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Mark Nelson - One of the best experts on this subject based on the ideXlab platform.

  • a plcγ1 dependent force sensitive signaling network in the myogenic constriction of Cerebral Arteries
    Science Signaling, 2014
    Co-Authors: Albert L Gonzales, Mark Nelson, Fabrice Dabertrand, Ying Yang, Michelle N Sullivan, Lindsey Sanders, David C Hilleubanks, Scott Earley
    Abstract:

    Maintaining constant blood flow in the face of fluctuations in blood pressure is a critical autoregulatory feature of Cerebral Arteries. An increase in pressure within the artery lumen causes the vessel to constrict through depolarization and contraction of the encircling smooth muscle cells. This pressure-sensing mechanism involves activation of two types of transient receptor potential (TRP) channels: TRPC6 and TRPM4. We provide evidence that the activation of the γ1 isoform of phospholipase C (PLCγ1) is critical for pressure sensing in Cerebral Arteries. Inositol 1,4,5-trisphosphate (IP3), generated by PLCγ1 in response to pressure, sensitized IP3 receptors (IP3Rs) to Ca2+ influx mediated by the mechanosensitive TRPC6 channel, synergistically increasing IP3R-mediated Ca2+ release to activate TRPM4 currents, leading to smooth muscle depolarization and constriction of isolated Cerebral Arteries. Proximity ligation assays demonstrated colocalization of PLCγ1 and TRPC6 with TRPM4, suggesting the presence of a force-sensitive, local signaling network comprising PLCγ1, TRPC6, TRPM4, and IP3Rs. Src tyrosine kinase activity was necessary for stretch-induced TRPM4 activation and myogenic constriction, consistent with the ability of Src to activate PLCγ isoforms. We conclude that contraction of Cerebral artery smooth muscle cells requires the integration of pressure-sensing signaling pathways and their convergence on IP3Rs, which mediate localized Ca2+-dependent depolarization through the activation of TRPM4.

  • Ca2+ Sparks and Their Function in Human Cerebral Arteries
    Stroke, 2002
    Co-Authors: George C. Wellman, David J. Nathan, Christine M. Saundry, Guillermo J. Pérez, Adrian D. Bonev, Paul L. Penar, Bruce I. Tranmer, Mark Nelson
    Abstract:

    Background and Purpose — Local Ca2+ release events (Ca2+ sparks) caused by the opening of ryanodine-sensitive Ca2+ channels in the sarcoplasmic reticulum have been suggested to oppose constriction in Cerebral Arteries through the activation of large-conductance Ca2+-activated K+ (BK) channels. We report the first identification and characterization of Ca2+ sparks and associated BK channel currents in smooth muscle cells isolated from human Cerebral Arteries. Methods — Membrane currents and intracellular Ca2+ were measured with the use of the patch-clamp technique and laser scanning confocal microscopy. Results — Ca2+ sparks with a peak fractional fluorescence change (F/F) of 2.02±0.04 and size of 8.2±0.5 μm2 (n=108) occurred at a frequency of approximately 1 Hz in freshly isolated, Cerebral artery myocytes from humans. At a holding potential of −40 mV, the majority of, but not all, Ca2+ sparks (61 of 85 sparks) were associated with transient BK currents. Consistent with a role for Ca2+ sparks in the control of Cerebral artery diameter, agents that block Ca2+ sparks (ryanodine) or BK channels (iberiotoxin) were found to contract human Cerebral Arteries. Conclusions — This study provides evidence for local Ca2+ signaling in human arterial myocytes and suggests that these events may play an important role in control of Cerebral artery diameter in humans.

  • chloride channel blockers inhibit myogenic tone in rat Cerebral Arteries
    The Journal of Physiology, 1997
    Co-Authors: Mark Nelson, Harm J Knot, Mathew A Conway, Joseph E Brayden
    Abstract:

    1. We have investigated the role of chloride channels in pressure-induced depolarization and contraction of Cerebral artery smooth muscle cells. 2. Two chloride channel blockers, indanyloxyacetic acid (IAA-94) and 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS), caused hyperpolarizations (10-15 mV) and dilatations (up to 90%) of pressurized (80 mmHg), rat posterior Cerebral Arteries. Niflumic acid, a blocker of calcium-activated chloride channels, did not affect arterial tone. 3. Dilatations to IAA-94 and DIDS were unaffected by potassium channel blockers, but were prevented by elevated potassium. IAA-94 and DIDS had no effect on membrane potential or diameter of Arteries at low intravascular pressure, where myogenic tone is absent. Reduction of extracellular chloride (60 mM Cl-) increased the pressure-induced contractions. Removal of extracellular sodium did not affect the pressure-induced responses. 4. Our results suggest that intravascular pressure activates DIDS- and IAA-94-sensitive chloride channels to depolarize arterial smooth muscle, thereby contributing to the myogenic constriction.

