A lumped parameter model of cerebral blood flow control combining cerebral autoregulation and neurovascular coupling

2012 ◽  
Vol 303 (9) ◽  
pp. H1143-H1153 ◽  
Author(s):  
Bart Spronck ◽  
Esther G. H. J. Martens ◽  
Erik D. Gommer ◽  
Frans N. van de Vosse
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Control ◽  
Cerebral Autoregulation ◽  
Neurovascular Coupling ◽  
Flow Regulation ◽  
Lumped Parameter Model ◽  
Blood Flow Regulation ◽  
Lumped Parameter ◽  
Blood Flow Control

Cerebral blood flow regulation is based on a variety of different mechanisms, of which the relative regulatory role remains largely unknown. The cerebral regulatory system expresses two regulatory properties: cerebral autoregulation and neurovascular coupling. Since partly the same mechanisms play a role in cerebral autoregulation and neurovascular coupling, this study aimed to develop a physiologically based mathematical model of cerebral blood flow regulation combining these properties. A lumped parameter model of the P2 segment of the posterior cerebral artery and its distal vessels was constructed. Blood flow regulation is exerted at the arteriolar level by vascular smooth muscle and implements myogenic, shear stress based, neurogenic, and metabolic mechanisms. In eight healthy subjects, cerebral autoregulation and neurovascular coupling were challenged by squat-stand maneuvers and visual stimulation using a checkerboard pattern, respectively. Cerebral blood flow velocity was measured using transcranial Doppler, whereas blood pressure was measured by finger volume clamping. In seven subjects, the model proposed fits autoregulation and neurovascular coupling measurement data well. Myogenic regulation is found to dominate the autoregulatory response. Neurogenic regulation, although only implemented as a first-order mechanism, describes neurovascular coupling responses to a great extent. It is concluded that our single, integrated model of cerebral blood flow control may be used to identify the main mechanisms affecting cerebral blood flow regulation in individual subjects.

scholarly journals IL-17A Contributes to the Angiotensin II-induced Neurovascular Coupling impairment through Oxidative Stress

2021 ◽  
Author(s):  
Jessica Youwakim ◽  
Diane Vallerand ◽  
Helene Girouard
Keyword(s):  
Oxidative Stress ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Neurovascular Coupling ◽  
Flow Regulation ◽  
Ang Ii ◽  
Superoxide Anion Production ◽  
Blood Flow Regulation ◽  
Chronic Inflammatory Condition ◽  
The Relationship

Abstract Hypertension, a multifactorial chronic inflammatory condition, is a risk factor for neurodegenerative diseases including stroke and Alzheimer’s disease. These diseases have been associated with higher concentration of blood interleukin (IL)-17A. However, the role that IL-17A plays in the relationship between hypertension and brain remains misunderstood. Cerebral blood flow regulation may be the crossroads of these conditions. Hypertension alters cerebral blood flow regulation including neurovascular coupling (NVC). In the present study, the effects of IL-17A on NVC in the context of hypertension induced by angiotensin (Ang) II will be examined. Our results show that the neutralization of IL-17A or the specific inhibition of its receptor prevent the Ang II- induced NVC impairment. These treatments reduce the Ang II-induced cerebral oxidative stress. Tempol and NOX-2 depletion prevent NVC impairment induced by IL-17A. These findings suggest that IL-17A, through superoxide anion production, is an important mediator of cerebrovascular dysregulation induced by Ang II.

scholarly journals Cerebral hemodynamics: a mathematical model including autoregulation, baroreflex and extracranial peripheral circulation

2021 ◽  
Author(s):  
Francisco Ambrosio Garcia ◽  
Deusdedit Lineu Spavieri Junior ◽  
Andreas Linninger
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cerebral Autoregulation ◽  
Peripheral Circulation ◽  
Flow Regulation ◽  
Pressure Waves ◽  
Vascular Bed ◽  
Blood Flow Regulation

Increasing evidence supports that cerebral autoregulation and mean arterial pressure regulation via baroreflex contribute to cerebral blood flow regulation. It is unclear whether the extracranial vascular bed of the head and neck helps reestablishing cerebral blood flow during changes in mean arterial pressure. Current computational models of cerebral blood flow regulation do not address the relationships between the intracranial and extracranial blood flow dynamics. We present a model of cerebral autoregulation, extracranial peripheral circulation and baroreflex control of heart rate and of peripheral vasculature that was included to the model of intracranial dynamics proposed by Linninger et al. (2009), which incorporates the fully coupled blood, cerebrospinal fluid and brain parenchyma systems. Autoregulation was modelled as being pressure-mediated at the arteries and arterioles and flow-mediated at the microcirculation. During simulations of a bout of acute hypotension, cerebral blood flow returns rapidly to baseline levels with a very small overshoot, whereas the blood flow to the peripheral circulation of the head and neck suffers a prolonged suppression in accordance with experimental evidence. The inclusion of baroreflex regulation at the extracranial vascular bed had a negligible effect on cerebral blood flow regulation during dynamic changes in mean arterial pressure. Moreover, the results suggest that the extracranial blood flow carries only modest information about cerebral blood flow in dynamic situations in which cerebral autoregulation is preserved and mean arterial pressure suffers alterations. This information is likely higher when the autoregulation is impaired. Steady-state cerebral blood flow in the model is kept within normal ranges despite variations in mean arterial pressure from 50 to 175 mmHg. By inputting aortic pressure waves from individuals with increasing arterial rigidity, increasing arterial systolic and pulse pressures, the model predicts the generation of intracranial pressure waves with accordingly increasing peaks and amplitudes.

Relationship of cerebral blood flow regulation to acute mountain sickness.

1989 ◽  
Vol 8 (3) ◽  
pp. 143-148 ◽  
Author(s):  
S M Otis ◽  
M E Rossman ◽  
P A Schneider ◽  
M P Rush ◽  
E B Ringelstein
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Acute Mountain Sickness ◽  
Flow Regulation ◽  
Blood Flow Regulation ◽  
Mountain Sickness ◽  
Relationship Of

Dynamics of cerebral blood flow regulation explained using a lumped parameter model

2002 ◽  
Vol 282 (2) ◽  
pp. R611-R622 ◽  
Author(s):  
Mette S. Olufsen ◽  
Ali Nadim ◽  
Lewis A. Lipsitz
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cardiovascular Response ◽  
Lumped Parameter Model ◽  
Initial Increase ◽  
Windkessel Model ◽  
Cerebrovascular Resistance ◽  
Posture Change ◽  
Lumped Parameter ◽  
Young Subjects

The dynamic cerebral blood flow response to sudden hypotension during posture change is poorly understood. To better understand the cardiovascular response to hypotension, we used a windkessel model with two resistors and a capacitor to reproduce beat-to-beat changes in middle cerebral artery blood flow velocity (transcranial Doppler measurements) in response to arterial pressure changes measured in the finger (Finapres). The resistors represent lumped systemic and peripheral resistances in the cerebral vasculature, whereas the capacitor represents a lumped systemic compliance. Ten healthy young subjects were studied during posture change from sitting to standing. Dynamic variations of the peripheral and systemic resistances were extracted from the data on a beat-to-beat basis. The model shows an initial increase, followed approximately 10 s later by a decline in cerebrovascular resistance. The model also suggests that the initial increase in cerebrovascular resistance can explain the widening of the cerebral blood flow pulse observed in young subjects. This biphasic change in cerebrovascular resistance is consistent with an initial vasoconstriction, followed by cerebral autoregulatory vasodilation.

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