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Poulin, Marc J. "Aspects of cerebral blood flow in humans." Thesis, University of Oxford, 1998. http://ora.ox.ac.uk/objects/uuid:a2af655f-9198-4cd0-a126-57c070f6399d.
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The technique of transcranial Doppler ultrasound (TCD) was used to assess cerebral blood flow (CBF) in humans. Studies were performed at rest and during dynamic submaximal exercise. In the resting experiments, TCD was combined with the technique of dynamic end-tidal forcing to study the dynamics of the CBF response to step changes in end-tidal (i.e. arterial) PC02 and PO2 In the resting and exercise experiments, the degree of consistency was examined between three indices of CBF that can be extracted from the TCD spectrum. Finally, the ventilatory and the CBF responses to acute isocapnic hypoxia were examined to try to quantify the possible reduction in ventilation that could be attributed to changes in CBF with hypoxia. In the studies performed at rest, during either hypoxia and/or hypercapnia (Chapter 2), the three indices of CBF extracted from the TCD spectrum were all consistent. However, during submaximal exercise (Chapter 5), the indices were less consistent and results suggest that the increase in CBF with exercise that has been reported with TCD needs to be treated with caution. The dynamic studies of the CBF response to step changes in end-tidal PC02 and PO2 in humans revealed that the CBF response to hypercapnia (Chapter 3) is characterised by a significant asymmetry, with a slower on-transient than off-transient, and also by a degree of undershoot following the relief of hypercapnia. The CBF response to hypocapnia (Chapter 4) is also characterised by a significant asymmetry, with a faster on-transient than off-transient. Furthermore, there is a slow progressive adaptation throughout the hypocapnic period. These studies show that the CBF responses to hypercapnia and hypocapnia are much faster than previously been thought. Finally, the work described in Chapter 6 attempts to quantify the possible reduction in ventilation that could be attributed to changes in CBF with hypoxia to determine whether it could be of sufficient magnitude to underlie hypoxic ventilatory decline (HVD). The results suggest that, in awake humans, changes in CBF during acute isocapnic hypoxia are quantitatively insufficient to underlie HVD.
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Mazzeo, M. D. "Lattice-Boltzmann simulations of cerebral blood flow." Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/19357/.
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Computational haemodynamics play a central role in the understanding of blood behaviour in the cerebral vasculature, increasing our knowledge in the onset of vascular diseases and their progression, improving diagnosis and ultimately providing better patient prognosis. Computer simulations hold the potential of accurately characterising motion of blood and its interaction with the vessel wall, providing the capability to assess surgical treatments with no danger to the patient. These aspects considerably contribute to better understand of blood circulation processes as well as to augment pre-treatment planning. Existing software environments for treatment planning consist of several stages, each requiring significant user interaction and processing time, significantly limiting their use in clinical scenarios. The aim of this PhD is to provide clinicians and researchers with a tool to aid in the understanding of human cerebral haemodynamics. This tool employs a high performance fluid solver based on the lattice-Boltzmann method (coined HemeLB), high performance distributed computing and grid computing, and various advanced software applications useful to efficiently set up and run patient-specific simulations. A graphical tool is used to segment the vasculature from patient-specific CT or MR data and configure boundary conditions with ease, creating models of the vasculature in real time. Blood flow visualisation is done in real time using in situ rendering techniques implemented within the parallel fluid solver and aided by steering capabilities; these programming strategies allows the clinician to interactively display the simulation results on a local workstation. A separate software application is used to numerically compare simulation results carried out at different spatial resolutions, providing a strategy to approach numerical validation. This developed software and supporting computational infrastructure was used to study various patient-specific intracranial aneurysms with the collaborating interventionalists at the National Hospital for Neurology and Neuroscience (London), using three-dimensional rotational angiography data to define the patient-specific vasculature. Blood flow motion was depicted in detail by the visualisation capabilities, clearly showing vortex fluid ow features and stress distribution at the inner surface of the aneurysms and their surrounding vasculature. These investigations permitted the clinicians to rapidly assess the risk associated with the growth and rupture of each aneurysm. The ultimate goal of this work is to aid clinical practice with an efficient easy-to-use toolkit for real-time decision support.
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Willie, Christopher Kenneth. "Cerebral blood flow in man : regulation by arterial blood gases." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/47074.
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Due to the high metabolic rate of brain tissue and nominal substrate storage, brain perfusion must be precisely regulated to ensure continuous delivery of oxygen and substrates. Cerebral blood flow (CBF) is principally regulated by tissue metabolism, perfusion pressure, autonomic nervous activity, and the partial pressures of arterial oxygen (PaO₂)and carbon dioxide (PaCO₂) – an integrative process thus involving the marked influence of pulmonary gas exchange and cardiovascular function, in addition to intracranial mediators of cerebrovascular resistance. This thesis explicates the roles of PaO₂ and PaCO₂ in human regulation of regional CBF. In study 1, to elucidate their discrete roles, PaO₂ and PaCO₂ were independently manipulated at sea level through the widest range tolerated in humans. Flow reactivity to hypocapnia (low PaCO₂) and hypoxia (low PaO₂) was greater in the vertebral (VA) than internal carotid (ICA) artery, whereas similar reactivity was observed during hypercapnia (high PaCO₂) and hyperoxia (high PaO2₂. Cerebral oxygen delivery was well protected except in cases of extreme hypocapnia. The ventilatory response to hypoxia mitigates falling PaO₂ and reduces PaCO₂, particularly during initial exposure to high altitude. Study 2 assessed regional CBF during ascent to 5050m and every 12 hours during the first 3 days of acclimatization. Although total CBF increased by ~50% and was modestly related to reductions in oxygen saturation of hemoglobin, no regional CBF differences were observed. To extend these findings, Study 3 aimed to determine if cerebrovascular responses to changes in PaO₂ and PaCO₂ differed at 5050m compared to sea level. Despite respiratory alkalosis and partial metabolic compensation at 5050m restoration of PaO₂ to sea level values decreased CBF, and CBF sensitivity to acutely altered PaCO₂ remained similar to sea level. To elucidate the interactive effect on CBF of profound hypoxemia and hypercapnia, study 4 examined the temporal changes in elite breath-hold divers during maximum apneas. Despite 40-50% reductions in arterial oxygen content, CBF elevations were regionally similar (up to +100%) thereby facilitating maintenance of brain oxygen delivery throughout apnea. Although the regulation of CBF is multifaceted, the cerebrovasculature prioritizes oxygen delivery and adjusts to chronic changes in arterial blood gases.
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Shi, Yulu. "Cerebral blood flow and intracranial pulsatility in cerebral small vessel disease." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/29625.
