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Of mice and men: essential considerations in the translation of collateral therapeutics.

To the Editor:

Shin and colleagues detail an elegant study of collateral perfusion in the ischemic penumbra of mice treated with induced hypertension after distal middle cerebral artery occlusion (MCAO).1 Using optical imaging techniques, they demonstrate that early augmentation of systemic blood pressure with phenylephrine after MCAO improves collateral flow from ipsilateral leptomeningeal branches of the anterior and posterior cerebral arteries. Such collateral perfusion is noted to markedly improve cerebral blood flow (CBF) in penumbra and core, with associated enhancement of oxygenation and cerebral metabolic rate of oxygen in these ischemic regions. After prompt reversal of distal MCAO, infarct size is reduced by induced hypertension in concentric fashion around a focus emanating from the site of distal MCAO. There are subtle yet critical details embedded in this sophisticated cerebrovascular pathophysiology experiment that must be considered regarding the potential of induced hypertension and other therapeutic approaches using collateral perfusion in acute ischemic stroke patients.2

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