Abstract
IT is widely recognized that hyperventilation occurs as a compensatory event in metabolic acidosis. The details of the mechanisms mediating this secondary response, however, are not completely clear. Recently, Mitchell and his co-workers1 proposed a comprehensive hypothesis to explain the chemical regulation of respiration in this and other disorders of acid–base equilibrium. The hypothesis envisions an interaction of respiratory stimuli arising from or related to changes in the acid–base composition of the blood, mediated through peripheral chemoreceptors, and those arising from the altered acid–base composition of the cerebrospinal fluid, mediated through medullary chemoreceptors sensitive to cerebrospinal-fluid pH. The drive to . . .
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