Relevant bibliographies by topics / Cerebral Arteriole

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  1. Journal articles
  2. Dissertations / Theses
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  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Cerebral Arteriole'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Cerebral Arteriole"

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Baker, Wesley B., Ashwin B. Parthasarathy, Kimberly P. Gannon, Venkaiah C. Kavuri, David R. Busch, Kenneth Abramson, Lian He, et al. "Noninvasive optical monitoring of critical closing pressure and arteriole compliance in human subjects." Journal of Cerebral Blood Flow & Metabolism 37, no. 8 (May 25, 2017): 2691–705. http://dx.doi.org/10.1177/0271678x17709166.

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The critical closing pressure ( CrCP) of the cerebral circulation depends on both tissue intracranial pressure and vasomotor tone. CrCP defines the arterial blood pressure ( ABP) at which cerebral blood flow approaches zero, and their difference ( ABP − CrCP) is an accurate estimate of cerebral perfusion pressure. Here we demonstrate a novel non-invasive technique for continuous monitoring of CrCP at the bedside. The methodology combines optical diffuse correlation spectroscopy (DCS) measurements of pulsatile cerebral blood flow in arterioles with concurrent ABP data during the cardiac cycle. Together, the two waveforms permit calculation of CrCP via the two-compartment Windkessel model for flow in the cerebral arterioles. Measurements of CrCP by optics (DCS) and transcranial Doppler ultrasound (TCD) were carried out in 18 healthy adults; they demonstrated good agreement (R = 0.66, slope = 1.14 ± 0.23) with means of 11.1 ± 5.0 and 13.0 ± 7.5 mmHg, respectively. Additionally, a potentially useful and rarely measured arteriole compliance parameter was derived from the phase difference between ABP and DCS arteriole blood flow waveforms. The measurements provide evidence that DCS signals originate predominantly from arteriole blood flow and are well suited for long-term continuous monitoring of CrCP and assessment of arteriole compliance in the clinic.
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2

Xi, Qi, Edward Umstot, Guiling Zhao, Damodaran Narayanan, Charles W. Leffler, and Jonathan H. Jaggar. "Glutamate regulates Ca2+ signals in smooth muscle cells of newborn piglet brain slice arterioles through astrocyte- and heme oxygenase-dependent mechanisms." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 2 (February 2010): H562—H569. http://dx.doi.org/10.1152/ajpheart.00823.2009.

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Glutamate is the principal cerebral excitatory neurotransmitter and dilates cerebral arterioles to match blood flow to neural activity. Arterial contractility is regulated by local and global Ca2+ signals that occur in smooth muscle cells, but modulation of these signals by glutamate is poorly understood. Here, using high-speed confocal imaging, we measured the Ca2+ signals that occur in arteriole smooth muscle cells of newborn piglet tangential brain slices, studied signal regulation by glutamate, and investigated the physiological function of heme oxygenase (HO) and carbon monoxide (CO) in these responses. Glutamate elevated Ca2+ spark frequency by ∼188% and reduced global intracellular Ca2+ concentration ([Ca2+]i) to ∼76% of control but did not alter Ca2+ wave frequency in brain arteriole smooth muscle cells. Isolation of cerebral arterioles from brain slices abolished glutamate-induced Ca2+ signal modulation. In slices treated with l-2-α-aminoadipic acid, a glial toxin, glutamate did not alter Ca2+ sparks or global [Ca2+]i but did activate Ca2+ waves. This shift in Ca2+ signal modulation by glutamate did not occur in slices treated with d-2-α-aminoadipic acid, an inactive isomer of l-2-α-aminoadipic acid. In the presence of chromium mesoporphyrin, a HO blocker, glutamate inhibited Ca2+ sparks and Ca2+ waves and did not alter global [Ca2+]i. In isolated arterioles, CORM-3 [tricarbonylchloro(glycinato)ruthenium(II)], a CO donor, activated Ca2+ sparks and reduced global [Ca2+]i. These effects were blocked by 1 H-(1,2,4)-oxadiazolo-(4,3-a)-quinoxalin-1-one, a soluble guanylyl cyclase inhibitor. Collectively, these data indicate that glutamate can modulate Ca2+ sparks, Ca2+ waves, and global [Ca2+]i in arteriole smooth muscle cells via mechanisms that require astrocytes and HO. These data also indicate that soluble guanylyl cyclase is involved in CO activation of Ca2+ sparks in arteriole smooth muscle cells.
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Liang, Guo Hua, Adebowale Adebiyi, M. Dennis Leo, Elizabeth M. McNally, Charles W. Leffler, and Jonathan H. Jaggar. "Hydrogen sulfide dilates cerebral arterioles by activating smooth muscle cell plasma membrane KATP channels." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 6 (June 2011): H2088—H2095. http://dx.doi.org/10.1152/ajpheart.01290.2010.