  • extracellular k induced hyperpolarizations and dilatations of rat coronary and Cerebral Arteries involve inward rectifier k channels
    The Journal of Physiology, 1996
    Co-Authors: Harm J Knot, Paul A Zimmermann, Mark Nelson
    Abstract:

    1. The hypothesis that inward rectifier K(+) channels are involved in the vasodilatation of small coronary and Cerebral Arteries (100-200 microm diameter) in response to elevated [K+]o was tested. The diameters and membrane potentials of pressurized Arteries from rat were measured using a video-imaging system and conventional microelectrodes, respectively. 2. Elevation of [K+]o from 6 to 16 mM caused the membrane potential of pressurized (60 mmHg) Arteries to hyperpolarize by 12-14 mV. Extracellular Ba(2+) (Ba2+(o)) blocked K(+)-induced membrane potential hyperpolarizations at concentrations (IC(50), 6 microM) that block inward rectifier K(+) currents in smooth muscle cells isolated from these Arteries. 3. Elevation of [K+]o from 6 to 16 mM caused sustained dilatations of pressurized coronary and Cerebral Arteries with diameters increasing from 125 to 192 microm and 110 to 180 microm in coronary and Cerebral Arteries, respectively. Ba2+(o) blocked K(+)-induced dilatations of pressurized coronary and Cerebral Arteries (IC50, 3-8 microM). 4. Elevated [K+]o-induced vasodilatation was not prevented by blockers of other types of K(+) channels (1 mM 4-aminopyridine, 1 mM TEA+, and 10 mu M glibenclamide), and blockers of Na(+)-K(+)-ATPase. Elevated [K+]o-induced vasodilatation was unaffected by removal of the endothelium. 5. These findings suggest that K+(o) dilates small rat coronary and Cerebral Arteries through activation of inward rectifier K(+) channels. Furthermore, these results support the hypothesis that inward rectifier K(+) channels may be involved in metabolic regulation of coronary and Cerebral blood flow in response to changes in [K+]o.

  • regulation of membrane potential and diameter by voltage dependent k channels in rabbit myogenic Cerebral Arteries
    American Journal of Physiology-heart and Circulatory Physiology, 1995
    Co-Authors: Harm J Knot, Mark Nelson
    Abstract:

    The hypothesis that voltage-dependent K+ channels are involved in the regulation of arterial smooth muscle membrane potential and blood vessel diameter was tested by examining the effects of inhibitors [4-aminopyridine (4-AP) and 3,4-diaminopyridine (3,4-DAP)] of voltage-dependent K+ channels on the membrane potential and diameter of pressurized small (100- to 300-microns diam) Cerebral Arteries from rabbit. In response to graded elevations in transmural pressure (20-100 mmHg), the membrane potential of smooth muscle cells in these Arteries depolarized and the Arteries constricted. 4-AP (1 mM) and 3,4-DAP (1 mM) depolarized Cerebral Arteries by 19 and 21 mV, respectively, when they were subjected to a transmural pressure of 80 mmHg. 3-Aminopyridine (3-AP, 1 mM), which is a relatively poor inhibitor of voltage-dependent K+ channels, depolarized smooth muscle cells in the Arteries by 1 mV. 4-AP and 3,4-DAP constricted pressurized (to 80 mmHg) Cerebral Arteries. 3-AP had little effect on arterial diameter. 4-AP increased the arterial constriction to transmural pressure over a wide range of pressures (40-90 mmHg). The effects of 4-AP and 3,4-DAP on membrane potential and diameter were not prevented by inhibitors of calcium channels, calcium-activated K+ channels, ATP-sensitive K+ channels, inward rectifier K+ channels, blockers of adrenergic, serotonergic, muscarinic, and histaminergic receptors, or removal of the endothelium. These results suggest that voltage-dependent K+ channels are involved in the regulation of membrane potential and response of small Cerebral Arteries to changes in intravascular pressure.

Frank M Faraci - One of the best experts on this subject based on the ideXlab platform.

