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

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.