Brain intracellular pH and metabolism during hypercapnia and hypocapnia in the new‐born lamb.

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Abstract
1. The effects of hypercapnia and hypocapnia on brain intracellular pH (pHi) and metabolism were investigated in new-born lambs under barbiturate anaesthesia. 2. 31P nuclear magnetic resonance (n.m.r.) spectroscopy was used to determine brain pHi and the relative concentrations of compounds containing mobile phosphorous nuclei including phosphocreatine (PCr), nucleoside triphosphates (NTP) and inorganic phosphate (Pi). Simultaneous measurements were made of the molar ratio of glucose to oxygen uptake by the brain. 3. During normocapnia (arterial partial pressure of CO2 Pa.CO2. 39 .+-. 1 mmHg mean .+-. S.E. of mean, n = 9) brain pHi was 7.13 .+-. 0.02. Hypercapnia (Pa,CO2, 98 .+-. 3 mmHg) was associated with a fall in brain pHi to 6.94 .+-. 0.03 (n = 19, P < 0.001), whereas no significant change in brain pHi occurring during hypocapnia (Pa,CO2, 16 .+-. 1 mmHg: brain pHi 7.15 .+-. 0.01). 4. During hypercapnia there was an increase in the ratio of Pi to NTP from 1.09 .+-. 0.08 to 1.47 .+-. 0.06 (P < 0.001) and a decrease in the ratio PCr/Pi from 1.60 .+-. 0.08 to 0.93 .+-. 0.04 (P < 0.001). There was a linear correlation between Pi/NTP and brain pHi. 5. Alterations in arterial PCO2 had no significant effect on the molar ratio of glucose to oxygen uptake by the brain, which remained close to unity. 6. The change in brain pHi observed during hypercapnia can be accounted for by the known physico-chemical buffering capacity of brain tissue. Homoeostasis of brain pHi during hypocapnia provides further evidence that additional regulatory mechanisms operate in these circumstances. 7. The observed changes in PCr and Pi can be accounted for in part by the [H+] dependence of the creatine kinase reaction.