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Caryl E. Hill – One of the best experts on this subject based on the ideXlab platform.

  • non Linear Relationship between hyperpolarisation and relaxation enables long distance propagation of vasodilatation
    The Journal of Physiology, 2011
    Co-Authors: Stephanie E Wolfle, Daniel J Chaston, Kenichi Goto, Shaun L. Sandow, F R Edwards, Caryl E. Hill
    Abstract:

    Non-technical summary  Microvascular dilatations initiated locally in metabolically active tissues spread rapidly upstream, with little attenuation, to larger vessels whose relaxation results in the necessary increases in local blood flow. While this rapidly spreading response occurs due to the propagation of hyperpolarisation through gap junctions, it is not understood why the dilatation does not attenuate unless a regenerative electrical mechanism is involved. We show in skeletal muscle arterioles in vivo that no such regenerative electrical phenomenon exists. Instead, the local dilatation spreads without attenuation because the initial hyperpolarisation is supramaximal and the impact of voltage on dilatation is restricted to a narrow voltage window near the resting membrane potential. Knowledge of this mechanism increases our understanding of the processes which control blood flow to organs and explains how these processes can be compromised in diseases in which endothelial function is reduced. Abstract  Blood flow is adjusted to tissue demand through rapidly ascending vasodilatations resulting from conduction of hyperpolarisation through vascular gap junctions. We investigated how these dilatations can spread without attenuation if mediated by an electrical signal. Cremaster muscle arterioles were studied in vivo by simultaneously measuring membrane potential and vessel diameter. Focal application of acetylcholine elicited hyperpolarisations which decayed passively with distance from the local site, while dilatation spread upstream without attenuation. Analysis of simultaneous recordings at the local site revealed that hyperpolarisation and dilatation were only Linearly related over a restricted voltage range to a threshold potential, beyond which dilatation was maximal. Experimental data could be simulated in a computational model with electrotonic decay of hyperpolarisation but imposition of this threshold. The model was tested by reducing the amplitude of the local hyperpolarisation which led to entry into the Linear range closer to the local site and decay of dilatation. Serial section electron microscopy and light dye treatment confirmed that the spread of dilatation occurred through the endothelium and that the two cell layers were tightly coupled. Generality of the mechanism was demonstrated by applying the model to the attenuated propagation of dilatation found in larger arteries. We conclude that long distance spread of locally initiated dilatations is not due to a regenerative electrical phenomenon, but rather a restricted Linear Relationship between voltage and vessel tone, which minimises the impact of electrotonic decay of voltage. Disease-related alterations in endothelial coupling or ion channel expression could therefore decrease the ability to adjust blood flow to meet metabolic demand.

  • Non-Linear Relationship between hyperpolarisation and relaxation enables long distance propagation of vasodilatation.
    The Journal of physiology, 2011
    Co-Authors: Stephanie E Wolfle, Daniel J Chaston, Kenichi Goto, Shaun L. Sandow, F R Edwards, Caryl E. Hill
    Abstract:

    Blood flow is adjusted to tissue demand through rapidly ascending vasodilatations resulting from conduction of hyperpolarisation through vascular gap junctions. We investigated how these dilatations can spread without attenuation if mediated by an electrical signal. Cremaster muscle arterioles were studied in vivo by simultaneously measuring membrane potential and vessel diameter. Focal application of acetylcholine elicited hyperpolarisations which decayed passively with distance from the local site,while dilatation spread upstream without attenuation. Analysis of simultaneous recordings at the local site revealed that hyperpolarisation and dilatation were only Linearly related over a restricted voltage range to a threshold potential, beyond which dilatation was maximal. Experimental data could be simulated in a computational model with electrotonic decay of hyperpolarisation but imposition of this threshold. The model was tested by reducing the amplitude of the local hyperpolarisation which led to entry into the Linear range closer to the local site and decay of dilatation. Serial section electron microscopy and light dye treatment confirmed that the spread of dilatation occurred through the endothelium and that the two cell layers were tightly coupled. Generality of the mechanism was demonstrated by applying the model to the attenuated propagation of dilatation found in larger arteries.We conclude that long distance spread of locally initiated dilatations is not due to a regenerative electrical phenomenon, but rather a restricted Linear Relationship between voltage and vessel tone, which minimises the impact of electrotonic decay of voltage. Disease-related alterations in endothelial coupling or ion channel expression could therefore decrease the ability to adjust blood flow to meet metabolic demand.

