Lactate as a modulator of hypoxia-induced hyperventilation

Abstract 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 (HCO 3 − ) 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 .