scholarly journals Mathematical Modelling of Cerebral Blood Circulation and Cerebral Autoregulation: Towards Preventing Intracranial Hemorrhages in Preterm Newborns

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Renée Lampe ◽  
Nikolai Botkin ◽  
Varvara Turova ◽  
Tobias Blumenstein ◽  
Ana Alves-Pinto
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Cerebral Autoregulation ◽  
Coupled Model ◽  
Equation Model ◽  
Polynomial Coefficients ◽  
Arterial Blood ◽  
Cerebral Blood Circulation ◽  
Preterm Newborns

Impaired cerebral autoregulation leads to fluctuations in cerebral blood flow, which can be especially dangerous for immature brain of preterm newborns. In this paper, two mathematical models of cerebral autoregulation are discussed. The first one is an enhancement of a vascular model proposed by Piechnik et al. We extend this model by adding a polynomial dependence of the vascular radius on the arterial blood pressure and adjusting the polynomial coefficients to experimental data to gain the autoregulation behavior. Moreover, the inclusion of a Preisach hysteresis operator, simulating a hysteretic dependence of the cerebral blood flow on the arterial pressure, is tested. The second model couples the blood vessel system model by Piechnik et al. with an ordinary differential equation model of cerebral autoregulation by Ursino and Lodi. An optimal control setting is proposed for a simplified variant of this coupled model. The objective of the control is the maintenance of the autoregulatory function for a wider range of the arterial pressure. The control can be interpreted as the effect of a medicament changing the cerebral blood flow by, for example, dilation of blood vessels. Advanced numerical methods developed by the authors are applied for the numerical treatment of the control problem.

Cerebral blood flow and interstitial fluid adenosine during hemorrhagic hypotension

1988 ◽  
Vol 255 (5) ◽  
pp. H1211-H1218 ◽  
Author(s):  
D. G. Van Wylen ◽  
T. S. Park ◽  
R. Rubio ◽  
R. M. Berne
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Adenosine Receptor ◽  
Cerebral Autoregulation ◽  
Interstitial Fluid ◽  
Adenosine Receptor Antagonist ◽  
Arterial Blood ◽  
Artificial Cerebrospinal Fluid ◽  
Adenosine Concentration ◽  
Group 2

This study was designed to assess the role of adenosine in autoregulation of cerebral blood flow (CBF) with the use of the brain dialysis technique to sample cerebral interstitial fluid (ISF) and hydrogen clearance to measure local CBF in ketamine-anesthetized rats. In group 1 (n = 11), animals were hemorrhaged to reduce mean arterial blood pressure (MABP) from control levels (MABP = 101.1 +/- 2.6) to 80, 70, 60, 50, 40, and 30 mmHg. Cerebral autoregulation was evidenced by no significant decrease in CBF until MABP decreased to 60 mmHg. However, dialysate adenosine concentration did not increase until MABP decreased to 50 mmHg. In group 2 (bilateral dialysis; n = 11), in which the left carotid artery was ligated before reductions in MABP, left-side dialysate adenosine concentration increased at a MABP of 70 mmHg. In group 3 (bilateral dialysis; n = 6), one dialysis probe was perfused with artificial cerebrospinal fluid containing 10(-3) M 8(p-sulfophenyl)theophylline (8-SPT), an adenosine receptor antagonist, during reduction of MABP to 50 mmHg. Although there were similar reductions in CBF with or without adenosine receptor blockade, dialysate adenosine concentration was greater on the side of locally infused 8-SPT at a MABP of 50 mmHg. These data suggest that adenosine is not responsible for cerebral autoregulation at blood pressures greater than 50 mmHg but may contribute to the decrease in cerebral vascular resistance observed at arterial pressures below the autoregulatory range.

