Demonstrates reduced cerebral blood flow in mice after carotid artery occlusion, suggesting impaired blood vessel function.
In this rUCCAO model, the principal hemodynamic deficit is a selective impairment in vasodilation, unmasked by sevoflurane, rather than sustained hypoperfusion. This identifies compromised cerebrovascular reactivity as a key pathophysiological alteration post-carotid occlusion.
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Hao et al. (2026) studied this question.
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