The integration of real and virtual magnetic resonance imaging experiments in a single instrument.

We present the design of an integrated system for performing both real and virtual (simulated) magnetic resonance imaging (MRI) experiments. We emphasize the approaches used to maximize the level of integration and also the benefits that tight real-virtual integration brings for a scientific instrument. The system has been implemented for both low field (0.2 T) and high field (9.4 T) imaging systems. The simulations can run for any MRI experiment and we demonstrate the operation of the system for T(1), T(2), T(2) ( *), and diffusion contrasts.

Differential neuronal and glial metabolic response during hypothermia in an experimental animal model.

OBJECTIVE: To study the effect of hypothermia on metabolic compartmentalization in an animal model. METHODS: [1-(13)C] glucose, [2-(13)C] glucose, [3-(13)C] lactate, and [2-(13)C] acetate were infused into male Sprague-Dawley rats. The (13)C label was detected using (13)C-edited H magnetic resonance spectroscopy or (13)C magnetic resonance spectroscopy to determine the isotopic enrichment of both glutamate and glutamine. The infusion was carried out at either normothermia (37 degrees C) or hypothermia (31 degrees C). RESULTS: The [1-(13)C] glucose infusion during hypothermia resulted in decreased labeling of glutamate and glutamine consistent with decreased metabolism or the shunting of glucose through the pentose phosphate pathway. Unexpectedly, [2-(13)C] glucose infusion during hypothermia resulted in decreased labeling of glutamate but not glutamine, implying decreased neuronal but unaltered glial metabolism. The lactate and acetate infusion showed no temperature effect on labeling, indicating that the dampened neuronal metabolism occurred during glycolysis. CONCLUSION: The results may explain the mechanism of action of hypothermia by differentially preserving the protective metabolism in glia while selectively dampening neuronal metabolism.

Truncation of the krebs cycle during hypoglycemic coma.

There is a misconception that hypoglycemic nerve cell death occurs easily, and can happen in the absence of coma. In fact, coma is the prerequisite for neuronal death, which occurs via metabolic excitatory amino acid release. The focus on nerve cell death does not explain how most brain neurons and all glia survive. Brain metabolism was interrogated in rats during and following recovery from 40 min of profound hypoglycemia using ex vivo (1)H MR spectroscopy to determine alterations accounting for survival of brain tissue. As previously shown, a time-dependent increase in aspartate was equaled by a reciprocal decrease in glutamate/glutamine. We here show that the kinetics of aspartate formation during the first 30 min (0.36 +/- 0.03 micromol g(-1) min(-1)) are altered such that glutamate, via aspartate aminotransferase, becomes the primary source of carbon when glucose-derived pyruvate is unavailable. Oxaloacetate is produced directly from alpha-ketoglutarate, so that reactions involving the six-carbon intermediates of the tricarboxylic acid cycle are bypassed. These fundamental observations in basic metabolic pathways in effect redraw the tricarboxylic acid cycle from a tricarboxylic to a dicarboxylic acid cycle during hypoglycemia. The basic neurochemical alterations according to the chemical equilibrium of mass action augments flux through a truncated Krebs cycle that continues to turn during hypoglycemic coma. This explains the partial preservation of energy charge and brain cell survival during periods of glucose deficiency.