Relationship of cerebral blood flow to cardiac output, mean arterial pressure, blood volume, and alpha and beta blockade in cats

1980 ◽  
Vol 52 (6) ◽  
pp. 745-754 ◽  
Author(s):  
Dudley H. Davis ◽  
Thoralf M. Sundt
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Blood Volume ◽  
Cerebral Autoregulation ◽  
Major Change ◽  
Beta Blockade ◽  
Content Type ◽  
Therapeutic Implications ◽  
Arterial Blood

✓ The relationship among cerebral blood flow (CBF), blood volume, cardiac output (CO), and mean arterial blood pressure (MABP) at varying levels of arterial CO2 tensions (PaCO2) were studied in 70 normal cats. The CBF was measured from the clearance curve of xenon−133 and CO with a thermal dilution catheter placed in the pulmonary artery. The CBF, CO, and MABP values varied appropriately with changes in PaCO2, confirming the reliability of the preparations and the presence of normal autoregulatory responses. Moderate hypovolemia that did not change MABP did, nevertheless, significantly decrease CO and CBF. In an effort to determine if this decrease in CO and CBF were coupled responses, the effects of beta stimulation, hypervolemia, and alpha and beta blockade were investigated. Propranolol, in a dosage insufficient to change MABP, decreased both CO and CBF. This agent abolished the CO response to elevations in PaCO2 but not the CBF response, making it unlikely that this CBF reduction resulted from impaired cerebral autoregulation. Isoproterenol, which, in contrast to propranolol, does not cross the normal blood-brain barrier, alone or in combination with phenoxybenzamine, produced a 38% and 72% increase in CO, respectively, without a change in CBF. Alpha blockade (no major change in CO) and beta blockade (major decrease in CO) did not significantly effect cerebral autoregulation to changes in MABP from angiotensin. The ability of the brain to resist increases in MABP and CO and maintain normal CBF is explained by normal cerebral autoregulation. However, its vulnerability to modest decreases in blood volume, which cannot be attributed to variations in perfusion pressure, is unexplained but obviously has important therapeutic implications. This may be related to reduction in CO, changes in autonomic activity, or a decrease in the size of the perfused capillary bed.

scholarly journals Defining the characteristic relationship between arterial pressure and cerebral flow

2012 ◽  
Vol 113 (8) ◽  
pp. 1194-1200 ◽  
Author(s):  
Can Ozan Tan
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Cerebral Autoregulation ◽  
Lower Body Negative Pressure ◽  
Pressure Fluctuations ◽  
Projection Pursuit ◽  
Projection Pursuit Regression ◽  
Cerebrovascular Events ◽  
Characteristic Relationship

Reliable assessment of cerebrovascular effectiveness in buffering against pressure fluctuations may have important implications for the timing and the outcome of therapy after adverse cerebrovascular events. Although linear approaches may indicate the presence or absence of cerebral autoregulation, they are inadequate to describe its characteristics and its effectiveness. Establishing a simple yet robust methodology to reliably measure the effectiveness of cerebral autoregulation could provide a tool to guide screening and clinical options to characterize and treat adverse cerebrovascular events associated with alterations in cerebral perfusion. To test the utility of one such methodology, an oscillatory lower body negative pressure of 30–40 mmHg was used at six frequencies from 0.03 to 0.08 Hz in 43 healthy volunteers, and the pressure-flow relation and the effectiveness of autoregulation was quantified using projection pursuit regression. Projection pursuit regression explained the majority of the relationship between pressure and cerebral blood flow fluctuations and revealed its nature consistently across individuals and across separate study days. The nature of this relationship entailed an autoregulatory region wherein slow arterial pressure fluctuations are effectively counterregulated and two passive regions wherein pressure fluctuations resulted in parallel changes in flow. The effectiveness of autoregulation was significantly reduced as pressure fluctuations became faster. These results demonstrate the characteristic relationship between arterial pressure and cerebral blood flow. Furthermore, the methodology utilized in this study provides a tool that can provide unique insight to integrated cerebrovascular control and may allow diagnosis of physiological alterations underlying impaired cerebral autoregulation.

scholarly journals Phase dynamics of cerebral blood flow in subarachnoid haemorrhage in response to sodium nitrite infusion

2020 ◽  
Author(s):  
Martyn Ezra ◽  
Payashi Garry ◽  
Matthew J Rowland ◽  
Georgios D Mitsis ◽  
Kyle TS Pattinson
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Haemorrhage ◽  
Sodium Nitrite ◽  
Cerebral Autoregulation ◽  
Physiological Stress ◽  
Delayed Cerebral Ischemia ◽  
Aneurysmal Subarachnoid Haemorrhage ◽  
Phase Dynamics ◽  
Arterial Blood

