Mechanisms of Cerebral Vasoconstriction
Basic, Organ-Based and Clinical Sciences
There are several factors that influence vasoconstriction of the cerebral vascular bed. Perhaps the most notable is the carbon dioxide (PaCO2). Hypocapnia, via an increase in perivascular pH, will cause vasoconstriction such that on average, each 7.5 mmHg change in PaCO2 will produce a change of 15 mL/100g/min in CBF. The elevated pH in the extracellular space and CSF will be buffered by a compensatory decline in bicarbonate over 6 hours. Vasoconstriction and reduction in cerebral blood flow and volume may be a desired effect; however, care should be taken to avoid dangerously low cerebral blood flow and vasoconstriction that can lead to ischemia.
Hyperoxia (PaO2 >112 mmHg) can also induce cerebral vasoconstriction, thought to be an adaptation to protect the brain from elevated PaO2 and oxygen free radicals. Autonomic nervous system stimulation has effects on the cerebral vasculature, predominantly the larger vessels, and vasoconstriction is produced by α2 receptor stimulation. Other neurogenic pathways play a role in the autoregulation of cerebral blood flow, including serotonin, dopamine, substance P, and neuropeptide Y.
Flow-metabolism coupling is an important component of cerebral blood flow regulation. Hypothermia decreases CMRO2 and subsequent cerebral blood flow via vasoconstriction. Metabolic factors such as free Ca2+, Thromboxane A2 (via arachidonate), and Endothelin (vascular smooth muscle endothelin A receptors) all have demonstrated vasoconstrictive effects.