scholarly journals The Effects of Cerebral Vasospasm on Cerebral Blood Flow and the Effects of Induced Hypertension: A Mathematical Modelling Study

2019 ◽  
Vol 8 (2-6) ◽  
pp. 152-163
Author(s):  
Pervinder Bhogal ◽  
Leonard Leong Yeo ◽  
Lucas O. Müller ◽  
Pablo J. Blanco

Background: Induced hypertension has been used to promote cerebral blood flow under vasospastic conditions although there is no randomised clinical trial to support its use. We sought to mathematically model the effects of vasospasm on the cerebral blood flow and the effects of induced hypertension. Methods: The Anatomically Detailed Arterial Network (ADAN) model is employed as the anatomical substrate in which the cerebral blood flow is simulated as part of the simulation of the whole body arterial circulation. The pressure drop across the spastic vessel is modelled by inserting a specific constriction model within the corresponding vessel in the ADAN model. We altered the degree of vasospasm, the length of the vasospastic segment, the location of the vasospasm, the pressure (baseline mean arterial pressure [MAP] 90 mm Hg, hypertension MAP 120 mm Hg, hypotension), and the presence of collateral supply. Results: Larger decreases in cerebral flow were seen for diffuse spasm and more severe vasospasm. The presence of collateral supply could maintain cerebral blood flow, but only if the vasospasm did not occur distal to the collateral. Induced hypertension caused an increase in blood flow in all scenarios, but did not normalise blood flow even in the presence of moderate vasospasm (30%). Hypertension in the presence of a complete circle of Willis had a marginally greater effect on the blood flow, but did not normalise flow. Conclusion: Under vasospastic condition, cerebral blood flow varies considerably. Hypertension can raise the blood flow, but it is unable to restore cerebral blood flow to baseline.

2009 ◽  
Vol 24 (5) ◽  
pp. 275-281 ◽  
Author(s):  
Teresa Rodriguez-Cano ◽  
Luis Beato-Fernandez ◽  
Inmaculada Garcia-Vilches ◽  
Ana Garcia-Vicente ◽  
Victor Poblete-Garcia ◽  
...  

AbstractObjectiveThe aim of the present study is to see if the changes in the regional cerebral blood flow (rCBF) experienced by restrictive anorexia nervosa (AR) and bulimia nervosa (BN) patients, following the exposure to their own body image, persist at follow-up.MethodsThree single photon emission computed tomography (SPECT) were performed on nine patients with a DSM-IV diagnosis of AR, 13 with BP, and 12 controls: at rest, following a neutral stimulus, and after exposure to their previously filmed whole body image. Body dissatisfaction was measured by means of the Body Dissatisfaction Questionnaire (BSQ). One year later the same assessment was repeated.ResultsFollowing the exposure to their own body image, BN showed an increase in body dissatisfaction, which was associated with the increase in the rCBF of the Right Temporal Area. Those changes persisted at follow-up.DiscussionMore specific long term therapies are needed for the treatment of the averse response showed by ED patients to their own body image exposure that is associated with the hyperactivation of the right temporal area when they are confronted with their whole body image.


1999 ◽  
Vol 91 (3) ◽  
pp. 677-677 ◽  
Author(s):  
Basil F. Matta ◽  
Karen J. Heath ◽  
Kate Tipping ◽  
Andrew C. Summors

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. Methods Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. Results Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P<0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. Conclusions In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.


2006 ◽  
Vol 14 (7S_Part_30) ◽  
pp. P1571-P1571
Author(s):  
Natanya S. Russek ◽  
Sara Elizabeth Berman ◽  
Karen K. Lazar ◽  
Yue Ma ◽  
Carson A. Hoffman ◽  
...  

1998 ◽  
Vol 274 (5) ◽  
pp. H1715-H1728 ◽  
Author(s):  
Mauro Ursino ◽  
Carlo Alberto Lodi