AbstractAneurysmal subarachnoid haemorrhage (SAH) is a devastating subset of stroke. One of the major determinates of morbidity is the development of delayed cerebral ischemia (DCI). Disruption of the nitric oxide (NO) pathway and consequently the control of cerebral blood flow (CBF), known as cerebral autoregulation, is believed to play a role in its pathophysiology. Through the pharmacological manipulation of in vivo NO levels using an exogenous NO donor we sought to explore this relationship.Phase synchronisation index (PSI), an expression of the interdependence between CBF and arterial blood pressure (ABP) and thus cerebral autoregulation, was calculated before and during sodium nitrite administration in 10 high-grade SAH patients acutely postrupture. In patients that did not develop DCI, there was a significant increase in PSI around 0.1 Hz during the administration of sodium nitrite (33%; p-value 0.006). In patients that developed DCI, PSI did not change significantly.Synchronisation between ABP and CBF at 0.1 Hz has been proposed as a mechanism by which organ perfusion is maintained, during periods of physiological stress. These findings suggest that functional NO depletion plays a role in impaired cerebral autoregulation following SAH, but the development of DCI may have a distinct pathophysiological aetiology.

Abstract TMP103: New Blood Velocity Indices Can Improve the Accuracy of Transcranial Doppler to Detect Vasospasm After Subarachnoid Hemorrhage

Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Jaiyoung Ryu ◽  
Xiao Hu ◽  
Shawn C Shadden
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Transcranial Doppler ◽  
Cerebral Autoregulation ◽  
Blood Velocity ◽  
Arterial Blood Flow ◽  
Flow Rates ◽  
Arterial Blood ◽  
Basilar Arteries

Background and Objectives: Early diagnosis of vasospasm after subarachnoid hemorrhage (SAH) can prompt aggressive treatment and improve neurological outcomes. Transcranial Doppler (TCD) is the only diagnosis modality that is noninvasive and available bedside. The purpose of this study was to numerically evaluate the relevance of various blood velocity indices in detection of unbalanced cerebral blood flow due to vasospasm, and to improve the accuracy of diagnosis using TCD. Methods: We employed a well-validated numerical model of arterial blood flow coupled with a sophisticated intracranial model to generate a cerebral blood flow database. Anterior (MCA and/or ACA) and posterior (PCA and/or basilar arteries) vasospasms were considered under normal and impaired cerebral autoregulation conditions. For each case, mean blood velocities and their ratios between ipsilateral and contralateral, downstream and upstream, and anterior and posterior arteries were monitored during the progress of vasospasm. Results: Blood velocities at vasospastic arterial segments demonstrated non-monotonic behavior, i.e. the velocities increased initially with mild and moderate vasospasm, however further vasospasm leads to decreasing values. This may lead to false-negative decisions clinically. Blood flow rates, however, decreased monotonically at the affected arteries. Blood velocities upstream of the vasospastic artery decreased in proportion to the blood flow rates (e.g. for MCA vasospasm, 30% and 20% reduction at ICA and CCA). For all vasospasm locations considered, normalization of velocities by upstream and contralateral velocities provided more robust detection. Moreover, the improvements were most compelling in cases with impaired cerebral autoregulation. Conclusions: The velocity indices and diagnosis strategy proposed in this study can improve the accuracy of TCD diagnosis for cerebral vasospasm. These indices are particularly effective in cases of severe vasospasm where traditional indices (e.g. absolute velocities, Lindegaard index) become problematic.

Brain adenosine production in rat during sustained alteration in systemic blood pressure

1980 ◽  
Vol 239 (5) ◽  
pp. H636-H641 ◽  
Author(s):  
H. R. Winn ◽  
J. E. Welsh ◽  
R. Rubio ◽  
R. M. Berne
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Autoregulation ◽  
Adenine Nucleotides ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Arterial Blood ◽  
Adenosine Concentration ◽  
Severe Hypotension

