Our purpose was to quantitate the proportion of H+ removed by the bicarbonate buffer system (BBS) when a modest load of H+ was infused acutely. In addition, the quantitative impact of hyperventilation on the BBS in the extracellular fluid (ECF) and other compartments in this setting was assessed. Three groups of rats (399 +/- 3 g) were anesthetized and connected to a respirator to control their arterial PCO2 and to collect expired air. Metabolic acidosis (pH 7.26 +/- 0.01, bicarbonate 18 +/- 1 mM) was induced by infusion of HCl (0.15 M, 4 mmol/kg) over 60 min, and expired air was collected for two 20-min periods beginning 75 and 105 min after the start of the infusion of HCl in each group. Each rat served as its own control for the rate of production of CO2 from metabolism. The first two groups were time controls. Their arterial PCO2 was constant at either ambient (50 mmHg) or hyperventilation levels (30 mmHg) during both collections (n = 5 each). In the experimental group (n = 5), the PCO2 was decreased from 40 to 27 mmHg during the second collection. The rate of production of CO2 from metabolism did not rise in the second collection in the time control experiments (change = -13.4 +/- 1.7 and -1.4 +/- 2.5 mumol/min, respectively), whereas more CO2 was collected during the second period in the experimental group (change = 42 +/- 9 mumol/min, P = 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)