EFFECT OF CARBON-DIOXIDE ON CEREBRAL METABOLISM DURING HYPOXIA-ISCHEMIA IN THE IMMATURE RAT

We previously have demonstrated that hypocapnia aggravates and hyperca pnia protects the immature rat from hypoxic ischemic brain damage. To ascertain cerebral blood flow (CBF) and metabolic correlates, 7-d post natal rats were subjected to hypoxia-ischemia during which they were r endered either hypo- (3.5 kPa), normo- (5.1 kPa), or hypercapnic (7.3 kPa) by the inhalation of either 0, 3, or 6% CO2, 8% O-2, balance N-2. CBF during hypoxia-ischemia was better preserved in the normo- and hy percapnic rat pups; these animals also exhibited a stimulation of cere bral glucose utilization. Brain glucose concentrations were higher and lactate lower in the normo- and hypercapnic animals, indicating that glucose was consumed oxidatively in these groups rather than by anaero bic glycolysis, as apparently occurred in the hypocapnic animals. ATP and phosphocreatine were better preserved in the normo- and hypercapni c rats compared with the hypocapnic animals. Cerebrospinal fluid gluta mate, as a reflection of the brain extracellular fluid concentration, was lowest in the hypercapnic rats at 2 h of hypoxia-ischemia. The dat a indicate that during hypoxia-ischemia in the immature rat, CBF is be tter preserved during normo- and hypercapnia; the greater oxygen deliv ery promotes cerebral glucose utilization and oxidative metabolism for optimal maintenance of tissue high energy phosphate reserves. An inhi bition of glutamate secretion into the synaptic cleft and its attenuat ion of N-methyl-D-aspartate receptor activation would further protect the hypercapnic animal from hypoxic-ischemic brain damage.