Brain production of adenosine and its metabolites, inosine and hypoxanthine was determined in 46 rats during sustained (5 min) reduction in mean arterial blood pressure (MABP) caused by hemorrhage. Also measured were ATP, ADP, AMP, phosphocreatine (PCr), and lactate. Brain tissue was obtained by the freeze-blowing technique. Ventilation was controlled to maintain constant arterial O2 tension, CO2 tension, and pH. When MABP was decreased from 135 + 3 (SE) mmHg to 72 +/- 2 mmHg, within the range of cerebral autoregulation, brain adenosine concentration doubled from 0.55 +/- 0.12 to 1.16 +/- 0.13 nmol/g (P < 0.015). Unlike the changes in adenosine concentrations, adenine nucleotides and PCr remained stable. Lactate varied inversely with MABP. With moderate to severe hypotension (MABP = 45 +/- 3 mmHg), adenosine levels increased almost sixfold. The increment in brain adenosine concentration within the autoregulatory range supports a role for this potent dilator of pial vessels in the regulation of cerebral blood flow.

scholarly journals Dynamic cerebral autoregulation estimates derived from near infrared spectroscopy and transcranial Doppler are similar after correction for transit time and blood flow and blood volume oscillations

2018 ◽  
Vol 40 (1) ◽  
pp. 135-149 ◽  
Author(s):  
Jan Willem J Elting ◽  
Jeanette Tas ◽  
Marcel JH Aries ◽  
Marek Czosnyka ◽  
Natasha M Maurits
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Transit Time ◽  
Phase Difference ◽  
Cerebral Autoregulation ◽  
Cerebral Blood Flow Velocity ◽  
Intraclass Correlation ◽  
Arterial Blood ◽  
Dynamic Cerebral Autoregulation

We analysed mean arterial blood pressure, cerebral blood flow velocity, oxygenated haemoglobin and deoxygenated haemoglobin signals to estimate dynamic cerebral autoregulation. We compared macrovascular (mean arterial blood pressure-cerebral blood flow velocity) and microvascular (oxygenated haemoglobin-deoxygenated haemoglobin) dynamic cerebral autoregulation estimates during three different conditions: rest, mild hypocapnia and hypercapnia. Microvascular dynamic cerebral autoregulation estimates were created by introducing the constant time lag plus constant phase shift model, which enables correction for transit time, blood flow and blood volume oscillations (TT-BF/BV correction). After TT-BF/BV correction, a significant agreement between mean arterial blood pressure-cerebral blood flow velocity and oxygenated haemoglobin-deoxygenated haemoglobin phase differences in the low frequency band was found during rest (left: intraclass correlation=0.6, median phase difference 29.5° vs. 30.7°, right: intraclass correlation=0.56, median phase difference 32.6° vs. 39.8°) and mild hypocapnia (left: intraclass correlation=0.73, median phase difference 48.6° vs. 43.3°, right: intraclass correlation=0.70, median phase difference 52.1° vs. 61.8°). During hypercapnia, the mean transit time decreased and blood volume oscillations became much more prominent, except for very low frequencies. The transit time related to blood flow oscillations was remarkably stable during all conditions. We conclude that non-invasive microvascular dynamic cerebral autoregulation estimates are similar to macrovascular dynamic cerebral autoregulation estimates, after TT-BF/BV correction is applied. These findings may increase the feasibility of non-invasive continuous autoregulation monitoring and guided therapy in clinical situations.

Cortical NOS inhibition raises the lower limit of cerebral blood flow-arterial pressure autoregulation

1999 ◽  
Vol 276 (4) ◽  
pp. H1253-H1262 ◽  
Author(s):  
Stephen C. Jones ◽  
Carol R. Radinsky ◽  
Anthony J. Furlan ◽  
Douglas Chyatte ◽  
Alejandro D. Perez-Trepichio
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Lower Limit ◽  
Blood Withdrawal ◽  
Arterial Blood ◽  
Pressure Autoregulation

