Sevoflurane-induced hemispheric cerebral blood flow reduction in mice with revived global perfusion after carotid artery occlusion.

BACKGROUND

Carotid artery disease (CAD) presents a significant risk for ischemic stroke. Understanding the pathophysiological changes following carotid artery occlusion, particularly regarding cerebral blood flow (CBF) and cerebrovascular reactivity (CVR), is essential for developing targeted treatments.

METHODS

We utilized right unilateral common carotid artery occlusion (rUCCAO) in adult male C57BL/6 J mice to model CAD's pathophysiology. CBF was assessed using awake animal functional magnetic resonance imaging (fMRI) to avoid anesthetic interference. Sevoflurane and dexmedetomidine were used to compare their effects on hemodynamic responses post-occlusion. Neurological assessments were conducted post-surgery and post-fMRI. Cerebrovascular reactivity was inferred from hemispheric CBF variations.

RESULTS

No acute neurological disorders or cerebral infarctions were observed following rUCCAO. Awake fMRI at 7 days post-occlusion revealed no significant difference in global or hemispheric CBF between rUCCAO and sham mice. Anesthetized conditions with sevoflurane demonstrated compromised vasodilation in the ipsilateral hemisphere. In contrast, dexmedetomidine did not elicit CBF variations, suggesting an intact response to vasoconstrictors and impaired vasodilatory reactivity post-occlusion.

CONCLUSION

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.