The brain requires a large amount of oxygen and glucose to meet its high metabolic demand. Therefore, its circulation has structural and functional adaptations to ensure a consistently high blood flow is maintained. Any interruptions to this supply will lead to a loss of consciousness in a few seconds and irreversible damage to neurones after 4 minutes. The brain is just one of many organs to have a specialised circulation.
This article will explore the structural and functional adaptations of the brain’s circulation.
Circle of Willis – anastomoses between the basilar and internal carotid arteries. It provides collateral blood flow, protecting the brain against ischemia. This means that even if one artery is damaged, blood flow is not compromised.
Blood-brain barrier – a highly selective barrier between the systemic circulation and the brain’s extracellular fluid formed by endothelial cells. It is permeable to lipophilic molecules such as O2 and CO2 and impermeable to lipid insoluble molecules like K+ and catecholamines.
Its main function is to protect the brain from potentially harmful neurotoxins and helps prevent infection from spreading to the brain (causing encephalitis).
This mechanism regulates local blood flow to the brain by allowing the blood vessel diameter to change with blood pressure. When pressure rises, vasoconstriction occurs to restrict the flow of blood. When blood pressure decreases, blood vessels dilate to increase blood flow.
This keeps cerebral blood flow relatively constant when there are changes in blood pressure. It begins to fail when mean arterial blood pressure falls below 50mmHg as the vessels cannot dilate any further. This reduction in blood flow causes syncope (fainting).
This mechanism also regulates local blood flow to the brain by allowing the blood vessel diameter to change in response to changes in the partial pressure of arterial CO2.
Metabolically active tissues may produce local hypercapnia (raised CO2) when their activity exceeds their blood supply. Therefore hypercapnia is a sign that the blood and oxygen supply is inadequate. This causes vasodilation to increase blood flow and supply the tissues that have a higher oxygen demand. Conversely, in hypocapnia, vasoconstriction occurs.
Raised intracranial pressure, such as in the case of a cerebral tumour or haemorrhage, can impair cerebral blood flow as it pushes against blood vessels and narrows their lumens.
When this occurs, it is detected by vasomotor control regions in the brainstem. This triggers an increase in the sympathetic vasomotor activity. An increase in sympathetic activity results in peripheral vasoconstriction, an increase in heart rate and force of contraction. This raises the arterial blood pressure to force the blood vessels to dilate and maintain adequate cerebral blood flow.
The increased blood pressure is detected by baroreceptors (mechanoreceptors which sense arterial pressure changes) in the aortic arch and carotid sinus. Baroreceptors increase the vagal tone to the sino-atrial node of the heart. This produces bradycardia (slow heart rate).
Additionally, as the intracranial pressure rises, the brainstem is compressed, resulting in an irregular breathing pattern. Therefore, clinically, hypertension combined with bradycardia and irregular breathing indicates high intracranial pressure.
Clinical Relevance – Panic Attacks
Panic attacks can cause an individual to hyperventilate. This causes hypocapnia as CO2 is being blown out faster than its production rate. The resulting hypocapnia causes cerebral vasoconstriction via metabolic autoregulation, reducing blood flow (and therefore oxygen and glucose) to the brain. Therefore, the brain tissue is not being perfused sufficiently to maintain consciousness. This causes syncope.