Abstract
The role of brain capillary endothelial cells in the reperfusion injury that follows transient global ischemia is not well understood. In a rat model of cardiac arrest and resuscitation, we observed an acute swelling of pericapillary astrocytes and accumulation of hypoxia-inducible factor (HIF1α). We found brainstem edema 1–2 days following reperfusion that was associated with elevated vascular endothelial growth factor (VEGF) localized to pericapillary astrocytes. We propose the hypothesis that HIF 1 α accumulating in response to oxidative stress during reperfusion upregulates VEGF. Elevated levels of VEGF lead to increased capillary permeability and hence vasogenic edema. As a result of brain stem vasogenic edema, critical autonomic functions such as respiration and blood pressure control may become compromised, increasing the risk of death during the first few days after resuscitation from cardiac arrest.
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