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Hydrogen sulfide (H2S) is a gaseous signaling molecule that appears to contribute to the regulation of vascular tone and blood pressure. Multiple potential mechanisms of vascular regulation by H2S exist. Here, we tested the hypothesis that piglet cerebral arteriole smooth muscle cells generate ATP-sensitive K+ (KATP) currents and that H2S induces vasodilation by activating KATP currents. Gas chromatography/mass spectrometry data demonstrated that after placing Na2S, an H2S donor, in solution, it rapidly (1 min) converts to H2S. Patch-clamp electrophysiology indicated that pinacidil (a KATP channel activator), Na2S, and NaHS (another H2S donor) activated K+ currents at physiological steady-state voltage (−50 mV) in isolated cerebral arteriole smooth muscle cells. Glibenclamide, a selective KATP channel inhibitor, fully reversed pinacidil-induced K+ currents and partially reversed (∼58%) H2S-induced K+ currents. Western blot analysis indicated that piglet arterioles expressed inwardly rectifying K+ 6.1 (Kir6.1) channel and sulfonylurea receptor 2B (SUR2B) KATP channel subunits. Pinacidil dilated pressurized (40 mmHg) piglet arterioles, and glibenclamide fully reversed this effect. Na2S also induced reversible and repeatable vasodilation with an EC50 of ∼30 μM, and this effect was partially reversed (∼55%) by glibenclamide. Vasoregulation by H2S was also studied in pressurized resistance-size cerebral arteries of mice with a genetic deletion in the gene encoding SUR2 (SUR2 null). Pinacidil- and H2S-induced vasodilations were smaller in arterioles of SUR2 null mice than in wild-type controls. These data indicate that smooth muscle cell KATP currents control newborn cerebral arteriole contractility and that H2S dilates cerebral arterioles by activating smooth muscle cell KATP channels containing SUR2 subunits.
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Wu, Xu-Dong, Chen Wang, Zhen-Ying Zhang, Yan Fu, Feng-Ying Liu, and Xiu-Hua Liu. "PuerarinAttenuates Cerebral Damage by Improving Cerebral Microcirculation in Spontaneously Hypertensive Rats." Evidence-Based Complementary and Alternative Medicine 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/408501.

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Puerariae Lobatae Radix(Gegen in Chinese) is the dried root ofPueraria lobata, a semiwoody, perennial, and leguminous vine native to China.Puerarinis one of the effective components of isoflavones isolated from the root ofPueraria lobata. Previous studies showed that extracts derived from the root ofPueraria lobatapossessed antihypertensive effect. Our study is to investigate whetherpuerarincontributes to prevention of stroke by improving cerebral microcirculation in rats.Materials and Methods. Video microscopy and laser Doppler perfusion imaging on the pia mater were used to measure the diameter of microvessel and blood perfusion in 12-week old spontaneously hypertensive rats (SHRs) and age-matched normotensive WKY rats. Histological alterations were observed by hematoxylin and eosin staining, and microvessel density in cerebral tissue was measured by immunohistochemical analysis with anti-Factor VIII antibody. Cell proliferation was detected by [3H]-TdR incorporation, and activities of p42/44 mitogen activated protein kinases (p42/44 MAPKs) were detected by western blot analysis in cultured cerebral microvascular endothelial cells (MECs).Results. Intravenous injection ofpuerarinrelaxed arterioles and increased the blood flow perfusion in the pia mater in SHRs.Puerarintreatment for 14 days reduced the blood pressure to a normal level in SHRs (P<0.05) and increased the arteriole diameter in the pia mater significantly as compared with vehicle treatment. Arteriole remodeling, edema, and ischemia in cerebral tissue were attenuated inpuerarin-treated SHRs. Microvessel density in cerebral tissue was greater withpuerarinthan with vehicle treatment.Puerarin-treated MECs showed greater proliferation and p42/44 MAPKs activities than vehicle treatment.Conclusions.Puerarinpossesses effects of antihypertension and stroke prevention by improved microcirculation in SHRs, which results from the increase in cerebral blood perfusion both by arteriole relaxation and p42/44 MAPKs-mediated angiogenesis.
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Beard, Daniel J., Damian D. McLeod, Caitlin L. Logan, Lucy A. Murtha, Mohammad S. Imtiaz, Dirk F. van Helden, and Neil J. Spratt. "Intracranial Pressure Elevation Reduces Flow through Collateral Vessels and the Penetrating Arterioles they Supply. a Possible Explanation for ‘Collateral Failure’ and Infarct Expansion after Ischemic Stroke." Journal of Cerebral Blood Flow & Metabolism 35, no. 5 (February 11, 2015): 861–72. http://dx.doi.org/10.1038/jcbfm.2015.2.

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Recent human imaging studies indicate that reduced blood flow through pial collateral vessels (‘collateral failure’) is associated with late infarct expansion despite stable arterial occlusion. The cause for ‘collateral failure’ is unknown. We recently showed that intracranial pressure (ICP) rises dramatically but transiently 24 hours after even minor experimental stroke. We hypothesized that ICP elevation would reduce collateral blood flow. First, we investigated the regulation of flow through collateral vessels and the penetrating arterioles arising from them during stroke reperfusion. Wistar rats were subjected to intraluminal middle cerebral artery (MCA) occlusion (MCAo). Individual pial collateral and associated penetrating arteriole blood flow was quantified using fluorescent microspheres. Baseline bidirectional flow changed to MCA-directed flow and increased by 4450% immediately after MCAo. Collateral diameter changed minimally. Second, we determined the effect of ICP elevation on collateral and watershed penetrating arteriole flow. Intracranial pressure was artificially raised in stepwise increments during MCAo. The ICP increase was strongly correlated with collateral and penetrating arteriole flow reductions. Changes in collateral flow post-stroke appear to be primarily driven by the pressure drop across the collateral vessel, not vessel diameter. The ICP elevation reduces cerebral perfusion pressure and collateral flow, and is the possible explanation for ‘collateral failure’ in stroke-in-progression.
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Ganjoo, Pragati, Neil E. Farber, Antal Hudetz, Jeremy J. Smith, Enric Samso, John P. Kampine, and William T. Schmeling. "In Vivo Effects of Dexmedetomidine on Laser-Doppler Flow and Pial Arteriolar Diameter." Anesthesiology 88, no. 2 (February 1, 1998): 429–39. http://dx.doi.org/10.1097/00000542-199802000-00022.

