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.
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.
Authors: R S Clark; P M Kochanek; C E Dixon; M Chen; D W Marion; S Heineman; S T DeKosky; S H Graham Journal: J Neurotrauma Date: 1997-04 Impact factor: 5.269
Authors: John H Chi; M Margaret Knudson; Mary J Vassar; Mary C McCarthy; Michael B Shapiro; Susan Mallet; John J Holcroft; Hugh Moncrief; Jennifer Noble; David Wisner; Krista L Kaups; Lynn D Bennick; Geoffrey T Manley Journal: J Trauma Date: 2006-11
Authors: Konstantin Salci; Per Enblad; Michel Goiny; Charles F Contant; Ian Piper; Pelle Nilsson Journal: Ups J Med Sci Date: 2010-11 Impact factor: 2.384
Authors: Massimo Antonelli; Elie Azoulay; Marc Bonten; Jean Chastre; Giuseppe Citerio; Giorgio Conti; Daniel De Backer; François Lemaire; Herwig Gerlach; Johan Groeneveld; Goran Hedenstierna; Duncan Macrae; Jordi Mancebo; Salvatore M Maggiore; Alexandre Mebazaa; Philipp Metnitz; Jerôme Pugin; Jan Wernerman; Haibo Zhang Journal: Intensive Care Med Date: 2009-01-06 Impact factor: 17.440