Abstract 14: Magnetic Resonance Characterization of Postresuscitation Hyperoxia-Induced Vasoconstriction and Neuronal Injury
Background: Cerebral perfusion is usually compromised after cardiac arrest and cardiopulmonary resuscitation (CPR). Hyperoxia has been reported to decrease cerebral blood flow. Post-CPR hyperoxia is associated with poor prognosis. We therefore sought to characterize the effects of hyperoxia on cerebral vasculature and neuronal injury in the post-resuscitation phase.
Methods: In an established rat model of asphyxia cardiac arrest and CPR, 100% O2 was employed in the post-resuscitation phase. Magnetic resonance (MR) imaging of the brain was done at baseline, after CPR and in hyperoxia sham control using a 7T PharmaScan 70/16 MR scanner with an active shielding gradient. Time-of-flight MR angiography (TOF MRA) was performed for demonstration of cerebral vasculature, and MR spectroscopy (MRS) done for measurement of cerebral metabolites.
Results: After cardiac arrest and CPR, the arterial diameter of the circle of Willis was reduced to about half that of baseline. The visible cerebral vasculature on TOF MRA was significantly decreased compared to baseline. In hyperoxia sham control, the arterial diameter was slightly reduced but the cerebral vasculature was relatively preserved. N-acetylaspartate (NAA), a reliable indicator of neuronal viability on MRS, decreased significantly after CPR in hyperoxic reperfusion group. In contrast, alanine and lactate increased remarkably after CPR, suggesting significant ischemia-reperfusion injury of the brain tissue.
Conclusion: Hyperoxic reperfusion in the post-resuscitation phase results in significant cerebral vasoconstriction. This leads to significant neuronal injury and may adversely impact neurological outcomes.
- Cerebrovascular circulation
- Cardiopulmonary resuscitation
- Magnetic resonance imaging
- Magnetic resonance spectroscopy
- © 2012 by American Heart Association, Inc.