Effect of posttraumatic hypoventilation on cerebral energy metabolism.
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.
Andersen
B J
BJ
Richard Roland Reynolds Neurosurgical Research Laboratories, Department of Surgery, Richmond, Virginia.
Unterberg
A W
AW
Clarke
G D
GD
Marmarou
A
A
D000818:Animals; D001921:Brain / Q000378:metabolism*; D001930:Brain Injuries / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism; D007040:Hypoventilation / Q000209:etiology* / Q000378:metabolism; D010101:Oxygen Consumption; D013997:Time Factors; D014949:Wounds, Nonpenetrating / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology
D005947:Glucose