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Background The alpha2-adrenergic agonist dexmedetomidine alters global cerebral blood flow (CBF). However, few studies have investigated the action of dexmedetomidine on the cerebral microcirculation. This investigation examined the effects of dexmedetomidine on (1) regional CBF in the rat cerebral cortex using laser-Doppler flowmetry and (2) on pial arteriolar diameter. Methods Halothane-anesthetized rats were fitted with instruments to measure CBF as determined by laser-Doppler flow (CBFldf) or to measure pial arteriolar diameter by preparing a cranial hollow deepened until a translucent plate of skull remained, thereby maintaining the integrity of the cranial vault. In both groups, 20 microg/kg dexmedetomidine was infused intravenously. Thirty minutes later, the mean arterial pressure was restored to control values with an infusion of phenylephrine (0.5 to 5 microg/kg/min). Results Administration of dexmedetomidine was associated with decreases in end-tidal and arterial carbon dioxide. The CBFldf and pial arteriolar diameter were measured during normocapnia (controlled carbon dioxide) and during dexmedetomidine-induced hypocapnia. Intravenous administration of dexmedetomidine significantly decreased systemic arterial pressure concurrent with a decrease in CBFldf (22% in normocapnic animals, 36% in hypocapnic animals). Restoration of mean arterial pressure increased CBFldf in normocapnic but not in hypocapnic animals. Similarly, dexmedetomidine significantly reduced pial vessel diameter in both normocapnic (9%) and hypocapnic animals (17%). However, vessel diameters remained decreased in the normocapnic and hypocapnic animals after the mean arterial pressure was restored. Conclusions These results suggest a modulation of cerebral vascular autoregulation by dexmedetomidine which may be mediated, in part, by alterations in carbon dioxide. Dexmedetomidine may have a direct action on the cerebral vessels to reduce the CBF during normo- or hypocapnia. The differences between CBFldf and pial arteriole responses to restoration of mean arterial pressure may reflect the difference in measurement techniques because laser-Doppler measurements reflect the net effect of several arterial segments on microvascular perfusion, whereas diameter measurements specifically examined individual pial arterioles, suggesting that dexmedetomidine vasoconstriction in the cerebral vasculature may be differentially and regionally mediated.
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Iddings, Jennifer A., Ki Jung Kim, Yiqiang Zhou, Haruki Higashimori, and Jessica A. Filosa. "Enhanced Parenchymal Arteriole Tone and Astrocyte Signaling Protect Neurovascular Coupling Mediated Parenchymal Arteriole Vasodilation in the Spontaneously Hypertensive Rat." Journal of Cerebral Blood Flow & Metabolism 35, no. 7 (March 11, 2015): 1127–36. http://dx.doi.org/10.1038/jcbfm.2015.31.

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Functional hyperemia is the regional increase in cerebral blood flow upon increases in neuronal activity which ensures that the metabolic demands of the neurons are met. Hypertension is known to impair the hyperemic response; however, the neurovascular coupling mechanisms by which this cerebrovascular dysfunction occurs have yet to be fully elucidated. To determine whether altered cortical parenchymal arteriole function or astrocyte signaling contribute to blunted neurovascular coupling in hypertension, we measured parenchymal arteriole reactivity and vascular smooth muscle cell Ca2+ dynamics in cortical brain slices from normotensive Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats. We found that vasoconstriction in response to the thromboxane A2 receptor agonist U46619 and basal vascular smooth muscle cell Ca2+ oscillation frequency were significantly increased in parenchymal arterioles from SHR. In perfused and pressurized parenchymal arterioles, myogenic tone was significantly increased in SHR. Although K+-induced parenchymal arteriole dilations were similar in WKY and SHR, metabotropic glutamate receptor activation-induced parenchymal arteriole dilations were enhanced in SHR. Further, neuronal stimulation-evoked parenchymal arteriole dilations were similar in SHR and WKY. Our data indicate that neurovascular coupling is not impaired in SHR, at least at the level of the parenchymal arterioles.
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Qi, Yujia, and Marcus Roper. "Control of low flow regions in the cortical vasculature determines optimal arterio-venous ratios." Proceedings of the National Academy of Sciences 118, no. 34 (August 19, 2021): e2021840118. http://dx.doi.org/10.1073/pnas.2021840118.

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The energy demands of neurons are met by a constant supply of glucose and oxygen via the cerebral vasculature. The cerebral cortex is perfused by dense, parallel arterioles and venules, consistently in imbalanced ratios. Whether and how arteriole–venule arrangement and ratio affect the efficiency of energy delivery to the cortex has remained an unanswered question. Here, we show by mathematical modeling and analysis of the mapped mouse sensory cortex that the perfusive efficiency of the network is predicted to be limited by low-flow regions produced between pairs of arterioles or pairs of venules. Increasing either arteriole or venule density decreases the size of these low-flow regions, but increases their number, setting an optimal ratio between arterioles and venules that matches closely that observed across mammalian cortical vasculature. Low-flow regions are reshaped in complex ways by changes in vascular conductance, creating geometric challenges for matching cortical perfusion with neuronal activity.
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Asano, Y., R. C. Koehler, T. Kawaguchi, and R. W. McPherson. "Pial arteriolar constriction to alpha 2-adrenergic agonist dexmedetomidine in the rat." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 6 (June 1, 1997): H2547—H2556. http://dx.doi.org/10.1152/ajpheart.1997.272.6.h2547.

