Blood and cerebrospinal fluid lactate during hyperventilation

Abstract

Twenty dogs were hyperventilated to produce hypocapnia (PaCO2. 7-23 mm Hg) with and without associated hypoxia (PaO2, 45- 65 mm Hg in 4 dogs). Arterial blood, sagittal sinus blood, and CSE [cerebrospinal fluid] were analyzed for pH, PCO2 [CO2 pressure], HCO3, lactate, and pyruvate before and at hourly intervals after hyperventilation lasting up to 6 hr. Brain samples were analyzed for lactate and pyruvate at the beginning and end of 4 experiments. Arterial and sagittal venous pH levels rose as high as 7.75, and were maintained there throughout hyperventilation with no tendency to fall. In no experiment did hyperventilation produce systemic acidosis. Mean blood lactate in the artery and sagittal sinus rose to a peak of 5.2 m[image] at 2 hr., but thereafter declined toward normal. The CSF pH rose rapidly to 7.44-7.67 but, after 2 hr., it gradually and progressively declined, reflecting a progressive increase in CSF lactate to a 6-hr, mean of 8.2 mM in eupoxic and 12.1 m[image] in hypoxic animals. Lactate concentrations in brain correlated closely with those in CSF, but neither brain nor CSF lactate correlated with the much lower sagittal blood lactate. Excess lactate comprised 14-69% of the total CSF lactate increase. The data are consistent with the hypothesis that selective cerebral hypoxia causes at least part of the CNS [central nervous system] effects of hyperventilation.