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J Cereb Blood Flow Metab. 2018 Jan;38(1):17-37. doi: 10.1177/0271678X17742548. Epub 2017 Nov 14.

Cerebral artery myogenic reactivity: The next frontier in developing effective interventions for subarachnoid hemorrhage.

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1 Department of Physiology, University of Toronto, Toronto, Canada.
2 Toronto Centre for Microvascular Medicine at TBEP, University of Toronto, Toronto, Canada.
3 Heart & Stroke/Richard Lewar Centre of Excellence for Cardiovascular Research, University of Toronto, Toronto, Canada.


Aneurysmal subarachnoid hemorrhage (SAH) is a devastating cerebral event that kills or debilitates the majority of those afflicted. The blood that spills into the subarachnoid space stimulates profound cerebral artery vasoconstriction and consequently, cerebral ischemia. Thus, once the initial bleeding in SAH is appropriately managed, the clinical focus shifts to maintaining/improving cerebral perfusion. However, current therapeutic interventions largely fail to improve clinical outcome, because they do not effectively restore normal cerebral artery function. This review discusses emerging evidence that perturbed cerebrovascular "myogenic reactivity," a crucial microvascular process that potently dictates cerebral perfusion, is the critical element underlying cerebral ischemia in SAH. In fact, the myogenic mechanism could be the reason why many therapeutic interventions, including "Triple H" therapy, fail to deliver benefit to patients. Understanding the molecular basis for myogenic reactivity changes in SAH holds the key to develop more effective therapeutic interventions; indeed, promising recent advancements fuel optimism that vascular dysfunction in SAH can be corrected to improve outcome.


Cerebral blood flow; cystic fibrosis transmembrane conductance regulator (CFTR); microvascular dysfunction; myogenic vasoconstriction; tumor necrosis factor

[Available on 2019-01-01]

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