  • subarachnoid haemorrhage what happens to the Cerebral Arteries
    Clinical and Experimental Pharmacology and Physiology, 1998
    Co-Authors: Christopher G Sobey, Frank M Faraci
    Abstract:

    1. Subarachnoid haemorrhage (SAH) is a unique disorder and a major clinical problem that most commonly occurs when an aneurysm in a Cerebral artery ruptures, leading to bleeding and clot formation. Subarachnoid haemorrhage results in death or severe disability of 50-70% of victims and is the cause of up to 10% of all strokes. Delayed Cerebral vasospasm, which is the most critical clinical complication that occurs after SAH, seems to be associated with both impaired dilator and increased constrictor mechanisms in Cerebral Arteries. Mechanisms contributing to development of vasospasm and abnormal reactivity of Cerebral Arteries after SAH have been intensively investigated in recent years. In the present review we focus on recent advances in our knowledge of the roles of nitric oxide (NO) and cGMP, endothelin (ET), protein kinase C (PKC) and potassium channels as they relate to SAH. 2. Nitric oxide is produced by the endothelium and is an important regulator of Cerebral vascular tone by tonically maintaining the vasculature in a dilated state. Endothelial injury after SAH may interfere with NO production and lead to vasoconstriction and impaired responses to endothelium-dependent vasodilators. Inactivation of NO by oxyhaemoglobin or superoxide from erythrocytes may also occur in the subarachnoid space after SAH. 3. Nitric oxide stimulates activity of soluble guanylate cyclase in vascular muscle, leading to intracellular generation of cGMP and relaxation. Subarachnoid haemorrhage appears to cause impaired activity of soluble guanylate cyclase, resulting in reduced basal levels of cGMP in Cerebral vessels and often decreased responsiveness of Cerebral Arteries to NO. 4. Endothelin is a potent, long-lasting vasoconstrictor that may contribute to the spasm of Cerebral Arteries after SAH. Endothelin is present in increased levels in the cerebrospinal fluid of SAH patients. Pharmacological inhibition of ET synthesis or of ET receptors has been reported to attenuate Cerebral vasospasm. Production of and vasoconstriction by ET may be due, in part, to the decreased activity of NO and formation of cGMP. 5. Protein kinase C is an important enzyme involved in the contraction of vascular muscle in response to several agonists, including ET. Activity of PKC appears to be increased in Cerebral Arteries after SAH, indicating that PKC may be critical in the development of Cerebral vasospasm. Recent evidence suggests that PKC activation may occur in Cerebral Arteries after SAH as a result of decreased negative feedback influence of NO/cGMP. 6. Cerebral Arteries are depolarized after SAH, possibly due to decreased activity of potassium channels in vascular muscle. Decreased basal activation of potassium channels may be due to several mechanisms, including impaired activity of NO (and/or cGMP) or increased activity of PKC. Vasodilator drugs that produce hyperpolarization, such as potassium channel openers, appear to be unusually effective in Cerebral Arteries after SAH. 7. Thus, endothelial damage and reduced activity of NO may contribute to Cerebral vascular dysfunction after SAH. Potassium channels may represent an important therapeutic target for the treatment of Cerebral vasospasm after SAH.

  • regulation of large Cerebral Arteries and Cerebral microvascular pressure
    Circulation Research, 1990
    Co-Authors: Frank M Faraci, D D Heistad
    Abstract:

    Resistance of large Arteries appears to be greater in the Cerebral circulation than in other vascular beds. Large Arteries contribute importantly to total Cerebral vascular resistance and are major determinants of local microvascular pressure. Recent studies have shown that resistance of large Arteries and Cerebral microvascular pressure are affected by several physiological stimuli, including changes in systemic blood pressure, increases in Cerebral metabolism, activity of sympathetic nerves, and humoral stimuli such as circulating vasopressin and angiotensin. Stimuli such as sympathetic stimulation and vasopressin produce selective responses of large Arteries and, thereby, regulate microvascular pressure without a significant change in Cerebral blood flow. These findings lead to the new hypothesis that the brain may be sensitive to changes in Cerebral microvascular pressure, resulting in activation of compensatory neurohumoral mechanisms. Important changes occur in large Cerebral Arteries under pathophysiological conditions. Chronic hypertension increases resistance of large Cerebral Arteries, which protects the microcirculation against hypertension. Atherosclerosis potentiates constrictor responses of large Cerebral Arteries to serotonin and thromboxane, which may contribute to vasospasm and transient ischemic attacks.

Anders Eklund - One of the best experts on this subject based on the ideXlab platform.

