Effect of posttraumatic hypoventilation on cerebral energy metabolism

B. J. Andersen, A. W. Unterberg, G. D. Clarke, A. Marmarou

Research output: Contribution to journalArticlepeer-review

44 Scopus citations

Abstract

Cerebral energy metabolism was studied in cats subjected to fluid-percussion brain trauma followed immediately by 30 minutes of controlled hypoventilation for the purpose of simulating a more realistic model of human head injury. The cerebral blood flow (CBF) and cerebral metabolic rates of oxygen (CMRO2) and glucose (CMRGl) were measured, with simultaneous phosphorus-31 magnetic resonance spectroscopy quantifications of cerebral tissue pH, phosphocreatine (PCr), and inorganic phosphate (Pi). Hypoventilation alone did not produce marked changes in CMRGl, tissue pH, or PCr:Pi ratios. When hypoventilation was combined with trauma, marked alterations in CBF, CMRGl, PCr:Pi ratio, and tissue pH were seen, indicating relative ischemia. The alterations of cerebral energy metabolism produced by combining trauma and hypoventilation are more severe than those caused by fluid-percussion trauma alone, and may provide a more realistic model of human head injury.

Original languageEnglish (US)
Pages (from-to)601-607
Number of pages7
JournalJournal of neurosurgery
Volume68
Issue number4
DOIs
StatePublished - Jan 1 1988

ASJC Scopus subject areas

  • Surgery
  • Clinical Neurology

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