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Dexmedetomidine (Dex) is an alpha 2-adrenergic agonist that decreases cerebral blood flow (CBF) when administered systemically. It is unclear whether cerebral vasoconstriction is mediated by a local effect on cerebral vessels or by a remote neural mechanism. In the present study, we compared the pial arteriole responses to locally and systemically administered Dex with and without local application of the specific alpha 2-adrenergic antagonist atipamezole. Six groups of male rats (n = 7 each) were anesthetized with isoflurane and prepared for measurements of small (20-39 microns), medium (40-59 microns), and large (60-79 microns) pial arteriole diameter by intravital microscopy or for regional CBF measurement by the radiolabeled-microsphere method. Local application of Dex caused dose-dependent constriction that was significant starting at 10(-8) M for small and medium-sized arterioles and at 10(-7) M for large arterioles. Constriction to 10(-5) M in small [21 +/- 2% (SE)], medium (21 +/- 2%), and large (15 +/- 1%) arterioles was almost completely blocked by local application of 10(-4) M atipamezole. Intravenous administration of Dex at 1 microgram/kg decreased CBF and caused modest arteriolar constriction that began to resolve 8 min after administration. A dose of 10 micrograms/kg constricted arterioles of all sizes with constriction beginning to resolve after approximately 10 min. Local application of atipamezole (10(-4) M) slightly blunted the response to 1 micrograms/kg of intravenous Dex but did not substantially limit constriction after 10 micrograms/kg. These data demonstrate that pial arterioles are capable of substantial constriction to Dex by a local alpha 2-adrenergic mechanism. However, the inability of locally applied atipamezole to substantially inhibit the vasoconstrictor response to systemically administered Dex suggests that Dex might also cause vasoconstriction indirectly through actions at other sites in the central nervous system.
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Iliff, Jeffrey J., Raimondo D'Ambrosio, Al C. Ngai, and H. Richard Winn. "Adenosine receptors mediate glutamate-evoked arteriolar dilation in the rat cerebral cortex." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 5 (May 1, 2003): H1631—H1637. http://dx.doi.org/10.1152/ajpheart.00909.2002.

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We tested the hypothesis that adenosine (Ado) mediates glutamate-induced vasodilation in the cerebral cortex by monitoring pial arteriole diameter in chloralose-anesthetized rats equipped with closed cranial windows. Topical application of 100 μM glutamate and 100 μM N-methyl-d-aspartate (NMDA) dilated pial arterioles (baseline diameter 25 ± 2 μm) by 17 ± 1% and 18 ± 4%, respectively. Coapplication of the nonselective Ado receptor antagonist theophylline (Theo; 10 μM) significantly reduced glutamate- and NMDA-induced vasodilation to 4 ± 2% ( P < 0.01) and 6 ± 2% ( P < 0.05), whereas the Ado A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (0.1 μM) had no effect. Moreover, application of the Ado A2A receptor-selective antagonist 4-{2-[7-amino-2-(2-furyl)(1,2,4)triazolo(2,3-a)(1,3,5)triazin-5-ylamino]ethyl}phenol (ZM-241385), either by superfusion (0.1 μM, 1 μM) or intravenously (1 mg/kg), significantly inhibited the pial arteriole dilation response to glutamate. Neither Theo nor ZM-241385 affected vascular reactivity to mild hypercapnia induced by 5% CO2 inhalation. These results suggest that Ado contributes to the dilation of rat cerebral arterioles induced by exogenous glutamate, and that the Ado A2A receptor subtype may be involved in this dilation response.
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Dissertations / Theses on the topic "Cerebral Arteriole"

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Li, Yao. "Contributions of TRPM4 and Rho Kinase to Myogenic Tone Development in Cerebral Parenchymal Arterioles." ScholarWorks @ UVM, 2016. http://scholarworks.uvm.edu/graddis/464.

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Cerebral parenchymal arterioles (PAs) play a critical role in assuring appropriate blood flow and perfusion pressure within the brain. PAs are unique in contrast to upstream pial arteries, as defined by their critical roles in neurovascular coupling, distinct sensitivities to vasoconstrictors, and enhanced myogenic responsiveness. Dysfunction of these blood vessels is implicated in numerous cardiovascular diseases. However, treatments are limited due to incomplete understanding of the fundamental control mechanisms at this level of the circulation. One of the key elements within most vascular networks, including the cerebral circulation, is the presence of myogenic tone, an intrinsic process whereby resistance arteries constrict and reduce their diameter in response to elevated arterial pressure. This process is centrally involved in the ability of the brain to maintain nearly constant blood flow over a broad range of systemic blood pressures. The overall goal of this dissertation was to investigate the unique mechanisms of myogenic tone regulation in the cerebral microcirculation. To reveal the contributions of various signaling factors in this process, measurements of diameter, intracellular Ca2+ concentration ([Ca2+]i), membrane potential and ion channel activity were performed. Initial work determined that two purinergic G protein-coupled receptors, P2Y4 and P2Y6 receptors, play a unique role in mediating pressure-induced vasoconstriction of PAs in a ligand-independent manner. Moreover, a particular transient receptor potential (TRP) channel in the melastatin subfamily, i.e. TRPM4, was also identified as a mediator of PA myogenic responses. Notably, the observations that inhibiting TRPM4 channels substantially reduces P2Y receptor-mediated depolarization and vasoconstriction, and that P2Y receptor ligands markedly activate TRPM4 currents provide definitive evidence that this ion channel functions as an important link between mechano-sensitive P2Y receptor activation and the myogenic response in PAs. Next, the signaling cascades that mediate stretch-induced TRPM4 activation in PA myocytes were explored. Interestingly, these experiments determined that the RhoA/Rho kinase signaling pathway is involved in this mechanism by facilitating pressure-induced, P2Y receptor-mediated stimulation of TRPM4 channels, leading to subsequent smooth muscle depolarization, [Ca2+]i increase and contraction. Since Rho kinase is generally accepted as a 'Ca2+-sensitization' mediator, the present, contrasting observations point to an underappreciated role of RhoA/Rho kinase signaling in the excitation-contraction mechanisms within the cerebral microcirculation. Overall, this dissertation provides evidence that myogenic regulation of cerebral PAs is mediated by mechano-sensitive P2Y receptors, which initiate the RhoA/Rho kinase signaling pathway, subsequent TRPM4 channel opening, and concomitant depolarization and contraction of arteriolar smooth muscle cells. Revealing the unique mechanochemical coupling mechanisms in the cerebral microcirculation may lead to development of innovative therapeutic strategies for prevention and treatment of microvascular pathologies in the brain.
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Catherall, Mark. "Modelling the role of nitric oxide in cerebral autoregulation." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:c15a49be-791f-47d5-91a0-f507f5856063.