  • Automatic labeling of Cerebral Arteries in magnetic resonance angiography
    Magnetic Resonance Materials in Physics Biology and Medicine, 2016
    Co-Authors: Tora Dunås, Laleh Zarrinkoob, Khalid Ambarki, Anders Wahlin, Richard Birgander, Jan Malm, Anders Eklund
    Abstract:

    Objectives In order to introduce 4D flow magnetic resonance imaging (MRI) as a standard clinical instrument for studying the cerebrovascular system, new and faster postprocessing tools are necessary. The objective of this study was to construct and evaluate a method for automatic identification of individual Cerebral Arteries in a 4D flow MRI angiogram. Materials and methods Forty-six elderly individuals were investigated with 4D flow MRI. Fourteen main Cerebral Arteries were manually labeled and used to create a probabilistic atlas. An automatic atlas-based artery identification method (AAIM) was developed based on vascular-branch extraction and the atlas was used for identification. The method was evaluated by comparing automatic with manual identification in 4D flow MRI angiograms from 67 additional elderly individuals. Results Overall accuracy was 93 %, and internal carotid artery and middle Cerebral artery labeling was 100 % accurate. Smaller and more distal Arteries had lower accuracy; for posterior communicating Arteries and vertebral Arteries, accuracy was 70 and 89 %, respectively. Conclusion The AAIM enabled fast and fully automatic labeling of the main Cerebral Arteries. AAIM functionality provides the basis for creating an automatic and powerful method to analyze arterial Cerebral blood flow in clinical routine.

  • blood flow distribution in Cerebral Arteries
    Journal of Cerebral Blood Flow and Metabolism, 2015
    Co-Authors: Laleh Zarrinkoob, Khalid Ambarki, Anders Wahlin, Richard Birgander, Anders Eklund, Jan Malm
    Abstract:

    High-resolution phase-contrast magnetic resonance imaging can now assess flow in proximal and distal Cerebral Arteries. The aim of this study was to describe how total Cerebral blood flow (tCBF) is ...

  • measuring pulsatile flow in Cerebral Arteries using 4d phase contrast mr imaging
    American Journal of Neuroradiology, 2013
    Co-Authors: Anders Wahlin, Khalid Ambarki, Richard Birgander, Jan Malm, Oliver Wieben, Kevin M Johnson, Anders Eklund
    Abstract:

    BACKGROUND AND PURPOSE: 4D PCMRI can be used to quantify pulsatile hemodynamics in multiple Cerebral Arteries. The aim of this study was to compare 4D PCMRI and 2D PCMRI for assessments of pulsatil ...

Jane A Madden - One of the best experts on this subject based on the ideXlab platform.

  • voltage gated k channels in rat small Cerebral Arteries molecular identity of the functional channels
    The Journal of Physiology, 2003
    Co-Authors: Sulayma Albarwani, Jane A Madden, Leah T Nemetz, Ann A Tobin, Sarah K England, Phillip F Pratt, Nancy J Rusch
    Abstract:

    Voltage-gated potassium (KV) channels represent an important dilator influence in the Cerebral circulation, but the composition of these tetrameric ion channels remains unclear. The goals of the present study were to evaluate the contribution of KV1 family channels to the resting membrane potential and diameter of small rat Cerebral Arteries, and to identify the α-subunit composition of these channels using patch-clamp, molecular and immunological techniques. Initial studies indicated that 1 μmol l−1 correolide (COR), a specific antagonist of KV1 channels, depolarized vascular smooth muscle cells (VSMCs) in pressurized (60 mmHg) Cerebral Arteries from -55 ± 1 mV to -34 ± 1 mV, and reduced the resting diameter from 152 ± 15 μm to 103 ± 20 μm. In patch clamped VSMCs from these Arteries, COR-sensitive KV1 current accounted for 65 % of total outward KV current and was observed at physiological membrane potentials. RT-PCR identified mRNA encoding each of the six classical KV1 α-subunits, KV1.1-1.6, in rat Cerebral Arteries. However, only the KV1.2 and 1.5 proteins were detected by Western blot. The expression of these proteins in VSMCs was confirmed by immunocytochemistry and co-immunoprecipitation of KV1.2 and 1.5 from VSMC membranes suggested KV1.2/1.5 channel assembly. Subsequently, the pharmacological and voltage-sensitive properties of KV1 current in VSMCs were found to be consistent with a predominant expression of KV1.2/1.5 heterotetrameric channels. The findings of this study suggest that KV1.2/1.5 heterotetramers are preferentially expressed in rat Cerebral VSMCs, and that these channels contribute to the resting membrane potential and diameter of rat small Cerebral Arteries.

