2 equilibrium of myocardial tissue homogenates showed no difference in nonbicarbonate buffer value between homogenates obtained from normal rats and from rats with myocardial hypertrophy. Therefore, it appears that the increased ability of the myocardial cell to regulate its pH during hypertrophy is not due to an increase in the cellular level of nonbicarbonate buffers, but seems to be related to a larger bicarbonate uptake by the myocardial cell during hypercapnia.
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González et al. (1979) studied Myocardial hypertrophy. Hypercapnia (breathing 7.5% or 10% CO2 in air) vs. Sham-operated rats was evaluated on Change in myocardial cell pH (pHi) during hypercapnia.
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