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Cerebral small vessel disease (SVD) is associated with increased risks of stroke and dementia, however the mechanisms remain unclear. Low cerebral blood flow (CBF) has long been suggested and accepted, but clinical evidence is conflicting. On the other hand, growing evidence suggests that increased intracranial pulsatility due to vascular stiffening might be an alternative mechanism. Pulse-gated phase-contrast MRI is an imaging technique that allows measuring of CBF contemporaneously with pulsatility in multiple vessels and cerebrospinal fluid (CSF) spaces. The overall aim of this thesis was to provide an overview of existing clinical evidence on both hypotheses, to test the reproducibility of CBF and pulsatility measures in phase-contrast MRI, and to explore the relationship between CBF and intracranial pulsatility and SVD features in a group of patients with minor stroke and SVD changes on brain imaging. I first systematically reviewed and meta-analysed clinical studies that have assessed CBF or intracranial pulsatility in SVD patients. There were 38 studies (n=4006) on CBF and 27 (n=3356) on intracranial pulsatility. Most were cross-sectional, and longitudinal studies were scarce. There were large heterogeneities in patient characteristics and indices used particularly for measuring and calculating pulsatility. Methods to reduce bias such as blinding and the expertise of structural image readers were generally poorly reported, and many studies did not account for the impact of confounding factors (e.g. age, vascular risk factors and disease severity) on CBF or pulsatility. Evidence for falling CBF predating SVD was not supported by longitudinal studies; high pulsatility in one large artery such as internal carotid arteries (ICA) or middle cerebral arteries might be related to SVD, but studies that measured arteries, veins and CSF in the same patients were very limited and the reliability of some pulsatility measures, especially in CSF, needs to be tested. In order to test the reproducibility of the CBF and intracranial pulsatility measures, I repeated 2D phase-contrast MRI scans of vessels and CSF on healthy volunteers during two visits. I also compared the ICA pulsatility index derived from the MRI flow waveform to that from the Doppler ultrasound velocity waveform in patients with minor stroke and SVD features. In 10 heathy volunteers (age 35.2±9.78 years), the reproducibility of CBF and vascular pulsatility indices was good, with within-subject coefficients of variability (CV) less than 10%; whereas CSF flow and pulsatility measures were generally less reproducible (CV > 20%). In 56 patients (age 67.8±8.27 years), the ICA pulsatility indices in Doppler ultrasound and MRI were acceptably well-correlated (r=0.5, p < 0.001) considering the differences in the two techniques. We carried out a cross-sectional study aiming to recruit 60 patients with minor stroke and SVD features. We measured CBF and intracranial pulsatility using phase-contrast MRI, as well as aortic augmentation index (AIx) using a SphygmoCor device. I first investigated the relationship between intracranial measures, and systemic blood pressure or aortic AIx, and then focused on how the intracranial haemodynamic measures related to two main SVD features (white matter hyperintensities (WMH) and perivascular spaces (PVS)). We obtained usable data from 56/60 patients (age 67.8±8.27 years), reflecting a range of SVD burdens. After the adjustment for age, gender, and history of hypertension, higher pulsatility in the venous sinuses was associated with lower diastolic blood pressure and lower mean arterial pressure (e.g. diastolic blood pressure on straight sinus pulsatility index (PI): β=-0.005, P=0.029), but not with aortic AIx. Higher aortic AIx was associated with low ICA PI (β=-0.011, P=0.040). Increased pulsatility in the venous sinuses, not low CBF, was associated with greater WMH volume (e.g. superior sagittal sinus PI: β=1.29, P=0.005) and more basal ganglia PVS (e.g. odds ratio=1.379 per 0.1 increase in superior sagittal sinus PI) after the adjustment for age, gender and blood pressure. The thesis is the first to summarise the literature on CBF and intracranial pulsatility in SVD patients, addressed the major limitations of current clinical studies of SVD, and also assessed CBF and intracranial pulsatility contemporaneously in well-characterised patients with SVD features. The overall results of the thesis challenge the traditional hypothesis of the cause and effect between low CBF and SVD, and suggest that increased cerebrovascular pulsatility, which might be due to intrinsic cerebral small vessel pathologies rather than just aortic stiffness, is important for SVD. More importantly, this pilot study also provides a reliable methodology for measuring intracranial pulsatility using phase-contrast MRI for future longitudinal or larger multicentre studies, and shows that intracranial pulsatility could be used as a secondary outcome in clinical trials of SVD. However, future research is required to elucidate the implication of venous pulsatility and to fully explore the passage of pulse wave transmission in the brain. Overall, this thesis advances knowledge and suggest potential targets for future SVD studies in terms of mechanisms, prevention and treatment.
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吳志萍 and Chi-ping Ng. "Cerebral blood flow monitoring of brain injured patients." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1996. http://hub.hku.hk/bib/B31214484.
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Ng, Chi-ping. "Cerebral blood flow monitoring of brain injured patients /." Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B18777077.
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Pathmanathan, Saidharshini. "Development of in vitro models of cerebral ischaemia." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249162.
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Bathula, Rajaram. "Ethnic differences in cerebral blood flow and its determinants." Thesis, Imperial College London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522845.
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Khlunovska, L. Yu. "Peculiarities of cerebral blood flow in children with headache." Thesis, БДМУ, 2017. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/17135.
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Appaji, Abhisara Apoorva. "Estimating Cerebral Blood Flow from a Flow from a Rotatinal Angiographic System." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.504287.
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Jayasinghe, Dulip. "The effect of blood pressure on the cerebral blood flow of preterm infants." Thesis, University of Leeds, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.490972.