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Malfunction of the system which regulates the bloodflow in the brain is a major cause of stroke and dementia, costing many lives and many billions of pounds each year in the UK alone. This regulatory system, known as cerebral autoregulation, has been the subject of much experimental and mathematical investigation yet our understanding of it is still quite limited. One area in which our understanding is particularly lacking is that of the role of nitric oxide, understood to be a potent vasodilator. The interactions of nitric oxide with the better understood myogenic response remain un-modelled and poorly understood. In this thesis we present a novel model of the arteriolar control mechanism, comprising a mixture of well-established and new models of individual processes, brought together for the first time. We show that this model is capable of reproducing experimentally observed behaviour very closely and go on to investigate its stability in the context of the vasculature of the whole brain. In conclusion we find that nitric oxide, although it plays a central role in determining equilibrium vessel radius, is unimportant to the dynamics of the system and its responses to variation in arterial blood pressure. We also find that the stability of the system is very sensitive to the dynamics of Ca2+ within the muscle cell, and that self-sustaining Ca2+ waves are not necessary to cause whole-vessel radius oscillations consistent with vasomotion.
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MOINARDEAU, VERONIQUE. "Traitement curatif du vasospasme arteriel cerebral apres hemorragie meningee par l'association remplissage vasculaire, hypertension arterielle moderee et nimodipine i. V." Lille 2, 1989. http://www.theses.fr/1989LIL2M308.

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Helps, Stephen. "Pathophysiological basis of cerebral arterial air embolism /." Title page, table of contents and summary only, 1994. http://web4.library.adelaide.edu.au/theses/09PH/09phh484.pdf.

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MARTINS, Islane Cristina. "Morfologia do círculo arterial cerebral em humanos: hipoplasia do segmento A1 da artéria cerebral anterior e padrão fetal da artéria cerebral posterior." Universidade Federal de Pernambuco, 2016. https://repositorio.ufpe.br/handle/123456789/20007.

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FACEPE
O círculo arterial cerebral é um polígono anastomótico na base do encéfalo que comunica o sistema carotídeo com o sistema vértebro-basilar e as carótidas entre si. Há muitas variações morfológicas nesse polígono e possíveis diferenças entre os sexos, particularmente no segmento A1 da artéria cerebral anterior e na origem da artéria cerebral posterior (ACP). O objetivo do presente estudo foi analisar comparativamente a frequência de hipoplasia do segmento A1 e do padrão fetal da artéria cerebral posterior no homem e na mulher. Foram analisadas retrospectivamente 848 angiografias por ressonância magnética arterial, em 426 homens e 422 mulheres, respectivamente, que se submeteram ao exame no Centro de Diagnóstico Multimagem. Os exames foram escolhidos aleatoriamente entre 1.000 angiorressonância realizadas entre 2010 e 2016, independente do motivo da solicitação médica. Hipoplasia do segmento A1 foi definido por analise qualitativa, quando havia uma nítida assimetria entre os dois segmentos A1 direito e esquerdo bem como o padrão fetal da artéria cerebral posterior. Para análise de hipoplasia foram medidos os diâmetros dos segmentos A1. Para análise do padrão fetal (diâmetro da ACP na origem da artéria carótida>diâmetro do segmento P1) foram analisadas 1.296 artérias carótidas em 648 indivíduos. Na análise estatística utilizouse o teste exato de Fisher. Os homens 152/326 (46,6%) apresentaram hipoplasia de A1 em comparação com 108/322 (33,5%) das mulheres (p<0,01, OR=1,7; IC95% 1,3-2,4). A hipoplasia de A1 nos homens foi mais frequente a direita (20% vs. 15%, p<0,01). O padrão fetal foi mais comum nas mulheres 151/644 (23,4%) do que em homens, 100/652 (15,3%) (p<0,001, OR=1,7; IC95% 1,3-2,2). As mulheres também apresentam mais padrão fetal bilateral do que os homens (8,0% vs. 3,4%; p<0,01; OR=0,4; IC 0,2-0,8). A hipoplasia do segmento A1 da artéria cerebral anterior é mais frequente nos homens e nas mulheres há uma maior frequência do padrão fetal da artéria cerebral posterior.
The Circle of Willis is an anastomotic polygon encephalon base that communicates the carotid system with vertebrobasilar system and carotid each other. There are lots of morphological variations that polygon and possible differences between genders particularly in the A1 segment of the anterior cerebral artery and the origin of the posterior cerebral artery (PCA) which are risk factors for anatomical brain aneurysms. The purpose of this study was to comparatively analyze the frequency of hypoplasia of the segment A1 and fetal type of cerebral posterior artery in man and woman. It was retrospectively reviewed 648 magnetic resonance angiographies in 326 men and 322 women, respectively. The tests were randomly chosen among about a thousand magnetic resonance angiographic performed between 2010 and 2016 in Multimagem Diagnostic Center, regardless of the medical reason request. Hypoplasia of the A1 segment was defined by qualitative analysis, when there was a clear asymmetry between the two segments A1, right and left. For hypoplasia analysis were also measured diameters of segments A1. For hypoplasia analysis were also measured diameters of segments A1. For analysis of the fetal type (diameter of the ACP origin of the carotid artery> diameter of the P1 segment of the ACP) were analyzed 1,296 carotid arteries (right and left) in 648 individuals. Statistical analysis was performed using Fisher's exact test. In men 152/326 (46.6%) showed hypoplasia A1 compared to 108/322 (33.5%) of women (p <0.01, OR = 1.7; 95% CI, 1.3-2, 4). Hypoplasia A1 was more common in men right (20% vs. 15%, p <0.01). Fetal type was more common in women 151/644 (23.4%) than in men (100/652; 15.3%) (p <0.001, OR = 1.7; 95% CI, 1.3-2, two). Women also have more bilateral fetal rate than men (8.0% vs. 3.4%; p <0.01). In conclusion, hypoplasia of the A1 segment of the anterior cerebral artery is more common in men and in women there is a greater frequency of fetal type of the posterior cerebral artery. Keywords: Circle of Willis
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6

