Unexpected reductions in regional cerebral perfusion during prolonged hypoxia

Hypoxia causes an increase in global cerebral blood flow, which maintains global cerebral oxygen delivery and metabolism. Yet neurological deficits are abundant under hypoxic conditions. We investigated regional cerebral microvascular responses to acute (2 h) and prolonged (10 h) poikilocapnic normobaric hypoxia. We found that 2 h of hypoxia caused an expected increase in frontal cortical grey matter perfusion, but unexpected perfusion decreases in regions of the brain normally associated with the "default mode" or "task negative" network. After 10 h in hypoxia, decreased blood flow to the major nodes of the default mode network became more pronounced and wide spread. Use of a hypercapnic challenge (5% CO₂) confirmed that these reduction in CBF from hypoxia were related to vasoconstriction. Our findings demonstrate steady-state deactivation of the default network under acute hypoxia, which become more pronounced over time. Moreover, these data provide a unique insight into the nuanced localized cerebrovascular response to hypoxia not attainable through traditional methods. That reduced perfusion was observed in the posterior cingulate and cuneal cortex, regions thought to play a role in declarative and procedural memory, provides an anatomical mechanism through which hypoxia may cause deficits in working memory.

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