Masatoshi Saito – One of the best experts on this subject based on the ideXlab platform.

  • conversion of the energy subtracted ct number to electron density based on a single Linear Relationship an experimental verification using a clinical dual source ct scanner
    Physics in Medicine and Biology, 2013
    Co-Authors: Masayoshi Tsukihara, Yoshiyuki Noto, Takahide Hayakawa, Masatoshi Saito
    Abstract:

    In radiotherapy treatment planning, the conversion of the computed tomography (CT) number to electron density is one of the main processes that determine the accuracy of patient dose calculations. However, in general, the CT number and electron density of tissues cannot be interrelated using a simple one-to-one correspondence. This study aims to experimentally verify the clinical feasibility of an existing novel conversion method proposed by the author of this note, which converts the energy-subtracted CT number (ΔHU) to the relative electron density (ρe) via a single Linear Relationship by using a dual-energy CT (DECT). The ΔHU-ρe conversion was performed using a clinical second-generation dual-source CT scanner operated in the dual-energy mode with tube potentials of 80 kV and 140 kV with and without an additional tin filter. The ΔHU-ρe calibration line was obtained from the DECT image acquisition for tissue substitutes in an electron density phantom. In addition, the effect of object size on ΔHU-ρe conversion was also experimentally investigated. The plot of the measured ΔHU versus nominal ρe values exhibited a single Linear Relationship over a wide ρe range from 0.00 (air) to 2.35 (aluminum). The ΔHU-ρe conversion performed with the tin filter yielded a lower dose and more reliable ρe values that were less affected by the object-size variation when compared to the corresponding values obtained for the case without the tin filter.

  • potential of dual energy subtraction for converting ct numbers to electron density based on a single Linear Relationship
    Medical Physics, 2012
    Co-Authors: Masatoshi Saito
    Abstract:

    Purpose: The conversion of the computed tomography(CT) number to electron density is one of the main processes that determine the accuracy of patient dose calculations in radiotherapy treatment planning. However, the CT number and electron density of tissues cannot be generally interrelated via a simple one-to-one correspondence because the CT number depends on the effective atomic number as well as the electron density. The purpose of this study is to present a simple conversion from the energy-subtracted CT number (ΔHU) by means of dual-energy CT (DECT) to the relative electron density (ρe) via a single Linear Relationship. Methods: The ΔHU–ρe conversion method was demonstrated by performing analytical DECT image simulations that were intended to imitate a second-generation dual-source CT (DSCT) scanner with an additional tin filtration for the high-kV tube. The ΔHU–ρecalibration line was obtained from the image simulation with a 33 cm-diameter electron density calibration phantom equipped with 16 inserts including polytetrafluoroethylene, polyvinyl chlochloride, and aluminum; the elemental compositions of these three inserts were quite different to those of body tissues. The ΔHU–ρe conversion method was also applied to previously published experimental CT data, which were measured using two different CTscanners, to validate the clinical feasibility of the present approach. In addition, the effect of object size on ρe-calibrated images was investigated by image simulations using a 25 cm-diameter virtual phantom for two different filtrations: with and without the tin filter for the high-kV tube. Results: The simulated ΔHU–ρe plot exhibited a predictable Linear Relationship over a wide range of ρe from 0.00 (air) to 2.35 (aluminum). Resultant values of the coefficient of determination, slope, and intercept of the Linear function fitted to the data were close to those of the ideal case. The maximum difference between the ideal and simulated ρe values was −0.7%. The satisfactory Linearity of ΔHU–ρe was also confirmed from analyses of the experimental CT data. In the experimental cases, the maximum difference between the nominal and simulated ρe values was found to be 2.5% after two outliers were excluded. When compared with the case without the tin filter, the ΔHU–ρe conversion performed with the tin filter yielded a lower dose and more reliable ρe values that were less affected by the object-size variation. Conclusions: The ΔHU–ρecalibration line with a simple one-to-one correspondence would facilitate the construction of a well-calibrated ρeimage from acquired dual-kV images, and currently, second generation DSCT may be a feasible modality for the clinical use of the ΔHU–ρe conversion method.