  • Effect of cocaine and cocaine metabolites on Cerebral Arteries in vitro.
    Life Sciences, 2002
    Co-Authors: Jane A Madden, Robert H. Powers
    Abstract:

    Cocaine has pronounced peripheral vasoconstrictor effects. Despite the short half life of cocaine in the body these effects are relatively long-lived. The role of cocaine metabolites in vasoconstriction attributed to cocaine has not been reported. We evaluated the contractile ability of cocaine and its major metabolites in isolated cat Cerebral Arteries. The primary cocaine metabolite, benzollecgonine was a potent contractile agent, causing a 50% decrease in cross sectional area at 10−5 M. This was less than caused by serotonin, but greater than caused by norepinehrine. Ecgonine and cocaine were less active contractile agents than was benzoylecgonine, and ecgonine methyl ester was a mild relaxant.

  • Responses to pulsatile flow in piglet isolated Cerebral Arteries.
    Pediatric research, 1998
    Co-Authors: Larissa A Shimoda, Nan A. Norins, Jane A Madden
    Abstract:

    Because cerebrovascular hemorrhage in newborns is often associated with fluctuations in Cerebral blood flow, this study was designed to investigate the effects of pulsatile flow in isolated Cerebral Arteries from neonatal piglets. Arteries mounted on cannulas were bathed in and perfused with a physiologic saline solution. An electronic system produced pulsations, the amplitude and frequency of which were independently controlled. At constant mean transmural pressure (20 mm Hg), increasing flow in steps from 0 to 1.6 mL/min under steady flow conditions caused a biphasic response, constriction at low flow, and dilation at high flow. Under pulsatile flow conditions (pulse amplitude 16-24 mm Hg; 2 Hz), the Arteries dilated upon flow initiation and continued to dilate as mean flow increased. Dilation to pulsatile flow did not depend on the level of mean flow because switching from steady to pulsatile flow at each flow step also caused dilation. Arteries dilated further upon increasing either pulse amplitude (12-28 mm Hg; 2 Hz) or frequency (16-24 mm Hg; 4 Hz). Inhibiting nitric oxide synthesis with Nomega-nitro-L-arginine or perfusing with glutaraldehyde to decrease endothelial cell deformability significantly reduced dilations to pulsatile flow and to increased amplitude and frequency. These data suggest that the arterial response to flow is highly dependent on the mode of flow. Dilation induced by initiating pulsatile flow or increasing either pulse amplitude or frequency appears to be mediated by augmented nitric oxide release as result of shear stress-induced deformation of the endothelial cells.

  • Responses to pulsatile flow in piglet isolated Cerebral Arteries
    Pediatric Research, 1998
    Co-Authors: Larissa A Shimoda, Nan A. Norins, Jane A Madden
    Abstract:

    Because cerebrovascular hemorrhage in newborns is often associated with fluctuations in Cerebral blood flow, this study was designed to investigate the effects of pulsatile flow in isolated Cerebral Arteries from neonatal piglets. Arteries mounted on cannulas were bathed in and perfused with a physiologic saline solution. An electronic system produced pulsations, the amplitude and frequency of which were independently controlled. At constant mean transmural pressure (20 mm Hg), increasing flow in steps from 0 to 1.6 mL/min under steady flow conditions caused a biphasic response, constriction at low flow, and dilation at high flow. Under pulsatile flow conditions (pulse amplitude 16-24 mm Hg; 2 Hz), the Arteries dilated upon flow initiation and continued to dilate as mean flow increased. Dilation to pulsatile flow did not depend on the level of mean flow because switching from steady to pulsatile flow at each flow step also caused dilation. Arteries dilated further upon increasing either pulse amplitude (12-28 mm Hg; 2 Hz) or frequency (16-24 mm Hg; 4 Hz). Inhibiting nitric oxide synthesis with Nω-nitro-L-arginine or perfusing with glutaraldehyde to decrease endothelial cell deformability significantly reduced dilations to pulsatile flow and to increased amplitude and frequency. These data suggest that the arterial response to flow is highly dependent on the mode of flow. Dilation induced by initiating pulsatile flow or increasing either pulse amplitude or frequency appears to be mediated by augmented nitric oxide release as result of shear stress-induced deformation of the endothelial cells.

