Cerebral metabolism after fluid-percussion injury and hypoxia in a feline model.
OBJECTIVE
Currently, there are no good clinical tools to identify the onset of secondary brain injury and/or hypoxia after traumatic brain injury (TBI). The aim of this study was to evaluate simultaneously early changes of cerebral metabolism, acid-base homeostasis, and oxygenation, as well as their interrelationship after TBI and arterial hypoxia.


METHODS
Cerebral biochemistry and O2 supply were measured simultaneously in a feline model of fluid-percussion injury (FPI) and secondary hypoxic injury. After FPI, brain tissue PO2 decreased from 33 +/- 5 mm Hg to 10 +/- 4 mm Hg and brain tissue PCO2 increased from 55 +/- 2 mm Hg to 81 +/- 9 mm Hg, whereas cerebral pH fell from 7.1 +/- 0.06 to 6.84 +/- 0.14 (p < 0.05 for all three measures). After 40 minutes of hypoxia, brain tissue PO2 and pH decreased further to 0 mm Hg and 6.48 +/- 0.28, respectively (p < 0.05), whereas brain tissue PCO2 remained high at 83 +/- 13 mm Hg. Secondary hypoxic injury caused a drastic increase in cerebral lactate from 513 +/- 69 microM/L to 3219 +/- 490 microM/L (p < 0.05). The lactate/glucose ratio increased from 0.7 +/- 0.1 to 9.1 +/- 2 after hypoxia was introduced. The O2 consumption decreased significantly from 18.5 +/- 1.1 microl/mg/hr to 13.2 +/- 2.1 microl/mg/hr after hypoxia was induced.


CONCLUSIONS
Cerebral metabolism, O2 supply, and acid-base balance were severely compromised ultra-early after TBI, and they declined further if arterial hypoxia was present. The complexity of pathophysiological changes and their interactions after TBI might explain why specific therapeutic attempts that are aimed at the normalization of only one component have failed to improve outcome in severely head injured patients.
Zauner
Alois
A
Division of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, Richmond, USA. Azauner@mednet.ucla.edu
Clausen
Tobias
T
Alves
Oscar L
OL
Rice
Ann
A
Levasseur
Joseph
J
Young
Harold F
HF
Bullock
Ross
R
D000136:Acid-Base Equilibrium / Q000502:physiology; D000818:Animals; D001921:Brain / Q000378:metabolism*; D001923:Brain Chemistry / Q000502:physiology; D001930:Brain Injuries / Q000378:metabolism*; D002245:Carbon Dioxide / Q000097:blood; D002415:Cats; D004195:Disease Models, Animal; D002534:Hypoxia, Brain / Q000378:metabolism*; D008297:Male; D008928:Mitochondria / Q000378:metabolism / Q000648:ultrastructure; D008933:Mitochondrial Swelling / Q000502:physiology; D010100:Oxygen / Q000097:blood
D002245:Carbon Dioxide; D010100:Oxygen