Lactate as a modulator of hypoxia-induced hyperventilation.

In the present study, we tested the hypothesis that lactate, which is a classic companion of hypoxic stress in mammals, is a modulator of hypoxia-induced hyperventilation. To this end, pulmonary ventilation (V(E)) of male Wistar rats was measured by whole body plethysmograph, and dichloroacetate (DCA, 100 mg/kg) was used to inhibit lactate production. Plasma lactate levels, arterial pH (pHa), arterial carbon dioxide partial pressure (PaCO(2)), arterial oxygen partial pressure (PaO(2)), plasma bicarbonate (HCO3(-)) and oxygen consumption (VO(2)) were determined as well. In normoxia, intraperitoneal DCA elicited a decrease only in plasma lactate levels. Hypoxia caused an increase in V(E), pHa and plasma lactate levels and parallel to decreases in PaCO(2), PaO(2) and VO(2) in the control group. DCA administration markedly reduced the ventilatory response to hypoxia by acting on tidal volume (V(T)). This reduced ventilatory response caused by DCA was independent of VO(2). In conclusion, the present study indicates that lactate contributes to the initiation and maintenance of hypoxia-induced hyperventilation in rats, modulating the adjustments in V(T).