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During the early postnatal period, some preterm infants experience periods of hypoxia, hypotension or both. Hypotension is associated with significant cerebral lesions and contributes to morbidity and mortality. The aetiology of the lesions is thought to be secondary to a loss of Cerebral Blood Flow (CBF) autoregulation, resulting in a pressure-passive CBF. Treatment of hypotension may require the use of inotropic agents that may also affect CBF. CBF can be measured by a number of techniques; one quantitative method is the intravenous 133Xe technique. To investigate the effects of blood pressure on the CBF of preterm infants, CBF was measured before and after treatment of hypotension. Infants received, in a stepwise manor, volume replacement, a dopamine. infusion of 5 JJ9/kg/min then randomisation between 10 JJ9/kg/min of dopamine (Group 1), or the addition of dobutamine infusion at 10 JJg/kg/min (Group 2). Analysis was performed in two stages; the infants were grouped according to blood pressure during acquisition of serial CBF estimates and analysed for the presence of autoregulation; secondly, the effect of inotropes on CBF was modelled. Sixty-one CBF recordings were obtained from 16 infants. Five infants were normotensive during CBF estimation, 11 were hypotensive at least once. CBF-MABP reactivity (95% CI) of the normotensive group was 1.9% (-0.8% to 4.7%) I mmHg llMABP; hypotensive group 1.9% (0.8% to 3.0). The PaCOz-CBF reactivity of the normotensive infants was 11.1% (6.8% to 15.5%) I KPa llPaCOz, that of the hypotensive infants was 4.1% (-5.0% to 14.1%). Twelve infants received at least 5 JJ9/kg/min of dopamine, 5 were SUbsequently randomised to Group1, 5 randomised to Group2. When the effects of MABP, PaC02 , postnatal age, dose of dopamine and dobutamine were modelled on CBF, MABP (2.1% (95% CI1.13.3%)/ mmHg L\MABP; p=0.0003) and postnatal age (1.1% (95% CI 0.12.1 %)/hour L\postnatal age; p=0.03) were found to be significant predictors of change in CBF. The 95% CI of MABP-CBF reactivity of the normotensive infants encompassed 0, interpreted as intact autoregulation, the lower CI of the hypotensive group did not, which was interpreted as absent autoregulation. Inotropes were not observed to affect CBF directly but could through increase in MABP via pressure-passive CBF.
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Wildfong, Kevin Wayne. "Regulation of cerebral blood flow during transient hypertension in humans." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/59126.
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Although the role of sympathetic nervous activity (SNA) in cerebral blood flow (CBF) regulation is poorly understood in humans, animal studies have demonstrated that elevations in cerebral SNA may protect against cerebral hyper-perfusion during elevations in blood pressure (BP). We examined the hypothesis that alpha-1 receptor blockade (Prazosin) would augment increases in CBF during acute hypertension. In 15 healthy volunteers, beat-by-beat BP, extra-cranial artery blood flow (internal carotid artery (QICA) & vertebral artery (QVA)), intra-cranial artery velocity (middle cerebral artery (MCAv) & posterior cerebral artery (PCAv)), and end-tidal gases (PETO₂ & PETCO₂) were controlled before and 90 min following oral Prazosin (1mg/20kg) at rest and during transient hypertension. Hypertension was non-pharmacologically induced using 30% maximal voluntary contraction (MVC) handgrip exercise (HG), lower-body positive pressure (LBPP), and combined LBPP & HG (LBPP+HG). Following Prazosin administration, baseline PETCO₂ (-1 mmHg), MAP (-7 mmHg) & MCAv (-5 cm/sec) were all significantly reduced (P<0.05), while PCAv, QICA and QVA and respective diameter were all unchanged; VA velocity was reduced (P=0.03), while ICA velocity was unchanged (P=0.96). Following Prazosin, MAP during 30% MVC HG was unchanged while MAP was significantly reduced during LBPP (-29 ± 68%) and LBPP+HG (-40 ± 38%); despite these changes in MAP, MCAv, PCAv, QICA & QVA all remained unchanged (P>0.05). There was significant attenuation of absolute PCAv CVC following Prazosin during LBPP and LBPP+HG (Δ0.036 ± 0.032 vs. Δ0.007 ± 0.019 & Δ0.053 ± 0.04 vs. Δ0.024 ± 0.025 cm/sec/mmHg; P<0.05), but not HG (P=0.4). Although changes in QICA and MAP were unrelated (r²=0.07; P=0.16) during 30% MVC HG, LBPP & LBPP+HG, QVA was positively correlated (r²=0.14; P=0.02) with changes in MAP following Prazosin. This latter observation is consistent with changes in PCAv CVC, potentially indicative of vasodilation in the PCA or alternatively redistribution of QVA before communicating with the PCA, or both. While these findings are contrary to our hypothesis, these differential findings are interpreted to indicate that there is a disparity between the extra- and intra-cranial arteries and that SNA serves a functional role in the regulation of the posterior region of the brain during transient hypertension.Graduate Studies, College of (Okanagan)
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Johansson, Jakob. "Cardiopulmonary Resuscitation : Pharmacological Interventions for Augmentation of Cerebral Blood Flow." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4281.
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Fellows, Lesley Kathleen. "In vivo monitoring of cerebral energy metabolism and blood flow." Thesis, University of Oxford, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314846.
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James, Peter Welbury. "Design and analysis of studies to estimate cerebral blood flow." Thesis, University of Newcastle Upon Tyne, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251020.
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Lucas, Claire. "An anatomical model of the cerebral vasculature and blood flow." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:37d408b6-b804-4085-b420-a9704aeb97eb.
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The brain accounts for around 2 % of human adult bodyweight but consumes 20 % of the resting oxygen available to the whole body. The brain is dependent on a constant supply of oxygen to tissue, transported from the heart via the vasculature and carried in blood. An interruption to flow can lead to ischaemia (a reduced oxygen supply) and prolonged interruption may result in tissue death, and permanent brain damage. The cerebral vasculature consists of many, densely packed, micro-vessels with a very large total surface area. Oxygen dissolved in blood enters tissue by passive diffusion through the micro-vessel walls. Imaging shows bursts of metabolic activity and flow in localised brain areas coordinated with brain activity (such as raising a hand). An appropriate level of oxygenation, according to physiological demand, is maintained via autoregulation; a set of response pathways in the brain which cause upstream or downstream vessels to expand or contract in diameter as necessary to provide sufficient oxygen to every region of the brain. Further, autoregulation is also evident in the response to pressure changes in the vasculature: the perfusing pressure can vary over a wide range from the basal-state with only a small effect on flow due to the constriction or dilation of vessels. Presented here is a new vasculature model where diameter and length are calculated in order to match the data available for flow velocity and blood pressure in different sized vessels. These vessels are arranged in a network of 6 generations each of bifurcating arterioles and venules, and a set of capillary beds. The input pressure and number of generations are the only specifications required to describe the network. The number of vessels, and therefore vessel geometry, is governed by how many generations are chosen and this can be altered in order to create more simple or complex networks. The flow, geometry and oxygen concentrations are calculated based on the vessel resistance due to flow from geometry based on Kirchoff circuit laws. The passive and active length-tension characteristics of the vasculature are established using an approximation of the network at upper and lower autoregulation limits. An activation model is described with an activation factor which governs the contributions of elastic andmuscle tension to the total vessel tension. This tension balances with the circumferential tension due to pressure and diameter and the change in activation sets the vessel diameter. The mass transport equation for oxygen is used to calculate the concentration of oxygen at every point in the network using data for oxygen saturation to establish a relationship between the permeability of the vessel wall to oxygen and the geometry and flow in individual vessels. A tissue compartment is introduced which enables the modelling of metabolic control. There is evidence for a coordinated response by surrounding vessels to local changes. A signal is proposed based on oxygen demand which can be conducted upstream. This signal decays exponentially with vessel length but also accumulates with the signal added from other vessels. The activation factor is therefore set by weighted signals proportional to changes in tissue concentration, circumferential tension, shear stress and conducted oxygen demand. The model is able to reproduce the autoregulation curve whereby a change in pressure has only a small effect on flow. The model is also able to replicate experimental results of diameter and tissue concentration following an increase in oxygen demand.
