Cerebral Circulation of Blood: Features and Regulation | Biology

In this article we will discuss about:- 1. General Features of Cerebral Circulation 2. Regulation of Cerebral Blood Flow 3. Measurement.

General Features of Cerebral Circulation:

1. Adult brain weighs 1400 gm (2% of body weight), 60% is composed of white matter, 40% is composed of grey matter.

2. Cerebral blood flow is 750 ml/min or 50-60 ml/ min/100 gm.

3. Cerebral O₂ consumption is 3.3 ml/min/100 g. Since grey matter consists of cell bodies, O₂ consumption is more here, i.e. 3 ml/min/100 gm white matter consists of only axons and so O₂ consumption is less, about 0.3 ml/min/100 gm.

4. Total O₂ consumption is 42-49 ml/min, which is nearly 17-20% of the total O₂ consumption of the body (250 ml).

5. Brain tissue is highly susceptible to O₂ lack. Sudden cessation of O₂ supply or blood flow to the brain results in loss of consciousness within 10 sec and deprivation of O₂ for 3-4 min results in irreversible brain damage. Minimum level of blood flow is essential for maintaining brain function. Critical blood flow level is approximately 18 ml/min/100 gm, i.e. flow less than this level causes uncon­sciousness.

6. Glucose is the chief source of energy for the brain. Hence, hypoglycemia also leads to damage of the brain tissue.

7. Cranium contains the brain (1400 gm), blood (75 ml) and CSF (75 ml). All these three are incompressible because of rigid cranium. Hence, the contents of the cranial cavity remain constant. This is known as Monro-Kellie doctrine.

Regulation of Cerebral Blood Flow:

CBF is tightly regulated to meet the brain’s metabolic demands. Too much blood (a condition known as hyperemia) can raise intracranial pressure (ICP), which can compress and damage delicate brain tissue. Too little blood flow (ischemia) results if blood flow to the brain is below 18 to 20 ml per 100 g per minute, and tissue death occurs if flow dips below 8 to 10 ml per 100 g per minute.

CBF is equal to the cerebral perfusion pressure (CPP) divided by the cerebrovascular resistance (CVR): CBF = CPP/CVR.

Control of CBF is considered in terms of the factors affecting CPP and the factors affecting CVR.

i. Cerebral Perfusion Pressure or CPP:

CPP is the net pressure gradient causing blood flow to the brain (brain perfusion). It is defined as the differ­ence between mean arterial and intracranial pressures.

CPP = MAP – ICP

Under normal circumstances cerebral blood flow is relatively constant due to protective auto-regulation. (MAP between 60 to 150 mm Hg and ICP about 10 mm Hg).

Outside of the limits of auto-regulation, raising MAP raises CPP and raising ICP lowers it (this is one reason that increasing ICP in traumatic brain injury is potentially deadly). CPP is normally between 70 and 90 mm Hg in an adult human, and cannot go below 70 mm Hg for a sustained period without causing ischemic brain damage.

ii. Cerebrovascular Resistance:

Cerebrovascular resistance can be modulated by local-chemical and endothelial factors, by autacoids, and by release of transmitters from perivascular nerves.

a. Local-chemical factors such as H⁺, K⁺, CO₂, adeno­sine, and osmolarity are involved in the regulation of cerebrovascular resistance during cortical activation and under pathological conditions such as hypoxia or ischemia. They cause vasodilation of cerebral vessels.

b. Endothelial factors such as thromboxane A2, endothelin (ET), endothelium derived constrictor factor and endothelium derived relaxing [EDRF, identified as nitric oxide (NO)] or hyperpolarizing (EDHF) factor, and prostacyclin (PGI₂), can be released by physical stimuli such as shear stress or hemorrhage, by autacoids, by neurotransmitters, and by cytokines. Several of these factors (NO, PGI₂, ET) can also be released from neurons and astrocytes thus enabling a coupling between parenchymal function and flow.

c. Autacoids like histamine, bradykinin, eicosanoids, and free radicals influence cerebrovascular resis­tance, capacitance vessels and the permeability of the blood-brain barrier under pathological condi­tions. They are released by trauma, ischemia, sei­zures and inflammation and causes vasodilation.

d. Neural control: Cerebral arteries are innervated by several systems. The sympathetic-noradrenergic fibers originate from the superior cervical ganglion. By releasing the constricting transmitter’s norepine­phrine and neuropeptide Y, this system extends the range of auto-regulation. The parasympathetic cholinergic system with the dilating transmitter’s acetylcholine and vasoactive intestinal polypeptide may prevent ischemia.

Measurement of Cerebral Blood Flow:

1945 Kety and Schmidt described a method of quantifying cerebral blood flow in humans, based on the Fick principle that utilized nitrous oxide, a metabolically inert and highly lipid-soluble gas, as the tracer of blood flow.

A major advance toward the broad clinical application of cerebral blood flow measurement came with the substitution of radiolabeled ⁸⁵Kr for nitrous oxide and scintillation counting as the direct measure of tracer movement within the tissue. The latter measure being substituted for the difference of the arterial and venous concentrations of the tracer. This approach provided a regionality of blood flow deter­mination that was lacking in the global blood flow measures provided by nitrous oxide.

In recent years most centers have turned to intravenous bolus introduction of ¹³³Xe as a simpler means of delivering the tracer.

Single photon emission computed tomography (SPECT) imaging system for ¹³³Xe. SPECT CBF derived with radiolabeled isotopes today provides relatively high-resolution three-dimensional qualitative CBF imaging.

Diffusion imaging with magnetic resonance imaging provides information concerning the presence or absence of blood movement.

Direct monitoring of cortical blood flow is available today utilizing either thermal dilution or laser Doppler technologies.