DECREASED BONE CARBONATE CONTENT IN RESPONSE TO METABOLIC, BUT NOT RESPIRATORY, ACIDOSIS

In vitro culture neonatal mouse calvariae release calcium and buffer t he medium proton concentration in response to a decrease in the medium pH caused by a reduction in bicarbonate concentration ([HCO3-]), a mo del of metabolic acidosis, but not to an equivalent decrease in pH cau sed by an increase in the partial pressure of carbon dioxide (PCO2), a model of respiratory acidosis. We have postulated that the medium is in equilibrium with the carbonated apatite in bone. To determine wheth er bone carbonate is depleted during models of acidosis, we cultured c alvariae in control medium (pH almost-equal-to 7.4, PCO2 almost-equal- to 43, [HCO3-] almost-equal-to 26) or in medium in which the pH was eq uivalently reduced by either a decrease in [HCO3-] (metabolic acidosis , pH almost-equal-to 7.1, [HCO3-] almost-equal-to 13) or an increase i n PCO2 (respiratory acidosis, pH almost-equal-to 7.1, PCO2 almost-equa l-to 86) and determined net calcium flux (J(Ca)) and bone carbonate co ntent. We found that compared with control, after 3, 24, and 48 h ther e was a decrease in bone carbonate content during metabolic but not du ring respiratory acidosis. Compared with control, at 3 h J(Ca) increas ed with both respiratory and metabolic acidosis; however, at 24 and 48 h J(Ca) increased only with metabolic acidosis. J(Ca) was correlated inversely with percent bone carbonate content in control and metabolic acidosis at all time periods studied (r = -0.809, n = 23, P < 0.001). Thus a model of metabolic acidosis appears to increase J(Ca) from bon e, perhaps due to the low [HCO3-] inducing bone carbonate dissolution. However, a model of respiratory acidosis does not substantially alter J(Ca), perhaps because the elevated PCO2 does not allow bone carbonat e dissolution despite the reduced pH.