The relationships among cerebral blood flow, cerebral blood volume, intracranial pressure (ICP), and the action of cerebrovascular regulatory mechanisms (autoregulation and CO2 reactivity) were investigated by means of a mathematical model. The model incorporates the cerebrospinal fluid (CSF) circulation, the intracranial pressure-volume relationship, and cerebral hemodynamics. The latter is based on the following main assumptions: the middle cerebral arteries behave passively following transmural pressure changes; the pial arterial circulation includes two segments (large and small pial arteries) subject to different autoregulation mechanisms; and the venous cerebrovascular bed behaves as a Starling resistor. A new aspect of the model exists in the description of CO2 reactivity in the pial arterial circulation and in the analysis of its nonlinear interaction with autoregulation. Simulation results, obtained at constant ICP using various combinations of mean arterial pressure and CO2 pressure, substantially support data on cerebral blood flow and velocity reported in the physiological literature concerning both the separate effects of CO2 and autoregulation and their nonlinear interaction. Simulations performed in dynamic conditions with varying ICP underline the existence of a significant correlation between ICP dynamics and cerebral hemodynamics in response to CO2 changes. This correlation may significantly increase in pathological subjects with poor intracranial compliance and reduced CSF outflow. In perspective, the model can be used to study ICP and blood velocity time patterns in neurosurgical patients in order to gain a deeper insight into the pathophysiological mechanisms leading to intracranial hypertension and secondary brain damage.


Nosotchu ◽  
1984 ◽  
Vol 6 (2) ◽  
pp. 223-229 ◽  
Author(s):  
Tomoaki Terada ◽  
Haruhiko Kikuchi ◽  
Jun Karasawa ◽  
Ikuo Ihara ◽  
Izumi Nagata

Trials ◽  
2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Zhi-peng Xiao ◽  
ke Jin ◽  
Jie-qing Wan ◽  
Yong Lin ◽  
Yao-hua Pan ◽  
...  

Abstract Background Cerebrovascular reactivity (CVR) is the change in cerebral blood flow in response to a vaso-active stimulus, and may assist the treatment strategy of ischemic stroke. However, previous studies reported that a therapeutic strategy for stroke mainly depends on the degree of vascular stenosis with steady-state vascular parameters (e.g., cerebral blood flow and CVR). Hence, measurement of CVR by multimodal imaging techniques may improve the treatment of ischemic stroke. Methods/design This is a prospective, randomized, controlled clinical trial that aimed to examine the capability of multimodal imaging techniques for the evaluation of CVR to improve treatment of patients with ischemic stroke. A total of 66 eligible patients will be recruited from Renji Hospital, Shanghai Jiaotong University School of Medicine. The patients will be categorized based on CVR into two subgroups as follows: CVR > 10% group and CVR < 10% group. The patients will be randomly assigned to medical management, percutaneous transluminal angioplasty and stenting, and intracranial and extra-cranial bypass groups in a 1:1:1 ratio. The primary endpoint is all adverse events and ipsilateral stroke recurrence at 6, 12, and 24 months after management. The secondary outcomes include the CVR, the National Institute of Health stroke scale and the Modified Rankin Scale at 6, 12, and 24 months. Discussion Measurement of cerebrovascular reserve by multimodal image is recommended by most recent studies to guide the treatment of ischemic stroke, and thus its efficacy and evaluation accuracy need to be established in randomized controlled settings. This prospective, parallel, randomized, controlled registry study, together with other ongoing studies, should present more evidence for optimal individualized accurate treatment of ischemic stroke. Trial registration Chinese Clinical Trial Registry, ID: ChiCTR-IOR-16009635; Registered on 16 October 2016. All items are from the World Health Organization Trial Registration Data Set and registration in the Chinese Clinical Trial Registry: ChiCTR-IOR-16009635.


Author(s):  
Hiroyuki Nakamura ◽  
Hirofumi Nagase ◽  
Takao Okazawa ◽  
Masami Yoshida ◽  
Akira Okada

To clarify the involvement of vasoactive intestinal polypeptide (VIP) in regional cerebral circulation during whole-body vibration (WBV), we determined regional cerebral blood flow and VIP-like immunoreactivity (VIP-LI) in rats following WBV for 90 min. at various accelerations (0, 2G and 4G rms), using the hydrogen gas electrolytic method. Interference electrodes were inserted into the frontal cortex and the hippocampus. Although we observed no change in hippocampal blood flow, the frontal cortical blood flow increased during the exposure in a manner that was dependent upon the acceleration. There was a significant reduction in hippocampal VIP-LI following WBV at an acceleration of 4G. The association between frontal cortical blood flow and hippocampal VIP-LI was significantly negative. Our results indicated that a local increase in blood flow in the frontal cortex of rats was induced by WBV. This increase seemed to be involved in the neural activation induced by WBV. Hippocampal VIP may have a role in the physiological regulation of frontal cortical circulation during WBV stress.


1985 ◽  
Vol 63 (6) ◽  
pp. 937-943 ◽  
Author(s):  
David J. Boarini ◽  
Neal F. Kassell ◽  
James A. Sprowell ◽  
Julie J. Olin ◽  
Hans C. Coester

✓ Profound arterial hypotension is à commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole. In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.


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