  • cocaine and benzoylecgonine constrict Cerebral Arteries by different mechanisms
    Life Sciences, 1995
    Co-Authors: Jane A Madden, Richard J Konkol, Peter A Keller, Tomas A Alvarez
    Abstract:

    This study was designed to determine possible mechanisms underlying the vasoconstrictor activity of cocaine and its principal metabolite, benzoylecgonine (BE) in cat isolated Cerebral Arteries. The Arteries constricted significantly in response to single doses of cocaine, BE and norepinephrine (NE; (P < 0.05). After 6-OHDA treatment to remove adrenergic nerve endings, NE-induced constrictions were essentially unchanged from those before treatment. Denervated Arteries exposed to cocaine dilated significantly (P < 0.05) but those exposed to BE constricted as much as before denervation. Following exposure to prazosin and yohimbine, arterial constrictions to NE and cocaine were significantly reduced from control (P < 0.05) but the BE-induced constriction was unchanged. Ryanodine eliminated the cocaine-induced contraction (P < 0.05) whereas verapamil eliminated the BE response (P < 0.05). These data suggest that while cocaine's vasoconstrictor action may be significantly mediated through adrenergic transmission, BE may act through a mechanism involving calcium (Ca2+) channels. Cocaine levels peak and decline in the body more rapidly than BE levels which can remain detectable for days. This study suggests there may also be different pharmacological mechanisms as well as temporal differences underlying the vasoreactivity of these two substances. Our findings may have implications for pharmacological management of cocaine-induced toxic vascular events.

Richard Wise - One of the best experts on this subject based on the ideXlab platform.

  • the major Cerebral Arteries proximal to the circle of willis contribute to cerebrovascular resistance in humans
    Journal of Cerebral Blood Flow and Metabolism, 2016
    Co-Authors: Esther A H Warnert, Kevin Murphy, Judith Elizabeth Hall, Emma C Hart, Richard Wise
    Abstract:

    Cerebral autoregulation ensures constant Cerebral blood flow during periods of increased blood pressure by increasing cerebrovascular resistance. However, whether this increase in resistance occurs at the level of major Cerebral Arteries as well as at the level of smaller pial arterioles is still unknown in humans. Here, we measure Cerebral arterial compliance, a measure that is inversely related to cerebrovascular resistance, with our novel non-invasive magnetic resonance imaging-based measurement, which employs short inversion time pulsed arterial spin labelling to map arterial blood volume at different phases of the cardiac cycle. We investigate the differential response of the cerebrovasculature during post exercise ischemia (a stimulus which leads to increased cerebrovascular resistance because of increases in blood pressure and sympathetic outflow). During post exercise ischemia in eight normotensive men (30.4 ± 6.4 years), Cerebral arterial compliance decreased in the major Cerebral Arteries at the level of and below the Circle of Willis, while no changes were measured in Arteries above the Circle of Willis. The reduction in arterial compliance manifested as a reduction in the arterial blood volume during systole. This study provides the first evidence that in humans the major Cerebral Arteries may play an important role in increasing cerebrovascular resistance.

  • noninvasive assessment of arterial compliance of human Cerebral Arteries with short inversion time arterial spin labeling
    Journal of Cerebral Blood Flow and Metabolism, 2015
    Co-Authors: Esther A H Warnert, Kevin Murphy, Judith Elizabeth Hall, Richard Wise
    Abstract:

    A noninvasive method of assessing Cerebral arterial compliance (AC) is introduced in which arterial spin labeling (ASL) is used to measure changes in arterial blood volume (aBV) occurring within the cardiac cycle. Short inversion time pulsed ASL (PASL) was performed in healthy volunteers with inversion times ranging from 250 to 850 ms. A model of the arterial input function was used to obtain the Cerebral aBV. Results indicate that aBV depends on the cardiac phase of the Arteries in the imaging volume. Cerebral AC, estimated from aBV and brachial blood pressure measured noninvasively in systole and diastole, was assessed in the flow territories of the basal Cerebral Arteries originating from the circle of Willis: right and left middle Cerebral Arteries (RMCA and LMCA), right and left posterior Cerebral Arteries (RPCA and LPCA), and the anterior Cerebral artery (ACA). Group average AC values calculated for the RMCA, LMCA, ACA, RPCA, and LPCA were 0.56%±0.2%, 0.50%±0.3%, 0.4%±0.2%, 1.1%±0.5%, and 1.1%±0.3% per mm Hg, respectively. The current experiment has shown the feasibility of measuring AC of Cerebral Arteries with short inversion time PASL.