Chan, Marcelo. "The design and development of a cerebral embolic implant." Thesis, Georgia Institute of Technology, 1995. http://hdl.handle.net/1853/17767.

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Wesołowski, Roman. "Development of arterial spin labelling methods for monitoring cerebral haemodynamics." Thesis, University of Nottingham, 2010. http://eprints.nottingham.ac.uk/13854/.

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The work described in this thesis was carried out at the Sir Peter Mansfield Magnetic Resonance Centre at the University of Nottingham between March 2006 and December 2009. All work described in this thesis was performed by the author, except where indicated. This thesis aims to develop and implement ASL techniques to measure haemodynamic responses to neural activity. The development of a new technique Double Acquisition Background Suppression (DABS) is presented as a remedy for a newly discovered artefact affecting Philips Achieva 7 T scanners and other sources of variation in baseline signals such as physiological noise. The new technique (DABS) was developed for simultaneous acquisition of ASL (with suppressed static tissue signal) and BOLD data using the FAIR scheme. This method not only provided a solution to obtaining ASL data at 7 T, despite the Roman Artefact, but also proved to reduce the contribution of physiological noise to ASL images, which is problematic, especially at ultra-high magnetic field strengths. The statistical verification was carried out based on the neural activation induced by a finger-tapping stimulus. A simplified model for quantifying CBVa.with the Look-Locker sampling method is proposed in this thesis to overcome the need for the Step-wise Compartmental Model (SCM). The Look-Locker sampling scheme acquires multiple readout pulses following the labelling and provides an estimation of transit time as well as CBVa. Here the simplified model is used to assess changes due to visual stimulation and validated against the SCM model. The application of LL-FAIR to form CBF and CBVa weighted data with improved SNR compared to traditional single TI FAIR technique is then shown. This method uses a summation over LL-EPI readout pulses and is used to asses the temporal characteristics and absolute changes in CBF and CBVa haemodynamic responses to a short (4.8 s) and long (9.6 s) visual stimulus. LL-FAIR methods are then used to appraise the neural coupling of haemodynamic parameters and assess Grubb's relationship. CBF and CBVa. Data were collected together with CBVtot data from a bolus injection of contrast agent. Assessing Grubb's power-law (CBVtot = CBFCI:)for neuronal activation, which was originally derived in primates during a steady state response of hypercapnia, a was found in this human study to be between 0.22 ± 0.08 and 0.29, dependent on the analysis method. In addition, the power-law relationship between CBVtot and CBVa.was assessed, and resulted in a similar relation, yielding aTA = 0.42 ± 0.14 and 0.40. Since CBF is thought to be driven by CBVa.the power-law between these parameters was also tested with a value of aFA = 1.35 ± 0.64 and 1.21, found in close agreement with earlier animal work.
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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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Nasi, Luiz Antonio. "Manipulação da pressão arterial no acidente vascular cerebral isquêmico agudo." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/132167.

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Figueiredo, P. M. "Measuring brain perfusion using arterial spin labelling by magnetic resonance imaging." Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275320.

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Books on the topic "Cerebral Arteriole"

1

1930-, Bevan John A., ed. Arterial behavior and blood circulation in the brain. New York: Consultants Bureau, 1986.

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Ultrasound diagnosis of cerebrovascular disease: Doppler sonography of the extra- and intracranial arteries duplex scanning. Stuttgart: Georg Thieme Verlag, 1993.

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Neurovascular imaging: MRI & microangiography. Dordrecht: Springer, 2010.

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Takahashi, Shōki. Neurovascular imaging: MRI & microangiography. Dordrecht: Springer, 2010.

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N, Tulenko Thomas, and Cox Robert H, eds. Recent advances in arterial diseases: Atherosclerosis, hypertension, and vasospasm : proceedings of the A.N. Richards Symposium, held in Philadelphia, Pennsylvania, May 10-11, 1984. New York: Liss, 1986.

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Schieuink. Cerebral and cervical Arterial Dissections. Dunitz Martin Ltd, 2004.

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Fisch, Adam. Arterial Supply. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199845712.003.0251.

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Chapter 19 discusses arterial supply, including the Circle of Willis, leptomeningeal cerebral arteries, deep cerebral arteries, arterial border zones, and arteries of the brainstem, cerebellum, spinal cord, and thalamus.
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Markus, Hugh, Anthony Pereira, and Geoffrey Cloud. Cerebral venous thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198737889.003.0012.

