Abstract
In the traditional approach to buffering of H(+) during metabolic acidosis, the sole focus is on lowering the H(+) concentration, but this overlooks several important points. First, increased binding of H(+) to proteins changes their charge, shape, and possibly function. Second, organs in which buffering of H(+) occurs is not assessed even though it would be advantageous to spare brain proteins in this process. Third, only the arterial and not the capillary PCO(2) of individual organs is considered. This article provides a "brain protein-centered" view, which leads to different conclusions concerning the way H(+) are removed physiologically.
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