Stephanie E Wolfle – One of the best experts on this subject based on the ideXlab platform.

  • non Linear Relationship between hyperpolarisation and relaxation enables long distance propagation of vasodilatation
    The Journal of Physiology, 2011
    Co-Authors: Stephanie E Wolfle, Daniel J Chaston, Kenichi Goto, Shaun L. Sandow, F R Edwards, Caryl E. Hill
    Abstract:

    Non-technical summary  Microvascular dilatations initiated locally in metabolically active tissues spread rapidly upstream, with little attenuation, to larger vessels whose relaxation results in the necessary increases in local blood flow. While this rapidly spreading response occurs due to the propagation of hyperpolarisation through gap junctions, it is not understood why the dilatation does not attenuate unless a regenerative electrical mechanism is involved. We show in skeletal muscle arterioles in vivo that no such regenerative electrical phenomenon exists. Instead, the local dilatation spreads without attenuation because the initial hyperpolarisation is supramaximal and the impact of voltage on dilatation is restricted to a narrow voltage window near the resting membrane potential. Knowledge of this mechanism increases our understanding of the processes which control blood flow to organs and explains how these processes can be compromised in diseases in which endothelial function is reduced. Abstract  Blood flow is adjusted to tissue demand through rapidly ascending vasodilatations resulting from conduction of hyperpolarisation through vascular gap junctions. We investigated how these dilatations can spread without attenuation if mediated by an electrical signal. Cremaster muscle arterioles were studied in vivo by simultaneously measuring membrane potential and vessel diameter. Focal application of acetylcholine elicited hyperpolarisations which decayed passively with distance from the local site, while dilatation spread upstream without attenuation. Analysis of simultaneous recordings at the local site revealed that hyperpolarisation and dilatation were only Linearly related over a restricted voltage range to a threshold potential, beyond which dilatation was maximal. Experimental data could be simulated in a computational model with electrotonic decay of hyperpolarisation but imposition of this threshold. The model was tested by reducing the amplitude of the local hyperpolarisation which led to entry into the Linear range closer to the local site and decay of dilatation. Serial section electron microscopy and light dye treatment confirmed that the spread of dilatation occurred through the endothelium and that the two cell layers were tightly coupled. Generality of the mechanism was demonstrated by applying the model to the attenuated propagation of dilatation found in larger arteries. We conclude that long distance spread of locally initiated dilatations is not due to a regenerative electrical phenomenon, but rather a restricted Linear Relationship between voltage and vessel tone, which minimises the impact of electrotonic decay of voltage. Disease-related alterations in endothelial coupling or ion channel expression could therefore decrease the ability to adjust blood flow to meet metabolic demand.

  • Non-Linear Relationship between hyperpolarisation and relaxation enables long distance propagation of vasodilatation.
    The Journal of physiology, 2011
    Co-Authors: Stephanie E Wolfle, Daniel J Chaston, Kenichi Goto, Shaun L. Sandow, F R Edwards, Caryl E. Hill
    Abstract:

    Blood flow is adjusted to tissue demand through rapidly ascending vasodilatations resulting from conduction of hyperpolarisation through vascular gap junctions. We investigated how these dilatations can spread without attenuation if mediated by an electrical signal. Cremaster muscle arterioles were studied in vivo by simultaneously measuring membrane potential and vessel diameter. Focal application of acetylcholine elicited hyperpolarisations which decayed passively with distance from the local site,while dilatation spread upstream without attenuation. Analysis of simultaneous recordings at the local site revealed that hyperpolarisation and dilatation were only Linearly related over a restricted voltage range to a threshold potential, beyond which dilatation was maximal. Experimental data could be simulated in a computational model with electrotonic decay of hyperpolarisation but imposition of this threshold. The model was tested by reducing the amplitude of the local hyperpolarisation which led to entry into the Linear range closer to the local site and decay of dilatation. Serial section electron microscopy and light dye treatment confirmed that the spread of dilatation occurred through the endothelium and that the two cell layers were tightly coupled. Generality of the mechanism was demonstrated by applying the model to the attenuated propagation of dilatation found in larger arteries.We conclude that long distance spread of locally initiated dilatations is not due to a regenerative electrical phenomenon, but rather a restricted Linear Relationship between voltage and vessel tone, which minimises the impact of electrotonic decay of voltage. Disease-related alterations in endothelial coupling or ion channel expression could therefore decrease the ability to adjust blood flow to meet metabolic demand.

Jane A Mitchell – One of the best experts on this subject based on the ideXlab platform.

  • aspirin and the in vitro Linear Relationship between thromboxane a2 mediated platelet aggregation and platelet production of thromboxane a2
    Journal of Thrombosis and Haemostasis, 2008
    Co-Authors: Paul C Armstrong, N J Truss, Ferhana Y Ali, A A Dhanji, Ivana Vojnovic, Zetty N Zain, David Bishopbailey, Mark J Paulclark, Art Tucker, Jane A Mitchell
    Abstract:

    Summary. Background: Currently, ‘aspirin resistance’, the anti-platelet effects of non-steroid anti-inflammatory drugs (NSAIDs) and NSAID-aspirin interactions are hot topics of debate. It is often held in this debate that the Relationship between platelet activation and thromboxane (TX) A2 formation is non-Linear and TXA2 generation must be inhibited by at least 95% to inhibit TXA2-dependent aggregation. This Relationship, however, has never been rigorously tested. Objectives: To characterize, in vitro and ex vivo, the concentration-dependent Relationships between TXA2 generation and platelet activity. Method: Platelet aggregation, thrombi adhesion and TXA2 production in response to arachidonic acid (0.03–1 mmol L−1), collagen (0.1–30 μg mL−1), epinephrine (0.001–100 μmol L−1), ADP, TRAP-6 amide and U46619 (all 0.1-30 μmol L−1), in the presence of aspirin or vehicle, were determined in 96-well plates using blood taken from naive individuals or those that had taken aspirin (75 mg, o.d.) for 7 days. Results: Platelet aggregation, adhesion and TXA2 production induced by either arachidonic acid or collagen were inhibited in concentration-dependent manners by aspirin, with logIC50 values that did not differ. A Linear Relationship existed between aggregation and TXA2 production for all combinations of arachidonic acid or collagen and aspirin (P < 0.01; R2 0.92; n = 224). The same Relationships were seen in combinations of aspirin-treated and naive platelets, and in blood from individuals taking an anti-thrombotic dose of aspirin. Conculsions: These studies demonstrate a Linear Relationship between inhibition of platelet TXA2 generation and TXA2-mediated aggregation. This finding is important for our understanding of the anti-platelet effects of aspirin and NSAIDs, NSAID–aspirin interactions and ‘aspirin resistance’.

Shaun L. Sandow – One of the best experts on this subject based on the ideXlab platform.

