Cerebral metabolism after fluid-percussion injury and hypoxia in a feline model

Alois Zauner, Tobias Clausen, Oscar L. Alves, Ann Rice, Joseph Levasseur, Harold F. Young, Ross Bullock

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Object. 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 μM/L to 3219 ± 490 μM/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 μl/mg/hr to 13.2 ± 2.1 μl/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.

Original languageEnglish
Pages (from-to)643-649
Number of pages7
JournalJournal of Neurosurgery
Volume97
Issue number3
StatePublished - Sep 1 2002
Externally publishedYes

Fingerprint

Percussion
Felidae
Brain Hypoxia
Wounds and Injuries
Brain Injuries
Lactic Acid
Acid-Base Equilibrium
Brain
Biochemistry
Homeostasis
Head
Glucose
Acids
Traumatic Brain Injury
Hypoxia

Keywords

  • Brain chemistry
  • Cat
  • Cerebral metabolism
  • Hypoxia
  • Traumatic brain injury

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Zauner, A., Clausen, T., Alves, O. L., Rice, A., Levasseur, J., Young, H. F., & Bullock, R. (2002). Cerebral metabolism after fluid-percussion injury and hypoxia in a feline model. Journal of Neurosurgery, 97(3), 643-649.

Cerebral metabolism after fluid-percussion injury and hypoxia in a feline model. / Zauner, Alois; Clausen, Tobias; Alves, Oscar L.; Rice, Ann; Levasseur, Joseph; Young, Harold F.; Bullock, Ross.

In: Journal of Neurosurgery, Vol. 97, No. 3, 01.09.2002, p. 643-649.

Research output: Contribution to journalArticle

Zauner, A, Clausen, T, Alves, OL, Rice, A, Levasseur, J, Young, HF & Bullock, R 2002, 'Cerebral metabolism after fluid-percussion injury and hypoxia in a feline model', Journal of Neurosurgery, vol. 97, no. 3, pp. 643-649.
Zauner A, Clausen T, Alves OL, Rice A, Levasseur J, Young HF et al. Cerebral metabolism after fluid-percussion injury and hypoxia in a feline model. Journal of Neurosurgery. 2002 Sep 1;97(3):643-649.
Zauner, Alois ; Clausen, Tobias ; Alves, Oscar L. ; Rice, Ann ; Levasseur, Joseph ; Young, Harold F. ; Bullock, Ross. / Cerebral metabolism after fluid-percussion injury and hypoxia in a feline model. In: Journal of Neurosurgery. 2002 ; Vol. 97, No. 3. pp. 643-649.
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abstract = "Object. 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 μM/L to 3219 ± 490 μM/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 μl/mg/hr to 13.2 ± 2.1 μl/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.",
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