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October 15, 2007
9:00 AM - 11:00 AM
Room Hall D, Area E,
HBO Alleviates Brain Injury and Improves Glucose Metabolism and Reduces Glutamate Release
Zhong-jin Yang, M.D., Yan Xie, M.D., Gerardo M. Bosco, M.D., Enrico M. Camporesi, M.D.
Anesthesiology, Upstate Medical University, Syracuse, New York
Numerous studies have shown that disturbed glucose metabolism and excessively increased extracellular concentration of glutamate due to cerebral ischemia provokes neuronal cell death. Others and our previous studies showed that hyperbaric oxygen (HBO2) alleviated focal ischemia-reperfusion brain injury. We hypothesized that the alleviation of focal brain injury by HBO2 may be associated with improved glucose metabolism and decreased glutamate release. In vivo microdialysis was used in the present study to examine the effect of HBO2 on 1) extracellular concentration of glucose, pyruvate and lactate; and 2) extracellular concentration of glutamate during middle cerebral artery occlusion (MCAO) and reperfusion in anesthetized male Sprague-Dawley rats. Probes were inserted with precise stereotaxic coordinates in the Striatum. Focal cerebral ischemia was induced with a surgically placed 4.0 polypropylene suture, causing reversible intraluminal occlusion of MCA. Control rats (n=8) were subjected to one-hour ischemia. Study rats (n=8) were treated with HBO2 (2.8 ATA, 100% O2) 15 minutes after ischemia was established for 1 hr and then returned to room air during 2 h reperfusion. Sham rats (n=6) were treated with HBO2 without MCAO. Artificial CSF was perfused at 1µl/min. The samples were continuously collected at 15-min intervals. Glucose, pyruvate, lactate and glutamate were analyzed using CMA 600 analyzer. The infarct size was determined by 2% TTC stain. One way ANOVA with Tukey's join tests and Fisher's pair wise tests were used to analyze the data. Results were considered significantly different at a value of p< 0.05.

Infarct size was significantly less in HBO2 group than in Control group, being 17.5±3.0% and 27.0± 6.0%, respectively (p<0.05%). There were no differences in the baseline levels of glucose, pyruvate, lactate and glutamate among groups. MCAO induced significant increase in the concentration of lactate and pyruvate and reached a peak at 30 min, being approximately 2-fold and 4-fold of baseline levels respectively; and maintained at elevated levels during reperfusion. The concentration of glucose decreased significantly in both Study and Control groups during ischemia period. During reperfusion phase, glucose rapidly returned to baseline in HBO group. In Control group, glucose continued to decrease and reached to approximately 20% of baseline level at the end of the experiment. The level of glutamate increased approximately 2 times during reperfusion phase and maintained at this high level in Control group. In the HBO2 treated rats, there was no significant changes in glutamate levels during ischemia and reperfusion periods.

The present study shows that HBO2, when administered early during ischemia, offers significant neuroprotection in this experimental transient focal cerebral ischemia-reperfusion rat model. Improved glucose metabolism and decreased glutamate release may contribute to the protective effect of HBO2 in brain ischemia-reperfusion injury.

Anesthesiology 2007; 107: A1134