Cerebral venous oxygen content as a measure of brain energy metabolism with increased intracranial pressure and hyperventilation.

In order to test the hypothesis that the cerebral arteriovenous oxygen difference (AVDO2) and venous oxygen content (VO2) could be used to monitor brain energy metabolism in the setting of increased intracranial pressure (ICP). 12 cats were studied with 31P-magnetic resonance spectroscopy. six cats were subjected to intracranial hypertension by cisternal infusion of saline. Energy failure occurred at an average AVDO2 of 8.4 +/- 3.2 vol% (+/- standard deviation) (range 4.7 to 14.7 vol%). The VO2 at the point of metabolic failure averaged 1.45 +/- 0.6 vol% and extended over a narrower range (1.0 to 2.9 vol%). In an additional six cats, ICP was raised to the threshold of metabolic failure and hyperventilation was then instituted (pCO2 10 to 18 torr). Five of the six cats experienced a drop in VO2 with hyperventilation. In two of these animals, hyperventilation resulted in a VO2 of 1.1 vol% or less and in metabolic failure as evidenced by a fall in phosphocreatine. It is concluded that a VO2 of less than 2 vol% is correlated with brain ischemia and that the safety of hyperventilation in the setting of increased ICP can be monitored by the use of VO2.

In vivo 31P nuclear magnetic resonance measurement of chronic changes in cerebral metabolites following neonatal intraventricular hemorrhage.

The purpose of this study was to determine whether cerebral metabolic changes occur after intraventricular hemorrhage in the newborn. Five babies with bilateral grade 3 to 4 intraventricular hemorrhage were compared with 15 preterm infants without intraventricular hemorrhage. Cerebral high-energy phosphorus metabolites and intracellular pH were measured with in vivo 31P nuclear magnetic resonance spectroscopy. Spectra were collected initially within the first 2 weeks of life, and then every other week until discharged from the hospital. The phosphocreatine to inorganic phosphate ratio and the phosphocreatine to adenosine triphosphate ratio were significantly lower in the group with intraventricular hemorrhage, but differences in intracellular pH were not significant. Differences between babies with and without intraventricular hemorrhage varied with postconceptional age: in those with intraventricular hemorrhage, the phosphocreatine to adenosine triphosphate ratio was decreased at all postconceptional ages, and the phosphocreatine to inorganic phosphate ratio was lower in babies with intraventricular hemorrhage and younger than 30 weeks. Results of this study confirm the presence of chronic metabolic changes following intraventricular hemorrhage which may exacerbate neurologic damage after intraventricular hemorrhage in the newborn.

An approach to the problem of metabolic heterogeneity in brain: ischemia and reflow after ischemia.

We have proposed that tissue metabolic failure during hypoxia or ischemia is related to the microheterogeneous distribution of tissue oxygen and not to failure of the creatine kinase equilibrium. This theory is based on the concept that sharp oxygen gradients exist in rapidly metabolizing tissue and that shifts in these gradients can place specific cells at risk for metabolic death while relatively adjacent cells escape unharmed; cells that are unharmed meet the steady-state requirements (V less than Vmax), those at risk do not (V greater than Vmax). Though it would seem that confirmation of such a hypothesis would require metabolic delineation at a high resolution, we have shown how 31P MRS provides information supporting this hypothesis. This possible use of MR spectroscopy to define microheterogeneous events suggests further clinical possibilities for this instrument in defining the rate of cell loss and the response to therapeutic interventions.