title: Posttraumatic brain vulnerability to hypoxia-hypotension: the importance of the delay between brain trauma and secondary insult.
abstract: OBJECTIVE
  To examine whether the effect of hypoxia-hypotension (HH) after traumatic brain injury (TBI) is affected by the delay between insults.
  
  
  METHODS
  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.
  
  
  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.
authors.affiliation: Département d'Anesthésie-Réanimation, Hôpital Bicêtre, AP-HP, 94276 Le Kremlin-Bicêtre, France. thgeeraerts@hotmail.com
authors.forename: Thomas
authors.initials: T
authors.lastname: Geeraerts
authors.forename: Arnaud
authors.initials: A
authors.lastname: Friggeri
authors.forename: Jean-Xavier
authors.initials: JX
authors.lastname: Mazoit
authors.forename: Dan
authors.initials: D
authors.lastname: Benhamou
authors.forename: Jacques
authors.initials: J
authors.lastname: Duranteau
authors.forename: Bernard
authors.initials: B
authors.lastname: Vigué
mesh_terms: D000818:Animals; D001921:Brain / Q000098:blood supply / Q000378:metabolism; D001929:Brain Edema / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D001930:Brain Injuries / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D002560:Cerebrovascular Circulation; D004195:Disease Models, Animal; D005947:Glucose / Q000378:metabolism; D005990:Glycerol / Q000378:metabolism; D002534:Hypoxia, Brain / Q000209:etiology* / Q000378:metabolism; D019585:Intracranial Hypotension / Q000209:etiology* / Q000378:metabolism; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D010100:Oxygen / Q000097:blood / Q000378:metabolism; D019289:Pyruvic Acid / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
chemical_list: D019344:Lactic Acid; D019289:Pyruvic Acid; D005947:Glucose; D005990:Glycerol; D010100:Oxygen