vasoreactivity

Vasoreactivity refers to the ability of blood vessels to change their diameter and hence regional blood flow in response to a vasoactive stimulus. It is commonly discussed in relation to cerebral circulation, where it describes how cerebral arteries dilate or constrict in response to triggers such as changes in carbon dioxide levels, pharmacologic challenges, or neural activity.

The governing mechanisms involve vascular smooth muscle tone, endothelial function, and neurovascular coupling. Carbon dioxide is a potent endogenous vasodilator: rising CO2 or falling pH in brain tissue leads to relaxation of smooth muscle and increased blood flow. Endothelial factors such as nitric oxide, prostacyclin, and endothelin modulate these responses, and autoregulatory mechanisms maintain stable flow across blood pressure ranges. Vasoreactivity is thus a composite readout of endothelial integrity, smooth muscle reactivity, and metabolic signaling.

Assessment methods vary by modality. In clinical research and practice, cerebral vasoreactivity is often evaluated with a CO2 challenge (breath-holding or rebreathing) while measuring cerebral blood flow or velocity with transcranial Doppler or perfusion imaging. Imaging approaches include BOLD fMRI, arterial spin labeling MRI, or positron emission tomography to quantify percent change in flow per unit CO2. Pharmacologic challenges, such as acetazolamide or adenosine, provide a controlled stimulus when physiological challenges are impractical.

Clinical relevance centers on cerebrovascular reserve: reduced vasoreactivity can indicate impaired endothelial or smooth muscle function and is associated with higher stroke risk, carotid stenosis, moyamoya disease, cerebral small vessel disease, and certain dementias. It also informs risk assessment for anesthesia and planning of revascularization strategies. Vasoreactivity is a versatile concept applied to other circulations, including coronary and pulmonary vasculature, where it aids in diagnosing and guiding treatment.