Simultaneous 31P- and 1H-Nuclear Magnetic Resonance Studies of Hypoxia and Ischemia in the Cat Brain

• Published in: Journal of cerebral blood flow and metabolism 1987-10, Vol.7 (5), p.543-551
• Main Authors: Gyulai, Laszlo, Schnall, Mitchell, McLaughlin, Alan C., Leigh, John S., Chance, Britton
• Format: Article
• Language: English
• Subjects: Adenosine Triphosphate - metabolism; Animals; Applied sciences; Biological and medical sciences; Brain - metabolism; Brain - physiopathology; Brain Ischemia - metabolism; Brain Ischemia - physiopathology; Cats; Electroencephalography - methods; Exact sciences and technology; Hydrogen; Hypoxia - metabolism; Hypoxia - physiopathology; Lactates - metabolism; Lactic Acid; Magnetic Resonance Spectroscopy; Male; Medical sciences; Nervous system involvement in other diseases. Miscellaneous; Neurology; Other techniques and industries; Phosphocreatine - metabolism; Phosphorus
• ISSN: 0271-678X; 1559-7016
• DOI: 10.1038/jcbfm.1987.103

The objective of this study was to evaluate simultaneous 31P/1H nuclear magnetic resonance (NMR) spectroscopy as a technique for monitoring and correlating changes in brain energy metabolism during hypoxia and ischemia. Five cats were studied with a protocol that involved 20 min of hypoxia (Pao2 20 mm), 60 min of recovery, 10 min of hypoxia with relative ischemia (bilateral carotid occlusion, PaO2 20 mm), and 60 min of recovery. Bifrontal and biparietal electrocorticograms (ECoG) were monitored continuously during the entire protocol. The results demonstrate that the degree of metabolic response is different in individual cats, but a number of quantitative relationships between metabolic parameters are consistently observed for all cats. First, there is agreement between increases in lactate and changes in intracellular pH; the observed relationship corresponds to an in vivo cerebral buffer capacity of 29 μmol/g/pH unit. Second, the delayed recovery of PCr is due to the effect of metabolic acidosis on the creatine kinase equilibrium and not to a delayed recovery of the ATP/ADP ratio. Third, the observed rate of lactate clearance from the cell is zero-order (k = 0.36 μmol/g/min) for lactate levels >5 μm/g and may be composed of both lactate efflux from the cell and lactate oxidation.