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Most stroke results from arterial disease but venous occlusion can also cause stroke, and other neurological complications. This condition is uncommon and needs a high index of suspicion if it is not to be missed. The clinical presentations are varied and can mimic other neurological conditions. The diagnosis is important because with appropriate treatment the prognosis can be much better than for arterial infarction.
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Perez, Victor Hugo. Atlas Del Sistema Arterial Cerebral Con Variantes Anatomicas. Editorial Limusa S.A. De C.V., 2002.

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De Deyne, Cathy, Ward Eertmans, and Jo Dens. Neurological assessment of the acute cardiac care patient. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0016_update_001.

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Many techniques are currently available for cerebral physiological monitoring in the intensive cardiac care unit environment. The ultimate goal of cerebral monitoring applied during the acute care of any patient with/or at risk of a neurological insult is the early detection of regional or global hypoxic/ischaemic cerebral insults. In the most ideal situation, cerebral monitoring should enable the detection of any deterioration before irreversible brain damage occurs or should at least enable the preservation of current brain function (such as in comatose patients after cardiac arrest). Most of the information that affects bedside care of patients with acute neurologic disturbances is now derived from clinical examination and from knowledge of the pathophysiological changes in cerebral perfusion, cerebral oxygenation, and cerebral function. Online monitoring of these changes can be realized by many non-invasive techniques, without neglecting clinical examination and basic physiological variables—with possible impact on optimal cerebral perfusion/oxygenation—such as invasive arterial blood pressure monitoring or arterial blood gas analysis.
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Book chapters on the topic "Cerebral Arteriole"

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Bradac, Gianni Boris. "Arterial Occlusive Diseases in Children." In Cerebral Angiography, 321. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54404-0_19.

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Bradac, Gianni Boris. "Arterial Occlusive Diseases in Children." In Cerebral Angiography, 283. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-15678-6_19.

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Lynn, Ridwan, and Alex Abou-Chebl. "Cerebral Arterial Anatomy." In Practical Carotid Artery Stenting, 63–74. London: Springer London, 2009. http://dx.doi.org/10.1007/978-1-84800-299-9_6.

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Bradac, Gianni Boris. "Arterial Occlusive Diseases in Children." In Applied Cerebral Angiography, 415–16. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57228-4_19.

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Muresian, Horia. "The Cerebral Circulation." In Arterial Revascularization of the Head and Neck, 1–43. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-34193-4_1.

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Lippert, Herbert, and Reinhard Pabst. "Cerebral arterial circle (circle of Willis)." In Arterial Variations in Man, 92–93. Munich: J.F. Bergmann-Verlag, 1985. http://dx.doi.org/10.1007/978-3-642-80508-0_46.

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Antochi, Florina, and Athena Mergeani. "Cervico-cerebral Arteries Dissection." In Arterial Revascularization of the Head and Neck, 301–23. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-34193-4_14.

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Agostoni, Elio Clemente, and Marco Longoni. "Cerebrovascular Interactions in Cerebral Disorders (Stroke, Transient Ischaemic Attacks, Microvascular Disease, Migraine)." In Arterial Disorders, 333–45. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14556-3_23.

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Trofimov, Alex, Michael Dobrzeniecki, and Denis E. Bragin. "Cerebral Arterial Compliance in Polytraumazed Patients with Cerebral Vasospasm." In Acta Neurochirurgica Supplement, 185–90. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-04615-6_29.

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Reisch, R., R. Filippi, H. Böcher-Schwarz, D. Mauer, K. Ringel, P. Stoeter, and A. Perneczky. "Effect of Intra-Arterial Infusion of Papaverine Hydrochloride on Brain Tissue Oxygen Pressure in the Management of Severe Vasospasm Following Aneurysmal Subarachnoid Hemorrhage." In Cerebral Vasospasm, 191–93. Vienna: Springer Vienna, 2001. http://dx.doi.org/10.1007/978-3-7091-6232-3_40.

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Conference papers on the topic "Cerebral Arteriole"

1

Lapi, D., M. Varanini, R. Scuri, and A. Colantuoni. "Effects of Catechin on cerebral arteriole vasomotion in spontaneously hypertensive rats." In 2020 11th Conference of the European Study Group on Cardiovascular Oscillations (ESGCO). IEEE, 2020. http://dx.doi.org/10.1109/esgco49734.2020.9158049.

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Baker, Wesley, Ashwin B. Parthasarathy, Lian He, Venkaiah C. Kavuri, Mamadou Diop, Daniel F. Milej, David R. Busch, et al. "Noninvasive Optical Monitoring of Cerebral Blood Flow, Critical Closing Pressure, and Arteriole Compliance in Adult Human Subjects." In Optical Tomography and Spectroscopy. Washington, D.C.: OSA, 2018. http://dx.doi.org/10.1364/ots.2018.of4d.1.

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Reymond, Philippe, Fabrice Merenda, Fabienne Perren, Daniel Rüfenacht, and Nikos Stergiopulos. "Validation of 1D Model of the Systemic Arterial Tree Including the Cerebral Circulation." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192529.

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The aim of this study is to develop a distributed model of the entire systemic arterial tree, coupled to a heart model and including a detailed description of the cerebral arteries. Distributed models of the arterial tree have been studied extensively in the past (Avolio [1], Stergiopulos et al [2], Westerhof et al [3]), however, no model has been developed so far that offers a physiologically relevant coupling to the heart and includes the entire cerebral arterial tree.
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Khe, A. K., A. P. Chupakhin, A. A. Cherevko, D. V. Parshin, A. L. Krivoshapkin, and K. Yu Orlov. "Personalized mathematical modeling of cerebral arterial aneurysms." In 2015 International Conference on Biomedical Engineering and Computational Technologies (SIBIRCON). IEEE, 2015. http://dx.doi.org/10.1109/sibircon.2015.7361889.

