ABSTRACT
Cerebral autoregulation, the physiological capability to regulate cerebral blood flow, may be assisted by short-term mean arterial pressure control via baroreflex, which, among several effects, modulates total peripheral resistance. It is unclear, however, whether the resistance of the head and neck vasculatures is also affected by baroreflex and whether these extracranial vessels assist autoregulation. Since sensing technologies such as functional Near-Infrared Spectroscopy and noninvasive intracranial pressure monitoring by strain gauge may be influenced by superficial tissue, it is clinically relevant to understand the relations between intracranial and extracranial hemodynamics. Therefore, we created an autoregulation model consisting of arteries and arterioles regulated by the intralumial pressure and microcirculation regulated by local blood flow. As the first critical step to quantify the signal deterioration introduced by the extracranial circulation on superficial sensors, the extracranial peripheral circulation of the head and neck and baroreflex regulation of the peripheral vasculature and of heart rate were also included. During simulations of a bout of acute hypotension, the model predicts a rapid return of cerebral blood flow to baseline levels and a prolonged suppression of the blood flow to the external carotid vasculature, in accordance with experimental evidence. The inclusion of peripheral control via baroreflex at the external carotid vasculature did not assist cerebral autoregulation, thus we raise the hypothesis that baroreflex may act on the head and neck vasculatures but this action has negligible effects on regulation of cerebral blood flow. When autoregulation is impaired, results suggest that the blood flow of the brain and of the head and neck present similar dynamics, while they are weakly coupled when autoregulation is intact. The model also provides a mechanistic explanation of the protection brought by cerebral autoregulation to the microvasculature and to the brain parenchyma. Our model forms the foundation for predicting the interference introduced by the superficial tissue to nonivasive sensors.
Competing Interest Statement
Francisco Ambrosio Garcia and Deusdedit Lineu Spavieri Junior received financial support from Braincare Desenvolvimento e Inovação Tecnológica S.A.. The sponsor (https://brain4.care/en/) has interest on understanding the fundamental aspects of intracranial and extracranial hemodynamics since the superficial tissue may interfere the measurements of noninvasive ICP monitoring developed by the sponsor and therefore participated in study design. Andreas Linninger received no specific funding for this work and has no commercial relationship with the company.
Footnotes
↵+ dspavieri{at}gmail.com
Second author name abbreviation updated.
- Abbreviations
- ABP
- Arterial blood pressure
- CBF
- Cerebral blood flow
- CBV
- Cerebral blood volume
- CA
- Cerebral autoregulation
- CPP
- Cerebral perfusion pressure
- MAP
- Mean arterial pressure
- ICP
- Intracranial pressure
- CSF
- Cerebrospinal fluid
- SV
- Stroke volume
- HR
- Heart rate
- Pxx
- Partial pressure
- CCA
- Common carotid artery
- ICA
- Internal carotid artery
- ECA
- External carotid artery
- XXint
- Intracranial compartment
- XXext
- Extracranial compartment
- Ar
- Arteries
- Al
- Arterioles
- Mc
- Microcirculation
- V
- Veins
- vSinus
- Venous sinus
- Lv
- Lateral ventricle
- 3V
- Third ventricle
- 4V
- Fourth ventricle
- cSAS
- Cranial subarachnoid space
- br
- Brain
- brsolid
- Brain solid cell matrix
- brexf
- Brain extracellular fluid
- pxx
- Pressure
- <.>
- Mean value using a low-pass filter
- xxn
- Baseline value of variable xx
- xxL,R
- Signifying two equations, one for the left and one for the right brain hemisphere
- xxR
- Right compartment
- xxL
- Left compartment
- fxxin
- Flow into the compartment
- fxxout
- Flow out of the compartment