This study published in 2014 provides an excellent review of the physiological mechanisms of cerebral blood flow regulation (open access):
Willie CK et al. Integrative regulation of human brain blood flow. J Physiol. 2014 Mar 1;592(5):841-59. doi: 10.1113/jphysiol.2013.268953.
Their list of references includes a very exhaustive list of studies conducted on this topic.
This study provides a figure which actually gives a good overview of the mechanisms of CBF regulation:
Here a small extract of the legend:
First, they give a small description of the brain vasculature
The central figure depicts the cerebrovasculature, comprised of two
pairs of large arteries that branch from the sublavian arteries, i.e.
the internal carotid arteries (ICAs) that carry ∼70% of total cerebral
blood flow (CBF) and the vertebral arteries (VAs) that distribute ∼30%
of total CBF to the brainstem, cerebellum and occipital cortex. The
internal carotid arteries and vertebral arteriess anastomose to form
the circle of Willis before branching out into the main intracerebral
arteries that ramify extensively en route to the brain surface. At the
surface, the vessels form a dense network of highly vasoactive
arterioles within the pia mater before they penetrate into the cortex
(inlay II).
Then they explain the role of intracranial pressure in the regulation of CBF
The driving pressure in this system is the cerebral perfusion pressure
(CPP) that is determined by the difference between mean arterial
pressure (MAP) and intracranial pressure (ICP), in conditions where
central venous pressure (CVP) is lower than ICP. In these conditions,
MAP approximates CPP. As a result of the enclosed nature of the skull,
ICP acts as a Starling resistor for cerebral venous outflow, a
mechanism that is likely to be of greater importance with marked
elevations in ICP or CVP, or both.
Cerebral arteries are the main actors in maintaining brain perfusion and react to changes in blood gases and to changes in perfusion pressure. Similarly, the pial vessels respond to changes in CPP, arterial partial pressures of O2 and CO2. Inlay III of their figure provides a good overview of the plial changes in response to blood gas alterations.