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Reinerman, Lauren E. "Cerebral Blood Flow Velocity and Stress as Predictors of Vigilance." University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1168111547.
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Miyamoto, Ikuya. "Rehabilitation with dental prosthesis can increase cerebral regional blood flow." Kyoto University, 2005. http://hdl.handle.net/2433/144467.
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Yang, Huijing. "Investigation of the correlation between cerebral blood flow and bold." Thesis, University of Iowa, 2014. https://ir.uiowa.edu/etd/4799.
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There are lots of dynamic process exist co-currently and spontaneously when the neurons in the brain are activated by the external stimulation, like cerebral blood flow (CBF) change, oxygen extraction change. The study of the dynamic relationship among these physiological variables, which describe the brain activity through different aspects, can help people understand the brain function when it gets excited and researchers can interpret the physiological meaning of these parameters better. The most common functional magnetic resonance imaging techniques are BOLD and ASL fMRI, in this research, the correlation between these two methods has been studied through a simultaneous data acquisition strategy. Assessing such correlation between BOLD fMRI measures and CBF offers a link of these two to the underlying of the spontaneous brain activities.
In the study, an ASL pulse sequence PICORE has been used to perform the fMRI experiment on 7 health subjects. A rapid median nerve electrical stimulation paradigm has been used to detect the activation of the brain from seven normal health right-handed human subjects. Three ROIs (SMA, S1, M1) have been selected and the data were analyzed to investigate the correlation between CBF value and BOLD signal change during brain activities. We found the CBF value rises for 5 - 6 ml/min/100g for fixed ROI and 11 - 12 ml/min/100g for non-fixed ROI and the BOLD signal change was around 0.8% for both situations. Our results shows for a fixed size ROI of each individual subject, no significant difference has been found for CBF value difference and the BOLD signal change between different runs and neither did the ratio of these two parameters (p > 0.05). When studied the activation area size for each run, we found significant difference for both CBF value difference and BOLD signal change (p < < 0.05) but no significant difference for the ratio of those two (p > 0.05). The dynamic relationship between CBF value difference and BOLD contrast signal change has been shown to be stable for a fixed ROI study. The amount of neurons being activated (activation size) for these two approaches has a habituation and decreased between runs, but the relationship between them remains typically the same since the ratio has no significant difference.
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Euser, Anna Gerrit. "Cerebral Blood Flow Autoregulation, Blood-Brain Barrier Permeability, and the Effects of Magnesium Sulfate Treatment During Pregnancy and Hypertension." ScholarWorks @ UVM, 2007. http://scholarworks.uvm.edu/graddis/81.
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Eclampsia is a hypertensive disorder of pregnancy and a leading cause of maternal death. The primary explanation for eclampsia is that it represents a form of hypertensive encephalopathy (HTE) with neurological symptoms including headaches, nausea, vomiting, visual disturbances, and seizures. The etiology of HTE involves an acute increase in arterial blood pressure that exceeds the autoregulatory capacity of the brain leading to forced dilatation of cerebral vessels, decreased cerebrovascular resistance, hyperperfusion, blood-brain barrier (BBB) disruption, and vasogenic cerebral edema formation. Due to the central role of the cerebral circulation in mediating these symptoms, a better understanding of how pregnancy affects the cerebral circulation is important to the treatment and prevention of eclampsia. A central goal of this dissertation was to determine pregnancy’s effect on cerebral blood flow (CBF) autoregulation, edema formation, and BBB permeability during acute hypertension. Women with eclampsia often seize at lower blood pressures than HTE patients. We hypothesized that pregnancy may predispose the brain to eclampsia by lowering the pressure of autoregulatory breakthrough and enhancing cerebral edema formation. Using an in vivo model of HTE, we found that the pressure of autoregulatory breakthrough was not different between nonpregnant (NP) and late-pregnant (LP) rats; however, cerebral edema formation was significantly increased only in LP animals. Nitric oxide synthase inhibition significantly increased the upper limit of autoregulation in both NP and LP animals and attenuated cerebral edema formation in LP animals. BBB permeability during acute hypertension was not different between these groups. Magnesium sulfate (MgSO4) is widely used to treat eclampsia despite an unclear mechanism of action. A second goal of this dissertation was to determine the cerebrovascular effects of MgSO4 during pregnancy. Specifically, we investigated the effect of MgSO4 on in vitro resistance artery vasodilation and in vivo BBB permeability during acute hypertension. We hypothesized that dilation to MgSO4 would be greater in mesenteric than cerebral vessels. MgSO4 elicited concentration-dependent vasodilation in all arteries, as determined by measuring lumen diameter of isolated and pressurized arteries, however, mesenteric arteries were considerably more sensitive than cerebral arteries. In addition, there was no effect of pregnancy on MgSO4 sensitivity in mesenteric arteries, whereas pregnancy decreased sensitivity to MgSO4 in cerebral arteries. We further hypothesized that MgSO4 would decrease BBB disruption during acute hypertension, thereby protecting the brain in eclampsia. Using an in vivo model of HTE, we showed that MgSO4 treatment decreased BBB permeability during acute hypertension in LP rats, with the greatest effect observed in the posterior cerebrum. In conclusion, this dissertation determined CBF autoregulation and cerebral edema formation during pregnancy, and also the effect of MgSO4 on cerebral resistance artery vasodilation and BBB permeability during acute hypertension in LP rats. Although pregnancy did not influence autoregulatory breakthrough, cerebral edema formation was enhanced in LP animals and this may potentiate neurological symptoms in eclampsia. In addition, MgSO4-induced cerebral vasodilation is likely not a primary mechanism of eclampsia treatment, rather MgSO4 may limit edema formation by attenuating BBB permeability during hypertension.
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Germon, Timothy John. "The validation of cerebral near infrared spectroscopy in adults." Thesis, University of Bristol, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299334.
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Smith, Kurt Jason. "Effects of arterial blood gas concentrations on regional cerebral blood flow and metabolism during exercise." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/54740.