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Shimogonya, Y., T. Ishikawa, Y. Imai, D. Mori, and T. Yamaguchi. "The Importance of Proliferation of the Arterial Wall in Formation of Saccular Cerebral Aneurysms." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193267.

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Cerebral aneurysms are an important cerebrovascular condition because aneurysm rupture is the most common cause of subarachnoid hemorrhage, which has a high mortality rate and a poor prognosis. Since the mechanism of cerebral aneurysm pathogenesis has not yet been understood, the preventative treatment for unruptured aneurysms is surgery only; however, the morbidity of the surgery is as high as over 10% [1]. On the other hand, the annual risk of rupture of cerebral aneurysms is not so high, reported to be 1.9% [2]. Consequently, it is difficult to judge whether a patient with an unruptured cerebral aneurysm should undergo surgery, when it is detected. Thus, it is important to develop a better understanding of the mechanism of cerebral aneurysm pathogenesis.
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Fonck, E., G. G. Feigl, J. Fasel, D. Sage, M. Unser, D. A. Rüfenacht, and N. Stergiopulos. "Effect of Ageing on Elastin Functionality in Human Cerebral Arteries." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192727.

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The ageing process affects elastin, a key component of the arterial wall integrity and functionality. Elastin may play an important role in cerebral vessels because elastin degradation is linked to cerebrovascular disease [1]. The goal of this study is to assess the biomechanical properties of human cerebral arteries, their composition and geometry, with particular focus on the functional alterations of elastin in cerebral arteries due to ageing.
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Shimogonya, Y., Y. Imai, T. Ishikawa, and T. Yamaguchi. "A Simulation Study on the Growth of Cerebral Aneurysms." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176106.

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Cerebral aneurysm is a cerebrovascular disease characterized by the local balloon-shaped expansion of the arterial wall. It is an extremely important disease on the clinical medicine, because the rupture of the cerebral aneurysm causes serious pathologic conditions such as the subarachnoid hemorrhage.
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Fabbri, Dario, Quan Long, Saroj Das, and Michele Pinelli. "Study of Embolic Particle Migration in Cerebral Arteries by Computational Modelling." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80314.

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As known, embolism is one of the major causes of stroke, which represents the rapid loss of brain functions. Two major sources of emboli which may cause ischemic attack were emboli formed in heart and from a ruptured arterial plaque in carotid arties. Due to the different characteristics of emboli formed from different mechanisms, the migration route of specific emboli in cerebral arteries may be different, so does the territory of the ischemic attack caused by them. Therefore, a good understanding of emboli migration in the complex cerebral arterial network may provide a good guidance for the diagnosis and treatment of stroke. Studies on the emboli motion in cerebral arteries so far were based on phantom models [1]. Although CFD simulation has been used on prediction of cerebral blood perfusion for many years, CFD particle tracking technique is rarely applied on study emboli migration in cerebral arteries. The present study aims to demonstrate the feasibility of using CFD particle tracking on emboli migration study with emphasis on the discussions of the particle tracking result by different coupling algorithms between blood flow and embolic particles.
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Reymond, Philippe, Fabrice Merenda, Fabienne Perren, Daniel Rüfenacht, and Nikos Stergiopulos. "One Dimensional Model of the Systemic Arterial Tree Including Cerebral Circulation." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176452.

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The aim of this study is to develop a distributed model of the entire systemic arterial tree, coupled to a heart model and including a detailed description of the cerebral arteries. Distributed models of the arterial tree have been studied extensively in the past (Avolio [1]; Cassot et al [2]; Meister [3]; Schaaf and Abbrecht [4]; Stergiopulos et al [5]; Westerhof et al [6]; Zagzoule and Marc-Vergnes [7]), however, no model has been developed so far that offers a physiologically relevant coupling to the heart and includes the entire cerebral artery network.
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Del Zoppo, G. J., S. M. Otis, J. Zyroff, W. Hacke, H. Zeumer, and L. A. Harker. "INTRA-ARTERIAL THROMBOLYTIC THERAPY IN ACUTE MIDDLE CEREBRAL ARTERY STROKE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643891.

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18 patients presenting with acute carotid territory stroke, secondary to angiographically demonstrated occlusion of the middle cerebral artery (MCA), have been treated within 8 hours of the onset of acute symptoms by local intra-arterial infusion of urokinase or streptokinase. All patients were screened by baseline CT cerebral scan to exclude intracerebral hemorrhage as a cause of the acute stroke. 14 patients demonstrated complete, 2 partial, and 2 no recanalization (reopening) of the previously occluded artery following a 1 to 2 hour infusion of the fibrinolytic agent.10 of the 14 patients displaying complete recanalization had complete neurological recovery or improvement with residual neurological deficits, while the 2 patients who did not display recanalization did not improve clinically. No clinical improvement was observed in the absence of recanalization.Hemorrhagic transformation of cerebral ischemic areas may be classified as hemorrhagic infarction (minimal hemorrhage, no clinical deterioraton) and parenchymatous hemorrhage (mass effect, clinical deterioration). Minor infarction-related hemorrhages without detectable neurological sequelae (hemorrhagic infarctions) were found by CT scan in 4 patients; all displayed complete recanalization; and all hemorrhagic infarctions resolved.This uncontrolled prospective clinical experience suggests that early local infusion of thrombolytic agents in selected patients may be efficacious and safe.
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