Effect of vestibular stimulation on volume velocity of the cerebral blood flow and systemic arterial pressure

1971 ◽  
Vol 72 (5) ◽  
pp. 1235-1236
Author(s):  
V. A. Romanov ◽  
M. D. Gaevyi
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Vestibular Stimulation ◽  
Systemic Arterial Pressure ◽  
Volume Velocity

Mathematical considerations for modeling cerebral blood flow autoregulation to systemic arterial pressure

1998 ◽  
Vol 274 (3) ◽  
pp. H1023-H1031 ◽  
Author(s):  
Erzhen Gao ◽  
William L. Young ◽  
John Pile-Spellman ◽  
Eugene Ornstein ◽  
Qiyuan Ma
Keyword(s):  
Experimental Data ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Systemic Arterial Pressure ◽  
Pressure Curve ◽  
Average Value ◽  
Upper Limits ◽  
In Series ◽  
Reported Data

The shape of the autoregulation curve for cerebral blood flow (CBF) vs. pressure is depicted in a variety of ways to fit experimentally derived data. However, there is no general empirical description to reproduce CBF changes resulting from systemic arterial pressure variations that is consistent with the reported data. We analyzed previously reported experimental data used to construct autoregulation curves. To improve on existing portrayals of the fitting of the observed data, a compartmental model was developed for synthesis of the autoregulation curve. The resistive arterial and arteriolar network was simplified as an autoregulation device (ARD), which consists of four compartments in series controlling CBF. Each compartment consists of a group of identical vessels in parallel. The response of each vessel category to changes in perfusion pressure was simulated using reported experimental data. The CBF-pressure curve was calculated from the resistance of the ARD. The predicted autoregulation curve was consistent with reported experimental data. The lower and upper limits of autoregulation (LLA and ULA) were predicted as 69 and 153 mmHg, respectively. The average value of the slope of the CBF-pressure curve below LLA and beyond ULA was predicted as 1.3 and 3.3% change in CBF per mmHg, respectively. Our four-compartment ARD model, which simulated small arteries and arterioles, predicted an autoregulation function similar to experimental data with respect to the LLA, ULA, and average slopes of the autoregulation curve below LLA and above ULA.

scholarly journals Impact of Systemic Arterial Pressure, Collateral Vascular Resistance and Degree of Carotid Stenosis on Cerebral Blood Flow, Reserve Blood Flow, Critical Carotid Stenosis, Cerebral Ischemia and Carotid Hemodynamics

2021 ◽  
Author(s):  
Joseph P Archie
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Carotid Artery ◽  
Arterial Pressure ◽  
Carotid Stenosis ◽  
Vascular Resistance ◽  
Systemic Arterial Pressure ◽  
Patient Specific ◽  
Carotid Blood Flow