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The magnitude of the cerebral blood flow (CBF) response to exercise is primarily related to the sensitive balance between arterial blood gases (partial pressure of arterial oxygen [PaO₂] and carbon dioxide [PaCO₂]) and cerebral metabolism. However, it has remained unclear whether experimentally or environmentally manipulating the oxygen tensions alters the regulatory influence of arterial blood gases on the intracranial velocities (CBV) and regional CBF responses to incremental exercise. The goal of the experimental chapters of this thesis (Chapter 4, 5 and 6) was to quantify the independent and combined influence of PaO₂ and PaCO₂ on global and regional CBV and CBF during exercise. Chapter 4 identified a heightened (nearly twice the expected response) posterior CBV response during hyperoxic (PO₂ ∼713 mmHg) compared to normoxic (PO₂ ∼160 mmHg) exercise. In contrast, both the anterior and posterior CBV responses were unaltered during mild hypoxic (PO₂ ∼121 mmHg) exercise compared to normoxic exercise. Chapter 5 demonstrated that during exercise in severe hypoxia (PO₂ ∼413 mmHg), following partial acclimatization to high altitude (5050 m), global CBF was elevated by ∼20% compared to sea-level exercise. The elevated global CBF during exercise at high altitude served to compensate for the hypoxemia, and in turn maintained cerebral oxygen delivery equivalent to sea-level values. Chapter 6 revisited and extended the observations during hyperoxic exercise from Chapter 4, whereby measures of extra-cranial CBF were compared with the intracranial velocities during normoxic and hyperoxic (PO₂ ∼300 mmHg) exercise, and also in a separate condition in which any exercise-induced rise in PaCO₂ was prevented (i.e., isocapnia was maintained). The differences observed between regional CBV and CBF during normoxic and hyperoxic incremental exercise trials were abolished when PaCO₂ was held constant. This final chapter also demonstrated that the increased ventilation, per se, is unlikely to influence the cerebrovascular response to exercise. In conclusion, changes in arterial blood gases (hypoxia and hyperoxia) can exacerbate the cerebrovascular response to exercise; however, during incremental exercise in hyperoxia, the regional differences, as well as the differential intracranial and extra-cranial flow responses, are mediated primarily by PaCO₂.Graduate Studies, College of (Okanagan)
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Wills, A. J. "Positron emission tomography studies of tremor." Thesis, Queen Mary, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297290.
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Wieckowska, Marguerite. "Cerebral blood flow measurement using fMRI and pet : a validation study." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=79271.
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Functional magnetic resonance imaging (fMRI) is a technique allowing the study of hemodynamic changes in the brain. Having a number of advantages over positron emission tomography (PET), the current gold standard, fMRI appears like an attractive alternative to study brain function. However, the measurements obtained with fMRI have not been rigorously validated.This thesis describes a study comparing cerebral blood flow (CBF) changes measured using a flow-sensitive alternating inversion recovery (FAIR) fMRI perfusion method, to the ones obtained using PET. We scanned 10 healthy normal volunteers under identical experimental conditions during presentation of 4 levels of visual stimulation and one level of hypercapnia. The CBF changes were compared in 4 regions-of-interest.
Good correspondence was found in the locations of the CBF changes. FAIR CBF changes had a higher signal-to-noise ratio and presented a monotonic increase with stimulation intensity, absent in PET measurements. FAIR measurements were correlated to PET but slightly lower. Statistical analysis of the data did not show that FAIR measurements were significantly different from PET ones.
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Su, Shen-Wei. "Modelling blood flow and oxygen transport in the human cerebral cortex." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:cee70abb-8c36-4244-920c-71305cf97bd0.
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Dementia, a stepwise deterioration of cognitive function, affects over 700,000 people in the UK, resulting in over 60,000 deaths and a cost of over £1.7 billion each year. It is believed to have a combination of vascular and degenerative origins and to have correlations with localised lesions, or infarctions, in the brains of affected patients. Mini-strokes are one of the causes for this disease as the presence of ischemia is highly related to the risk factors for dysfunction of the neurovascular unit. The underlying interacting mechanisms are, however, often very complex and they remain largely poorly understood. The cerebral microvascular bed is highly irregular and localised variations in its structure are large. To capture these variations, statistical algorithms are required, rather than large volumes of expensive experimental data. Therefore, accurate modelling of blood flow and oxygen transport at the microvascular level is important in improving our understanding of the structure and function of the cerebral vasculature and hence of brain diseases. A novel algorithm is proposed here to create artificial microvascular networks that match quantitatively experimental data previously obtained in human brain tissue. Blood flow and oxygen transport in the network and the tissue are analysed through both discretised and continuum transport models. By disabling flow sources, ischemic events can be simulated. Using multiple networks, the influence of individual network structures on the response to ischemia is analysed. The relationship between the discretised and continuum formulations of the model is quantified, providing a means for scaling up the model over multi length scales. Finally, the phenomenon of microvessel collapse under ischemic conditions is examined and it is shown that this is fundamentally dependent upon the variability found at the network level, since it cannot be modelled by a continuum model. An initial infarction is also found to facilitate the occurrence of collapse events for most networks.
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Tovedal, Thomas. "Cerebral perfusion during cardiopulmonary bypass with special reference to blood flow." Doctoral thesis, Uppsala universitet, Anestesiologi och intensivvård, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-248686.
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Cardiopulmonary bypass (CPB) is an important method that enables open heart surgery. There is a risk of neurological complications, and efforts to minimize those include optimization of the cerebral perfusion during CPB. This thesis focuses on such optimization of flow conditions in case of obstructed venous drainage, carotid stenosis and during selective antegrade cerebral perfusion (SACP). In a pig model of impaired venous drainage from the superior vena cava (SVC), stepwise obstruction increased the central venous pressure (CVP) and caused impaired oxygenation. Cerebral micro-dialysis revealed ischemic responses in some but not all of the pigs. Further experiments, using the same model, aimed to restore cerebral perfusion pressure (CPP) reduced by 75% superior venous obstruction. Both vasopressor treatment and increased venous drainage were effective in normalizing the CPP and improving the cerebral oxygenation. The intracranial pressure was elevated in the vasopressor group, but no signs of brain damage were observed. The arterial flow during CPB can be altered between pulsatile and non-pulsatile profiles. Switching between these modes was performed during CPB in 20 patients with or without carotid stenosis. The effects on cerebral oxygenation and mean arterial pressure (MAP) were examined. The MAP was significantly lowered by pulsatile flow, but the flow profile did not affect the cerebral oxygenation. No differences were seen between patients with or without carotid stenosis. SACP is used to ensure the cerebral perfusion during deep hypothermic circulatory arrest (HCA). The cerebral blood flow (CBF) was examined using positron-emission tomography (PET) technique in 8 pigs divided into HCA and HCA+SACP groups. The CBF was downregulated by 70% to 0.10 ml/cm3/min by 20°C hypothermia. A pump flow of 6 ml/kg/min preserved the CBF level without signs of cerebral desaturation. The fluorodeoxyglucose (FDG) uptake after re-warming to 37°C was similar after SACP compared with HCA alone. In conclusion, experimental SVC obstruction may impair the cerebral perfusion. Vasopressors can restore the CPP during SVC obstruction and improve cerebral oxygenation. In patients, pulsatile flow can lower the MAP in absence of effects on the cerebral oxygenation. During experimental HCA, SACP at 6 ml/kg/min can preserve the CBF at 0.10 ml/cm3/min.
