Posttraumatic brain vulnerability to hypoxia-hypotension: the importance of the delay between brain trauma and secondary insult.

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  • Additional Information
    • Source:
      Publisher: Springer Verlag Country of Publication: United States NLM ID: 7704851 Publication Model: Print-Electronic Cited Medium: Print ISSN: 0342-4642 (Print) Linking ISSN: 03424642 NLM ISO Abbreviation: Intensive Care Med Subsets: MEDLINE
    • Publication Information:
      Publication: New York : Springer Verlag
      Original Publication: Berlin ; New York, Springer International.
    • Subject Terms:
      Brain Injuries/*complications ; Hypoxia, Brain/*etiology ; Intracranial Hypotension/*etiology; Animals ; Brain/blood supply ; Brain/metabolism ; Brain Edema/etiology ; Brain Edema/metabolism ; Brain Edema/physiopathology ; Brain Injuries/metabolism ; Brain Injuries/physiopathology ; Brain Injuries/therapy ; Cerebrovascular Circulation ; Disease Models, Animal ; Glucose/metabolism ; Glycerol/metabolism ; Hypoxia, Brain/metabolism ; Intracranial Hypotension/metabolism ; Lactic Acid/metabolism ; Male ; Oxygen/blood ; Oxygen/metabolism ; Pyruvic Acid/metabolism ; Rats ; Rats, Sprague-Dawley ; Time Factors
    • Abstract:
      Objective: To examine whether the effect of hypoxia-hypotension (HH) after traumatic brain injury (TBI) is affected by the delay between insults.
      Design: Thirty Sprague-Dawley rats were randomized into five groups: sham, TBI alone (trauma alone, impact-acceleration, 450 g weight drop from 1.8 m), HH alone (blood depletion, mean arterial pressure 40 mmHg, FIO2=10%, 15 min), TBI+early HH (TBI followed by HH, 45-min delay), and TBI+late HH (225-min delay). Cerebral perfusion pressure was continuously recorded. Brain microdialysis and PtiO2 probes were inserted stereotaxically into the right thalamus.
      Measurements and Results: After the HH period and for 60 min a significant increase in cerebral lactate-pyruvate ratio was observed in groups subjected to HH vs. TBI alone and sham groups (33.0+/-5.1 for HH alone and 51.9+/-6.7 for TBI+early HH vs. 16.7+/-2.4 for TBI alone at the same time, 27.6+/-4.4 for TBI+late HH vs. 13.1+/-1 for TBI alone at the same time). There was no significant difference in lactate-pyruvate ratio peaks between HH alone and TBI+late HH while it was higher in TBI+early HH. Similar results were obtained for cerebral glycerol. PtiO2 during HH phase did not differ between HH alone, TBI+early HH and TBI+late HH (respectively, 4.2+/-3.1, 4.9+/-5.7, and 2.9+/-1.8 mmHg).
      Conclusions: A 45-min delay between HH and TBI has important metabolic consequences while a 225-min delay has a similar effect as HH in a noninjured brain. The posttraumatic brain vulnerability to HH depends on the delay between cerebral aggressions.
    • Comments:
      Comment in: Intensive Care Med. 2008 Mar;34(3):402-4. doi: 10.1007/s00134-007-0889-3. (PMID: 17938886)
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    • Accession Number:
      33X04XA5AT (Lactic Acid)
      8558G7RUTR (Pyruvic Acid)
      IY9XDZ35W2 (Glucose)
      PDC6A3C0OX (Glycerol)
      S88TT14065 (Oxygen)
    • Publication Date:
      Date Created: 20071017 Date Completed: 20080930 Latest Revision: 20211020
    • Publication Date:
      20250114
    • Accession Number:
      10.1007/s00134-007-0863-0
    • Accession Number:
      17938889