Tissue Pco 2 in Brain Ischemia Related to Lactate Content in Normo- and Hypercapnic Rats

The amount of lactate formed during ischemia determines the rise in tissue Pco₂ (P_tco₂). Conflicting results exist on the relationship between lactate and P_tco₂. The objective of this study was to settle this issue. We varied the preischemic plasma glucose concentration of normo- and hypercapnic rats, assessed tissue lactate and total CO₂ contents, and determined the Pco₂/lactate relationship over the lactate range 2–40 mmol kg⁻¹. The results showed that whatever the equilibration time, the Pco₂/lactate relationship was linear. The results obtained could be reproduced by a theoretical buffer system that mimics the buffering behavior of intracellular fluid. Our results bear on the question of whether compartmentation of H⁺ occurs during ischemia, with glial cells becoming more acid than neurons. A discontinuous Pco₂/lactate relationship, with a constant Pco₂ above a certain lactate content, would support this contention. Since our results demonstrate a linear relationship between lactate and Pco₂ over the lactate range 2–40 mmol kg⁻¹, they considerably weaken any argument for gross compartmentation of H⁺.