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Gentile, Russell. "Adding cerebral autoregulation to a lumped parameter model of blood flow." Honors in the Major Thesis, University of Central Florida, 2012. http://digital.library.ucf.edu/cdm/ref/collection/ETH/id/555.
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A mathematical model of blood flow in infants with hypoplastic left heart syndrome (HLHS) was improved by adding cerebral autoregulation. This is the process by which blood vessels constrict or dilate to keep blood flow steady in certain organs during pressure changes. The original lumped parameter model transformed the fluid flow into an electrical circuit. Its behavior is described using a system of thirty-three coupled differential equations that are solved numerically using a fourth-order Runge-Kutta method implemented in MATLAB. A literature review that includes a discussion of autoregulation mechanisms and approaches to modeling them is followed by a description of the model created for this paper. The model is based on the baroreceptor or neurogenic theory of autoregulation. According to this theory, nerves in certain places within the cardiovascular system detect changes in blood pressure. The brain then compensates by sending a signal to blood vessels to constrict or dilate. The model of the control system responded fairly well to a pressure drop with a steady state error of about two percent. Running the model with or without the control system activated had little effect on other parameters, notably cardiac output. A more complete model of blood flow control would include autonomic regulation. This would vary more parameters than local autoregulation, including heart rate and contractility. This is suggested as a topic of further research.B.S.M.E.
Bachelors
Engineering and Computer Science
Mechanical Engineering
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Boylan, Geraldine Bernadette. "EEG and cerebral blood flow velocity in the sick newborn baby." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268436.
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Smirl, Jonathan David. "The relationship between arterial blood pressure and cerebral blood flow : insights into aging, altitude and exercise." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/54000.
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The majority of previous research on the relationship between blood pressure and cerebral blood flow (CBF) through the application of transfer function analysis (TFA) has been performed under spontaneous conditions. Under these circumstances, there is little input signal power (blood pressure), which makes linear interpretation of the output (CBF) results tenuous. In five experimental studies, the general aim of this thesis was to provide new insights on the relationship(s) between blood pressure and CBF throughout the aging spectrum. The first study determined the reproducibility of TFA metrics during spontaneous and driven blood pressure oscillations. The results revealed that squat-stand maneuvers were the most robust and reliable method to evaluate this relationship throughout aging. Consequently, this methodology was employed for the research studies. The second study examined the pressure-flow response in younger adults with acutely elevated cerebrovascular resistance index (CVRi). Augmenting CVRi, even without changes in CO₂, resulted in increased phase lead and reduced amplitude modulation; therefore, the impact of CVRi needs to be considered for the parsimonious interpretation of TFA metrics. The third experiment examined the pressure-flow relationship in three adult populations: young and old healthy adults, and heart transplant recipients. Findings revealed comparable cerebral pressure-flow responses in all groups, despite elevated CVRi (older groups), and blunted cardiac baroreceptors (long-term heart transplant recipients). Thus, it appears the acutely increased phase and decreased gain noted in the second study may not accurately reflect the chronic elevations in CVRi in older adults.
Through the unique approach of oscillating blood pressure during exercise, the fourth study demonstrated that the cerebrovasculature high-pass filter model is intact in both young and older populations. The final study at high-altitude (5050m) explored the cerebral pressure-flow relationship prior to, during acclimatization, and return from high-altitude. Despite the marked oxygen desaturation, there were no changes to the pressure-flow response across the entire range of exposure acclimatization timelines. In conclusion: 1) squat-stand maneuvers provide a meritorious way to examine cerebral-pressure flow responses; and 2) effective pressure-flow relationships are maintained during healthy aging and exercise, and persist despite blunting of cardiac baroreflexes and reductions in arterial oxygen saturation.Graduate Studies, College of (Okanagan)
Graduate
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Shrewsbury-Gee, Joanne. "An investigation of compounds of potential value in experimental cerebral ischaemia." Thesis, University of Manchester, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.329110.
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Wong, Michael Lik Hang. "Transcranial doppler ultrasound pulsatility index and cerebral blood flow autoregulation in neurotrauma /." Title page and abstract only, 1994. http://web4.library.adelaide.edu.au/theses/09MS.B/09ms.bw872.pdf.
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Kunicki, Suzanne. "Cerebral blood flow regulation in the human and in a bovine model." Thesis, McGill University, 1991. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=60567.
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The role of perivascular nerve fibers, smooth muscle cells and endothelium in the regulation of human and bovine cerebral artery contractility was investigated in vitro and the effect of cold-storage on vessel function was determined. Stimulation of perivascular nerve endings over a range of transmural electric field stimulation produced frequency- and duration-dependent responses in arteries of both species. The pharmacological properties of the cerebral vessels were studied using 17 different vasoactive agents which acted directly on the smooth muscle and/or on the endothelium. Parallel studies on human and bovine vessels indicate that the cow may be a very useful source of tissue for further experimentation. Cold-storage of cerebral arteries did not significantly alter vessel viability or responsiveness to vasoactive compounds, although a reduction in sensitivity to transmural electric field stimulation in human middle and posterior arteries was observed.
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Meadows, Guy Ellis. "The regulation of cerebral blood flow during wakefulness and sleep in humans." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413672.
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Gallichan, Daniel. "Measuring cerebral blood flow using arterial spin labelling with magnetic resonance imaging." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.442955.
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Tingying, Peng. "Signal processing methods for the analysis of cerebral blood flow and metabolism." Thesis, University of Oxford, 2009. http://ora.ox.ac.uk/objects/uuid:ca84ac5b-7df0-488d-b390-d6f4f6e3ee52.
