Cerebrovascular resist – Vasodilators


Cerebral blood flow (CBF) is directly proportional to cerebral metabolic rate (CMR).  Cerebral perfusion pressure (CPP) is the difference between the mean arterial pressure (MAP) and intracranial pressure (ICP) or central venous pressure (CVP), whichever is greater.  Autoregulation maintains CBF relatively constant between a CPP of 50 and 150 mmHg in normotensive, healthy individuals.

In the systemic circulation, arterioles are typically the major site of vascular resistance; however, in the brain, both large arteries and small arterioles contribute significantly to vascular resistance.  Direct measure of the pressure gradient across different segments of the cerebral circulation found that the large extracranial vessels (internal carotid and vertebral) and intracranial pial vessels contribute 20-45% of cerebral vascular resistance; this large artery resistance attenuates changes in downstream microvascular pressure during increases in systemic arterial pressure. Thus, segmental vascular resistance in the brain is a protective mechanism that helps provide constant blood flow without pathologically increasing hydrostatic pressure that can cause vasogenic edema.

Several factors cause an increase in CBF, including increasing PaCO2 (>40 mmHg) and decreasing PaO2 (<50 mmHg). Various anesthetic agents have effects on CBF.  Most intravenous anesthetics reduce CBF and CMR in parallel (except for ketamine).  Most inhaled anesthetics (desflurane, sevoflurane, and isoflurane) produce cerebral vasodilation and result in dose-dependent increases in CBF at concentrations higher than 0.5 MAC.  A decrease in CMR is thought to counteract the vasodilation such that CBF is largely unchanged at concentrations less than 0.5 MAC.

Vasoactive agents may also have an effect on CBF.  Pure α1 agonists seem to have little direct effect on CBF.  Dexmedetomidine, an α2 agonist, has been shown to decrease CBF and CMR (likely in parallel).

β-agonists have little effect on cerebral vasculature in low doses; however, in high doses, they can cause an increase in CMR with accompanying increase in CBF.  There is evidence that this effect is enhanced in the setting of a defect in the BBB.  β-blockers have been variably reported to reduce or have no direct effect on CBF and cerebral metabolic rate (CMR); they could likely have an effect secondary to a change in cerebral perfusion pressure (CPP).



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  1. D D Heistad, M L Marcus, F M Abboud Role of large arteries in regulation of cerebral blood flow in dogs. J. Clin. Invest.: 1978, 62(4);761-8

  2. F M Faraci, D D Heistad Regulation of large cerebral arteries and cerebral microvascular pressure. Circ. Res.: 1990, 66(1);8-17