Pediatric research · 2013
Brain tissue oxygen monitoring identifies cortical hypoxia and thalamic hyperoxia after experimental cardiac arrest in rats.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
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Manole Mioara D, Kochanek Patrick M, Bayır Hülya, Alexander Henry, Dezfulian Cameron, Fink Ericka L, Bell Michael J, Clark Robert S B
Аннотация
BACKGROUND: Optimization of cerebral oxygenation after pediatric cardiac arrest (CA) may reduce neurological damage associated with the post-CA syndrome. We hypothesized that important alterations in regional partial pressure of brain tissue oxygen (PbO2) occur after resuscitation from CA and that clinically relevant interventions such as hyperoxia and blood pressure augmentation would influence PbO2.
METHODS: Cortical and thalamic PbO2 were monitored in immature rats subjected to asphyxial CA (9 or 12 min asphyxia) and sham-operated rats using oxygen sensors.
RESULTS: Thalamus and cortex showed similar baseline PbO2. Postresuscitation, there was early and sustained cortical hypoxia in an insult-duration dependent fashion. In contrast, thalamic PbO2 initially increased fourfold and afterwards returned to baseline values. PbO2 level was dependent on the fraction of inspired O2, and the response to oxygen was more pronounced after a 9 vs. 12 min CA. After a 12 min CA, PbO2 was modestly affected by blood pressure augmentation using epinephrine in the thalamus but not in the cortex.
CONCLUSION: After asphyxial pediatric CA, there is marked regional variability of cerebral oxygenation. Cortical hypoxia is pronounced and appears early, whereas thalamic hyperoxia is followed by normoxia. Compromised PbO2 in the cortex may represent a relevant and clinically measurable therapeutic target aimed at improving neurological outcome after pediatric CA.
METHODS: Cortical and thalamic PbO2 were monitored in immature rats subjected to asphyxial CA (9 or 12 min asphyxia) and sham-operated rats using oxygen sensors.
RESULTS: Thalamus and cortex showed similar baseline PbO2. Postresuscitation, there was early and sustained cortical hypoxia in an insult-duration dependent fashion. In contrast, thalamic PbO2 initially increased fourfold and afterwards returned to baseline values. PbO2 level was dependent on the fraction of inspired O2, and the response to oxygen was more pronounced after a 9 vs. 12 min CA. After a 12 min CA, PbO2 was modestly affected by blood pressure augmentation using epinephrine in the thalamus but not in the cortex.
CONCLUSION: After asphyxial pediatric CA, there is marked regional variability of cerebral oxygenation. Cortical hypoxia is pronounced and appears early, whereas thalamic hyperoxia is followed by normoxia. Compromised PbO2 in the cortex may represent a relevant and clinically measurable therapeutic target aimed at improving neurological outcome after pediatric CA.