  • non Linear Relationship between hyperpolarisation and relaxation enables long distance propagation of vasodilatation
    The Journal of Physiology, 2011
    Co-Authors: Stephanie E Wolfle, Daniel J Chaston, Kenichi Goto, Shaun L. Sandow, F R Edwards, Caryl E. Hill
    Abstract:

    Non-technical summary  Microvascular dilatations initiated locally in metabolically active tissues spread rapidly upstream, with little attenuation, to larger vessels whose relaxation results in the necessary increases in local blood flow. While this rapidly spreading response occurs due to the propagation of hyperpolarisation through gap junctions, it is not understood why the dilatation does not attenuate unless a regenerative electrical mechanism is involved. We show in skeletal muscle arterioles in vivo that no such regenerative electrical phenomenon exists. Instead, the local dilatation spreads without attenuation because the initial hyperpolarisation is supramaximal and the impact of voltage on dilatation is restricted to a narrow voltage window near the resting membrane potential. Knowledge of this mechanism increases our understanding of the processes which control blood flow to organs and explains how these processes can be compromised in diseases in which endothelial function is reduced. Abstract  Blood flow is adjusted to tissue demand through rapidly ascending vasodilatations resulting from conduction of hyperpolarisation through vascular gap junctions. We investigated how these dilatations can spread without attenuation if mediated by an electrical signal. Cremaster muscle arterioles were studied in vivo by simultaneously measuring membrane potential and vessel diameter. Focal application of acetylcholine elicited hyperpolarisations which decayed passively with distance from the local site, while dilatation spread upstream without attenuation. Analysis of simultaneous recordings at the local site revealed that hyperpolarisation and dilatation were only Linearly related over a restricted voltage range to a threshold potential, beyond which dilatation was maximal. Experimental data could be simulated in a computational model with electrotonic decay of hyperpolarisation but imposition of this threshold. The model was tested by reducing the amplitude of the local hyperpolarisation which led to entry into the Linear range closer to the local site and decay of dilatation. Serial section electron microscopy and light dye treatment confirmed that the spread of dilatation occurred through the endothelium and that the two cell layers were tightly coupled. Generality of the mechanism was demonstrated by applying the model to the attenuated propagation of dilatation found in larger arteries. We conclude that long distance spread of locally initiated dilatations is not due to a regenerative electrical phenomenon, but rather a restricted Linear Relationship between voltage and vessel tone, which minimises the impact of electrotonic decay of voltage. Disease-related alterations in endothelial coupling or ion channel expression could therefore decrease the ability to adjust blood flow to meet metabolic demand.

  • Non-Linear Relationship between hyperpolarisation and relaxation enables long distance propagation of vasodilatation.
    The Journal of physiology, 2011
    Co-Authors: Stephanie E Wolfle, Daniel J Chaston, Kenichi Goto, Shaun L. Sandow, F R Edwards, Caryl E. Hill
    Abstract:

    Blood flow is adjusted to tissue demand through rapidly ascending vasodilatations resulting from conduction of hyperpolarisation through vascular gap junctions. We investigated how these dilatations can spread without attenuation if mediated by an electrical signal. Cremaster muscle arterioles were studied in vivo by simultaneously measuring membrane potential and vessel diameter. Focal application of acetylcholine elicited hyperpolarisations which decayed passively with distance from the local site,while dilatation spread upstream without attenuation. Analysis of simultaneous recordings at the local site revealed that hyperpolarisation and dilatation were only Linearly related over a restricted voltage range to a threshold potential, beyond which dilatation was maximal. Experimental data could be simulated in a computational model with electrotonic decay of hyperpolarisation but imposition of this threshold. The model was tested by reducing the amplitude of the local hyperpolarisation which led to entry into the Linear range closer to the local site and decay of dilatation. Serial section electron microscopy and light dye treatment confirmed that the spread of dilatation occurred through the endothelium and that the two cell layers were tightly coupled. Generality of the mechanism was demonstrated by applying the model to the attenuated propagation of dilatation found in larger arteries.We conclude that long distance spread of locally initiated dilatations is not due to a regenerative electrical phenomenon, but rather a restricted Linear Relationship between voltage and vessel tone, which minimises the impact of electrotonic decay of voltage. Disease-related alterations in endothelial coupling or ion channel expression could therefore decrease the ability to adjust blood flow to meet metabolic demand.