Cerebral Intracellular Changes during Supercarbia: An in vivo 31P Nuclear Magnetic Resonance Study in Rats

• Published in: Journal of cerebral blood flow and metabolism 1985-12, Vol.5 (4), p.537-544
• Main Authors: Litt, Lawrence, González-Méndez, Ricardo, Severinghaus, John W., Hamilton, William K., Shuleshko, Julia, Murphy-Boesch, Joseph, James, Thomas L.
• Format: Article
• Language: English
• Subjects: Adenosine Diphosphate - metabolism; Adenosine Triphosphate - metabolism; Animals; Biological and medical sciences; Blood Gas Analysis; Brain - metabolism; Extracellular Space - metabolism; Hydrogen-Ion Concentration; Hypercapnia - metabolism; Magnetic Resonance Spectroscopy; Medical sciences; Nervous system involvement in other diseases. Miscellaneous; Neurology; Phosphocreatine - metabolism; Phosphorus; Rats; Rats, Inbred Strains; Space life sciences
• ISSN: 0271-678X; 1559-7016
• DOI: 10.1038/jcbfm.1985.81

31P nuclear magnetic resonance (NMR) spectroscopy was used noninvasively to measure in vivo changes in intracellular pH and intracellular phosphate metabolites in the brains of rats during supercarbia (Paco2 ⩾ 400 mm Hg). Five intubated rats were mechanically ventilated with inspired gas mixtures containing 70% CO2 and 30% O2. Supercarbia in the rat was observed to cause a greater reduction in cerebral intracellular pH (pHi) and increase in Pco2 than observed in other experiments with rats after 15 min of global ischemia. Complete neurologic and metabolic recovery was observed in these animals, despite an average decrease in pH; of 0.63 ± 0.02 pH unit during supercarbia episodes that raised Paco2 to 490 ± 80 mm Hg. No change was observed in cerebral intracellular ATP and only a 25% decrease was detected in phosphocreatine. The concentration of free cerebral intracellular ADP, which can be calculated if one assumes that the creatine kinase reaction is in equilibrium, decreased to approximately one-third of its control value. The calculated threefold decrease in the concentration of free ADP and twofold increase in the cytosolic phosphorylation potential suggest that there is increased intracellular oxygenation during supercarbia. Because a more than fourfold increase in intracellular hydrogen ion concentration was tolerated without apparent clinical injury, we conclude that so long as adequate tissue oxygenation and perfusion are maintained, a severe decrease in intracellular pH need not induce or indicate brain injury.