Effect of posttraumatic hypoventilation on cerebral energy metabolism

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

Producción científica: Articlerevisión exhaustiva

47 Citas (Scopus)


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.

Idioma originalEnglish (US)
Páginas (desde-hasta)601-607
Número de páginas7
PublicaciónJournal of neurosurgery
EstadoPublished - 1988

ASJC Scopus subject areas

  • Clinical Neurology
  • Surgery


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