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An important protective feature of the cerebral circulation is its ability to maintain sufficient cerebral blood flow and oxygen supply in accordance with the energy demands of the brain despite variations in a number of external factors such as arterial blood pressure, heart rate and respiration rate. If cerebral autoregulation is impaired, abnormally low or high CBF can lead to cerebral ischemia, intracranial hypertension or even capillary damage, thus contributing to the onset of cerebrovascular events. The control and regulation of cerebral blood flow is a dynamic, multivariate phenomenon. Sensitive techniques are required to monitor and process experimental data concerning cerebral blood flow and metabolic rate in a clinical setting. This thesis presents a model simulation study and 4 related signal processing studies concerned with CBF regulation. The first study models the regulation of the cerebral vasculature to systemic changes in blood pressure, dissolved blood gas concentration and neural activation in a integrated haemodynamic system. The model simulations show that the three pathways which are generally thought to be independent (pressure, CO₂ and activation) greatly influence each other, it is vital to consider parallel changes of unmeasured variability when performing a single pathway study. The second study shows how simultaneously measured blood gas concentration fluctuations can improve the accuracy of an existing frequency domain technique for recovering cerebral autoregulation dynamics from spontaneous fluctuations in blood pressure and cerebral blood flow velocity. The third study shows how the continuous wavelet transform can recover both time and frequency information about dynamic autoregulation, including the contribution of blood gas concentration. The fourth study shows how the discrete wavelet transform can be used to investigate frequency-dependent coupling between cerebral and systemic cardiovascular dynamics. The final study then uses these techniques to investigate the systemic effects on resting BOLD variability. The general approach taken in this thesis is a combined analysis of both modelling and data analysis. Physiologically-based models encapsulate hypotheses about features of CBF regulation, particularly those features that may be difficult to recover using existing analysis methods, and thus provide the motivation for developing both new analysis methods and criteria to evaluate these methods. On the other hand, the statistical features extracted directly from experimental data can be used to validate and improve the model.
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Xie, Jingyi. "Quantitative measurement of regional cerebral blood flow with arterial spin labelling imaging." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.504384.
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Doctors, G. M. "Towards patient-specific modelling of cerebral blood flow using lattice-Boltzmann methods." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1335721/.
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Patient-specific Computational fluid dynamics (CFD) studies of cerebral blood flow have the potential to help plan neurosurgery, but developing realistic simulation methods that deliver results quickly enough presents a major challenge. The majority of CFD studies assume that the arterial walls are rigid. Since the lattice-Boltzmann method (LBM) is computationally efficient on multicore machines, some methods for carrying out lattice-Boltzmann simulations of time-dependent fluid flow in elastic vessels are developed. They involve integrating the equations of motion for a number of points on the wall. The calculations at every lattice site and point on the wall depend only on information from neighbouring lattice sites or wall points, so they are suitable for efficient computation on multicore machines. The first method is suitable for three-dimensional axisymmetric vessels. The steady-state solutions for the wall displacement and flow fields in a cylinder at realistic parameters for cerebral blood ow agree closely with the analytical solutions. Compared to simulations with rigid walls, simulations with elastic walls require 13% more computational effort at the parameters chosen in this study. A scheme is then developed for a more complex geometry in two dimensions, which applies the full theory of linear elasticity. The steady-state wall profiles obtained from simulations of a Starling resistor agree closely with those from existing computational studies. I find that it is essential to change the lattice sites from solid to fluid and vice versa if the wall crosses any of them during the simulation. Simple tests of the dynamics show that when the mass of the wall is much greater than that of the fluid, the period of oscillation of the wall agrees within 7% of the expected period. This method could be extended to three dimensions for use in cerebral blood ow simulations.
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Wei, Datong. "Quantitative and continuous measurement of cerebral blood flow by a thermal method." Case Western Reserve University School of Graduate Studies / OhioLINK, 1993. http://rave.ohiolink.edu/etdc/view?acc_num=case1060354210.
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Beam, Christina Ashley. "Effects of Sensory and Cognitive Vigilance Tasks on Cerebral Blood Flow Velocity." University of Cincinnati / OhioLINK, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1036017621.
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Rubinstein, Abraham B. "An experimental investigation of spinal cord blood flow, it's autoregulation, and the effects of cerebral compression on spinal cord blood flow /." Thesis, McGill University, 1986. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66220.
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Helps, Stephen. "Cerebral blood flow in rats after treatment with the primary sensory neurotoxin capsaicin." Title page, contents and summary only, 1987. http://web4.library.adelaide.edu.au/theses/09SM/09smh484.pdf.
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McGleenon, Bronagh Mary. "Endothelial function and measures of oxidative stress in Alzheimer's disease." Thesis, Queen's University Belfast, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301745.
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Austin, Nicola Cecile. "A study of the effect of the patent ductus arteriosus on the intracranial and extracranial arterial blood flow velocity waveforms in preterm infants." Thesis, University of Southampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296274.
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Trangmar, Steven John. "Circulatory limitations to exercise capacity in humans : the impact of heat stress and dehydration on brain and muscle blood flow and metabolism." Thesis, Brunel University, 2015. http://bura.brunel.ac.uk/handle/2438/10609.
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Heat stress and dehydration pose a severe challenge to physiological function and the capability to perform physical work. There is, however, limited knowledge on the regional haemodynamic and metabolic responses to strenuous exercise in environmentally stressful conditions. The primary aim of this thesis was to examine whether dehydration and heat stress compromise brain, muscle and systemic blood flow and metabolism, and whether depressed brain and muscle oxygen delivery underpin reduced exercise capacity during graded incremental and prolonged exercise. This thesis makes an original contribution to the knowledge by showing for the first time that dehydration markedly accelerates the decline in cerebral blood flow during maximal incremental (Chapter 4) and prolonged sub-maximal exercise (Chapter 5) in the heat. Cerebral metabolism, however, is preserved by compensatory increases in substrate extraction. Falling carbon dioxide tension underpinned the decline in CBF. However, a distinct regional distribution of blood flow across the head was observed, suggesting that different mechanisms are responsible for the regulation of regional blood flow within the head. A reduced cerebral metabolism is therefore an unlikely factor explaining the compromised exercise capacity in physiologically stressful hot environments. Rather, restrictions in active muscle blood flow and oxygen supply, which are not apparent during sub-maximal exercise, may explain the reduced maximal aerobic power in heat stressed conditions. For the first time we have manipulated skin and core temperature to show that combined internal and skin hyperthermia reduces maximal aerobic power in association with restrictions in limb, brain and systemic blood flow and skeletal muscle metabolism (Chapter 6). Overall, the findings of the present thesis provide novel information on how circulatory limitations across contracting skeletal muscle, brain and systemic tissues and organs might underpin the impairment in exercise capacity in physiologically taxing environments evoking significant dehydration and hyperthermia.
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Ben-Yoseph, O. "Multinuclear magnetic resonance spectroscopy studies of perturbed cerebral metabolism in vitro." Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240078.
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Smirl, Jonathan David. "Cerebral blood flow in heart transplant recipients at rest and during incremental exercise." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/40296.
