Abstract

In Response: We appreciate the comments of Drs. Kolbitsch and Benzer regarding our study [1]. Unfortunately, blood glucose levels in the control group were not available, because in this particular set of animals, which was studied prior to the other groups, blood glucose was not routinely determined. Otherwise, the experimental protocol these animals were subjected to was the same. The different blood glucose levels of the other experimental groups might be related to the anesthetic method used. For example, a higher blood glucose level has been found with isoflurane anesthesia compared with barbiturates in a number of experiments in rats [2,3]. Also, with fentanyl/nitrous oxide increased blood glucose levels were observed in rats compared with halothane anesthesia [4]. Hyperglycemia in focal cerebral ischemia results in more pronounced brain edema, larger infarct size, and a more severe neurologic deficit [5]. However, similar effects of elevated blood glucose in traumatic brain injury have not been established. As demonstrated by Combs et al. [6] in a similar model of a focal cold cerebral lesion in rats, an increase of blood glucose from 166 to 772 mg/100 mL did not result in more pronounced cerebral edema. In another study, administration of glucose to animals subjected to fluid percussion brain injury did not alter the formation of posttraumatic cerebral edema or worsen neurologic outcome, although blood glucose increased from 146 to 315 mg/100 mL [7]. Therefore, in view of the comparatively moderate increases in blood glucose with fentanyl or isoflurane in our experiments, an influence on brain edema formation seems unlikely. R. Murr, MD Department of Anesthesiology University of Munich D-81366 Munich, Germany L. Schurer, MD Department of Neurosurgery Klinikum Mannheim University of Heidelberg D-68167 Mannheim, Germany

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