AbstractIntroductionCarotid artery stenosis related stroke is a major health care concern. Current risk management strategies for patients with asymptomatic carotid stenosis include ultrasound surveillance and occasionally an estimate of cerebral blood flow reserve. Other patient specific hemodynamic variables may be predictive of ischemic stroke risk. This study, based on a cerebral blood flow hemodynamic model, aims to investigate the impact of systemic arterial pressure, collateral vascular resistance and degree of carotid stenosis on cerebral ischemic risk, cerebrovascular blood flow reserve, critical carotid artery stenosis, carotid artery blood flow and carotid stenosis hemodynamics.MethodsThis study uses a three-component (carotid, collateral, brain) energy conservation cerebrovascular fluid mechanics model in combination with the Lassen cerebral blood flow autoregulation model that predicts cerebral blood flow in patients with carotid stenosis. It is a two-phase model, zone A when regional cerebral blood flow is autoregulated at normal values and zone B when cerebral blood flow is below normal and dependent on collateral perfusion pressure. The model solution with carotid artery occlusion defines collateral vascular resistance, with patient specific values calculated from clinical pressure measurements. In addition to cerebral blood flow the model predicts critical stenosis values and carotid and collateral blood flows as a function of systemic arterial pressure and percent diameter stenosis. Carotid stenosis blood flow velocities and energy dissipation are predicted from carotid blood flow solutions.ResultsThe model defines patient specific collateral vascular resistance, cerebral vascular resistance and critical carotid stenosis. It predicts carotid vascular resistance to be non-linearly proportional to area carotid stenosis. Solutions include reserve cerebral blood flow, the carotid and collateral components of cerebral blood flow, criteria for cerebral ischemia and carotid stenosis hemodynamics. Critical carotid stenosis is determined by mean systemic arterial pressure and the Lassen autoregulation threshold cerebral perfusion pressure. Critical stenosis values range from 61% to 76% diameter stenosis when mean systemic arterial pressures are 80mmHg to 120mmHg and the cerebral autoregulation pressure threshold is 50mmHg. When carotid stenosis is less than critical, cerebral blood flow is maintained normal and the ratios of carotid blood flow to collateral blood flow are inversely proportional to the carotid to collateral vascular resistance ratios. At stenosis greater than the critical, carotid blood flow is not adequate to maintain normal cerebral blood flow, cerebral blood flow is primarily collateral flow, all reserve blood flow is collateral and prevention of cerebral ischemia requires adequate collateral flow. Patient specific collateral vascular resistance values less than 1.0 predict normal cerebral blood flow at moderate to severe stenosis. Values greater than 1.0 predicts cerebral ischemia to be dependent on the magnitude of collateral vascular resistance. Systemic arterial pressure is a major determinant of carotid stenosis hemodynamics. Carotid blood flow velocities increase with carotid stenosis and have progressively higher variance depending on collateral blood flow as predicted by collateral vascular resistance. Turbulent flow energy dissipation intensity is similarly inversely proportional to collateral vascular resistance at severe carotid stenosis.ConclusionsCerebral, collateral and carotid blood flow solutions are determined by systemic arterial pressure, collateral vascular resistance and degree of stenosis. Critical carotid stenosis, systemic arterial pressure and collateral vascular resistance are primary determinants of cerebral ischemic risk in patients with significant carotid stenosis.

scholarly journals Autoregulation of Cerebral Blood Flow to Changes in Arterial Pressure in Mild Alzheimer's Disease

2010 ◽  
Vol 30 (11) ◽  
pp. 1883-1889 ◽  
Author(s):  
Allyson R Zazulia ◽  
Tom O Videen ◽  
John C Morris ◽  
William J Powers
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
The Elderly ◽  
Local Defect ◽  
Clinical Dementia Rating ◽  
Positron Emission ◽  
Before And After

Studies in transgenic mice overexpressing amyloid precursor protein (APP) demonstrate impaired autoregulation of cerebral blood flow (CBF) to changes in arterial pressure and suggest that cerebrovascular dysfunction may be critically important in the development of pathological Alzheimer's disease (AD). Given the relevance of such a finding for guiding hypertension treatment in the elderly, we assessed autoregulation in individuals with AD. Twenty persons aged 75±6 years with very mild or mild symptomatic AD (Clinical Dementia Rating 0.5 or 1.0) underwent 15O-positron emission tomography (PET) CBF measurements before and after mean arterial pressure (MAP) was lowered from 107±13 to 92±9 mm Hg with intravenous nicardipine; 11C-PIB-PET imaging and magnetic resonance imaging (MRI) were also obtained. There were no significant differences in mean CBF before and after MAP reduction in the bilateral hemispheres (−0.9±5.2 mL per 100 g per minute, P=0.4, 95% confidence interval (CI)=−3.4 to 1.5), cortical borderzones (−1.9±5.0 mL per 100 g per minute, P=0.10, 95% CI=−4.3 to 0.4), regions of T2W-MRI-defined leukoaraiosis (−0.3±4.4 mL per 100 g per minute, P=0.85, 95% CI=−3.3 to 3.9), or regions of peak 11C-PIB uptake (−2.5±7.7 mL per 100 g per minute, P=0.30, 95% CI=−7.7 to 2.7). The absence of significant change in CBF with a 10 to 15 mm Hg reduction in MAP within the normal autoregulatory range demonstrates that there is neither a generalized nor local defect of autoregulation in AD.

The Effects of Paco2 on Regional Cerebral Blood Flow and Internal Carotid Arterial Pressure during Carotid Clamping

1971 ◽  
Vol 35 (3) ◽  
pp. 286-300 ◽  
Author(s):  
Gudru n ◽  
H. J. Ladegaard-Pedersen ◽  
H. Henriksen ◽  
L. Olesen ◽  
O. B. Paulson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Regional Cerebral Blood Flow ◽  
Internal Carotid ◽  
Regional Cerebral Blood ◽  
Carotid Arterial
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