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Pathological impairments to cardiac output may impact cerebral blood flow (CBF). Prior studies on heart transplant recipients (HTR) have reported increases of 25-53% in CBF, 1-6 months following transplant. It is currently unknown if CBF is chronically altered in the years following transplant or during progressive exercise stress, when compared with aged-matched controls (AM). Donor population controls (DC) were included to determine if the responses observed in HTR are related to the age of the donor rather than the individual. The aim of this thesis was to examine the influence of long-term heart transplantation on the regulation of CBF velocity (CBFv) at rest and during incremental exercise. Two hypotheses were tested: 1) CBFv would be similar in HTR when compared to AM, but lower than DC; 2) that during incremental exercise, the HTR would have reduced elevations in CBFv compared with AM and DC.
To address these hypotheses, HTR were tested who have a reported inability to acutely increase cardiac output during exercise. Seven male clinically stable HTR (62 ± 9 yrs of age, 9 ± 7 yrs post-transplant), seven male AM (62 ± 7 yrs), and seven male DC (22 ± 3 yrs) were recruited for this study. Bilateral middle cerebral arteries were insonated using transcranial Doppler ultrasound to obtain an index of CBFv. Data were obtained while seated and during an incremental cycling test to volitional exhaustion. A repeated measures ANOVA was applied to identify differences across exercise intensity. Comparisons between groups were performed with Fisher's LSD post hoc test.
The main findings were: 1) Rest: CBFv was comparable between HTR and AM (40 vs. 41 cm/s), as expected, CBFv was 68% higher in the DC compared with the HTR and AM groups (P<0.05). 2) Incremental exercise: mean CBFv was not significantly different between the HTR and AM groups across any of the exercise intensities.
In conclusion, the CBFv of long-term HTR are comparable to AM both at rest and during incremental exercise that despite a suppressed VO₂ Peak (and likely Q) CBFv is well maintained during incremental exercise in long – term HTR.
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Chemtob, Sylvain. "The role of prostaglandins in autoregulation of cerebral blood flow of the newborn /." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=75940.
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The role of prostanoids in autoregulation of cerebral blood flow (CBF) of the newborn is unclear. We hypothesized that prostanoids not only exhibit cerebral vasoactive properties, but also play an important role in setting the limits of autoregulation of CBF in the newborn.Consequently, in the newborn piglet, we determined the effects of prostaglandins (PGs), PGE$ sb1$, PGE$ sb2$, PGF$ sb{2 alpha}$ and PGI$ sb2$, on CBF, and compared their vasoactive action on isolated internal carotid and basilar arteries of newborns and adults. Cerebrovascular prostanoid concentrations were also measured as a function of systemic blood pressure (BP), in animals subjected or not to prostanoid synthesis inhibition, using ibuprofen. Finally, we examined in the preterm infant the effects of indomethacin on CBF velocity (CBFV) during clinical procedures (endotracheal suctioning) known to increase BP and CBFV concomitantly.
All major cerebrovascular PGs (physiologically relevant doses) increased CBF, and contracted minimally isolated arteries. These effects were most evident for PGF$ sb{2 alpha}$, the most effective adult vasoconstrictor PG.
During hypotension, sagittal sinus concentrations of thromboxane exhibited the highest increase of all prostanoids. However, during hypertension, PGE, PGF$ sb{2 alpha}$, and 6-keto-PGF$ sb{1 alpha}$ increased, without changes in TXB$ sb2$. Ibuprofen, inhibited the changes in prostanoids that occurred as a function of BP, and widened CBF autoregulation from 50-90 mm Hg to 35-117 mm Hg of BP. Therefore, the potent vasoconstrictor, thromboxane, contributed to set the lower limit of the CBF autoregulatory range to 50 mm Hg of BP; and PGs (which increase newborn CBF) contributed to the pressure-passivity of CBF above 90 mm Hg.
In the preterm newborn infant, indomethacin attenuated the increases in CBFV that occur with endotracheal suctioning; thus, in accord with studies on animals subjected to changes in BP.
In conclusion, PGs possess minimal cerebral vasocontractile activity in the newborn. The findings confirm our hypothesis that prostanoids contribute significantly in establishing the range of CBF autoregulation of the newborn, which is principally narrowed at its upper limit compared to that of the adult. Thus, the difference in the CBF autoregulatory range of the newborn and adult animal appears to result mainly from age-related differences in the effects of PGs on cerebral hemodynamics. Finally, ibuprofen may provide therapeutic modes to prevent hemorrhagic and ischemic encephalopathies of the newborn.
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Laudignon, Nicole. "The rle of adenosine on regulation of cerebral blood flow in the newborn /." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=74338.
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The high vulnerability of the newborn brain to oxygen deficit strongly suggests a relative inadequacy in the adaptive cerebral vessel dilation. We hypothesized that this neonatal deficiency might be due to an insufficient brain adenosine production and/or a decreased sensitivity of the cerebral vessels to adenosine, a crucial metabolic regulator of adult cerebral blood flow. This hypothesis was tested on newborn (1-3 day old) and older pigs as the experimental model. Our findings are as follows: (1) Adenosine induced a concentration-dependent vasodilation of the newborn cerebral vessels, especially in the brain stem and periventricular area. (2) The cerebrospinal fluid concentration of adenosine and adenosine metabolites increased during both hypoxic-hypoxia and systemic hypotension. During hypoxia, these levels were inversely correlated to the arterial oxygen content and positively correlated to the increase in cerebral blood flow. (3) Adenosine receptor antagonism by 8-phenyltheophylline completely blocked the cerebral hyperemia during moderate hypoxia, partially reversed it during severe hypoxia, and abolished autoregulation (i.e. the maintenance of a constant cerebral blood flow over a wide range of systemic blood pressure). Moreover, adenosine receptor blockade altered the regional redistribution of cerebral blood flow during severe hypoxia and hypotension. (4) Cerebrospinal fluid concentrations of adenosine during normoxia and hypoxia were lower in the newborn than in the older animals. (5) Relative to adult internal carotid arteries (important cerebral resistance vessels), newborn vessels were less sensitive to adenosine.These data demonstrate that adenosine is a potent dilator of the cerebral vessels and an important mediator of the regional cerebral adaptive response to brain oxygen deficit in the newborn. Brain interstitial concentrations of adenosine and the cerebral vessel sensitivity to adenosine are lower in the newborn than in the older individual. These findings may explain the relative deficiency in the adaptation of the newborn cerebral vasculature during brain oxygen deficit, leading to an unusual vulnerability to hypoxic-ischemic encephalopathy.
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Wiersma, Jonna Alcide. "Measurement of cerebral blood flow in humans using MRI with arterial spin labelling." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.483504.
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Piechnik, Stefan K. "A mathematical and biophysical modelling of cerebral blood flow and cerebrospinal fluid dynamics." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269226.
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