Published in:
01-03-2008 | Experimental
Posttraumatic brain vulnerability to hypoxia-hypotension: the importance of the delay between brain trauma and secondary insult
Published in: Intensive Care Medicine | Issue 3/2008
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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.