The maintenance of constant cerebral blood flow (CBF) as arterial blood pressure is reduced, commonly referred to as CBF-pressure autoregulation, is typically characterized by a plateau until the vasodilatory capacity is exhausted at the lower limit, after which flow falls linearly with pressure. We investigated the effect of cortical, as opposed to systemic, nitric oxide synthase (NOS) inhibition on the lower limit of CBF-pressure autoregulation. Forty-four Sprague-Dawley rats were anesthetized with halothane and N2O in O2. With a closed cranial window placed the previous day in a ventilated and physiologically stable preparation, we determined the CBF using laser-Doppler flowmetry. Animals with low reactivity to inhaled CO2 and suffused ADP or ACh were excluded. Five arterial pressures from 100 to 40 mmHg were obtained with controlled hemorrhagic hypotension under cortical suffusion with artificial cerebrospinal fluid (aCSF) and then again after suffusion for 35 ( n = 5) and 105 min ( n = 10) with aCSF, 10−3 M N ω-nitro-l-arginine (l-NNA; n = 12), or 10−3 M N ω-nitro-d-arginine (d-NNA; n = 5). An additional group ( n = 7) was studied after a 105-min suffusion of l-NNA followed by a single blood withdrawal procedure. The lower limit of autoregulation was identified visually by four blinded reviewers as a change in the slope of the five-point plot of CBF vs. mean arterial blood pressure. The lower limit of 90 ± 4.3 mmHg after 105 min of 1 mMl-NNA suffusion was increased compared with the value in the time-control group of 75 ± 5.3 mmHg ( P < 0.01; ANOVA) and the initial value of 67 ± 3.7 mmHg ( P < 0.001). The lower limit of 84 ± 5.9 mmHg in seven animals with 105 min of suffusion of 1 mM l-NNA without previous blood withdrawal was significantly increased ( P < 0.01) in comparison with 70 ± 1.9 mmHg from those with just aCSF suffusion ( n = 37). No changes in lower limit for the other agents or conditions, including 105 or 35 min of aCSF or 35 min of l-NNA suffusion, were detected. The lack of effect on the lower limit withd-NNA suffusion suggests an enzymatic mechanism, and the lengthyl-NNA exposure of 105 min, but not 35 min, suggests inhibition of a diffusionally distant NOS source that mediates autoregulation. Thus cortical suffusion ofl-NNA raises the lower limit of autoregulation, strongly suggesting that nitric oxide is at least one of the vasodilators active during hypotension as arterial pressure is reduced from normal.

Cerebral autoregulation in migraine with aura: A case control study

Cephalalgia ◽  
2018 ◽  
Vol 39 (5) ◽  
pp. 635-640 ◽  
Author(s):  
Cédric Gollion ◽  
Nathalie Nasr ◽  
Nelly Fabre ◽  
Michèle Barège ◽  
Marc Kermorgant ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Transfer Function ◽  
Arterial Blood Pressure ◽  
Migraine With Aura ◽  
Cerebral Autoregulation ◽  
Arterial Blood ◽  
Transfer Function Analysis ◽  
History Of

Background Migraine with aura is independently associated with increased risk of ischemic stroke, especially in younger subjects. This association might be related to an impairment of cerebral autoregulation, which normally maintains cerebral blood flow independent of arterial blood pressure variations. Methods Patients aged 30–55, fulfilling ICHD-3 beta criteria for migraine with aura, were prospectively enrolled and compared with gender- and age-matched healthy controls without a history of migraine. Patients and controls with a history of stroke or any disease potentially impairing cerebral autoregulation were excluded. We assessed cerebral autoregulation with two different methods: Transfer function analysis, and the correlation coefficient index Mx. The transfer function phase and gain reflect responses of cerebral blood flow velocities to relatively fast fluctuations of arterial blood pressure, whereas Mx also reflects responses to slower arterial blood pressure fluctuations. Results A total of 22 migraine with aura patients (median age [IQR]: 39.5 [12.5] years) and 22 controls (39 [9.75] years) were included. Transfer function parameters and Mx were not different between patients and controls. However, Mx was inversely correlated with age in patients (ρ = −0.567, p = 0.006) and not in controls (ρ = −0.084, p = 0.509). Mx was also inversely correlated with migraine with aura duration (ρ = −0.617, p = 0.002), suggesting improvement of cerebral autoregulation efficiency with disease duration. Conclusions Cerebral autoregulation did not differ between patients and controls aged 30–55. However, cerebral autoregulation efficiency was strongly correlated with migraine with aura duration. Further studies in younger patients are needed to determine whether cerebral autoregulation is impaired early in the course of disease. Trial Registration NCT02708797.

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