1
40
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Text
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<a href="http://doi.org/10.1161/CIRCULATIONAHA.116.024826" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCULATIONAHA.116.024826</a>
Pages
1240–1252
Issue
13
Volume
135
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Augmentation of Muscle Blood Flow by Ultrasound Cavitation Is Mediated by ATP and Purinergic Signaling.
Publisher
An entity responsible for making the resource available
Circulation
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-03
Subject
The topic of the resource
Adenosine Triphosphate – Metabolism; Adenosine Triphosphate/*metabolism; Animal Studies; Animals; contrast echocardiography; Equipment and Supplies; Hemodynamics; Humans; Inbred C57BL; Male; Mice; microbubbles; Microbubbles; microcirculation; Muscle; Neurotransmitter Agents – Metabolism; perfusion; Purinergic Agents/*metabolism; Signal Transduction; Skeletal – Blood Supply; Skeletal/*blood supply; Ultrasonography – Methods; Ultrasonography/*methods
Creator
An entity primarily responsible for making the resource
Belcik J Todd; Davidson Brian P; Xie Aris; Wu Melinda D; Yadava Mrinal; Qi Yue; Liang Sherry; Chon Chae Ryung; Ammi Azzdine Y; Field Joshua; Harmann Leanne; Chilian William M; Linden Joel; Lindner Jonathan R
Description
An account of the resource
BACKGROUND: Augmentation of tissue blood flow by therapeutic ultrasound is thought to rely on convective shear. Microbubble contrast agents that undergo ultrasound-mediated cavitation markedly amplify these effects. We hypothesized that purinergic signaling is responsible for shear-dependent increases in muscle perfusion during therapeutic cavitation. METHODS: Unilateral exposure of the proximal hindlimb of mice (with or without ischemia produced by iliac ligation) to therapeutic ultrasound (1.3 MHz, mechanical index 1.3) was performed for 10 minutes after intravenous injection of 2x10(8) lipid microbubbles. Microvascular perfusion was evaluated by low-power contrast ultrasound perfusion imaging. In vivo muscle ATP release and in vitro ATP release from endothelial cells or erythrocytes were assessed by a luciferin-luciferase assay. Purinergic signaling pathways were assessed by studying interventions that (1) accelerated ATP degradation; (2) inhibited P2Y receptors, adenosine receptors, or KATP channels; or (3) inhibited downstream signaling pathways involving endothelial nitric oxide synthase or prostanoid production (indomethacin). Augmentation in muscle perfusion by ultrasound cavitation was assessed in a proof-of-concept clinical trial in 12 subjects with stable sickle cell disease. RESULTS: Therapeutic ultrasound cavitation increased muscle perfusion by 7-fold in normal mice, reversed tissue ischemia for up to 24 hours in the murine model of peripheral artery disease, and doubled muscle perfusion in patients with sickle cell disease. Augmentation in flow extended well beyond the region of ultrasound exposure. Ultrasound cavitation produced an approximately 40-fold focal and sustained increase in ATP, the source of which included both endothelial cells and erythrocytes. Inhibitory studies indicated that ATP was a critical mediator of flow augmentation that acts primarily through either P2Y receptors or adenosine produced by ectonucleotidase activity. Combined indomethacin and inhibition of endothelial nitric oxide synthase abolished the effects of therapeutic ultrasound, indicating downstream signaling through both nitric oxide and prostaglandins. CONCLUSIONS: Therapeutic ultrasound using microbubble cavitation to increase muscle perfusion relies on shear-dependent increases in ATP, which can act through a diverse portfolio of purinergic signaling pathways. These events can reverse hindlimb ischemia in mice for \textgreater24 hours and increase muscle blood flow in patients with sickle cell disease. CLINICAL TRIAL REGISTRATION: URL: http://clinicaltrials.gov. Unique identifier: NCT01566890.
Identifier
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<a href="http://doi.org/10.1161/CIRCULATIONAHA.116.024826" target="_blank" rel="noreferrer noopener">10.1161/CIRCULATIONAHA.116.024826</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
Adenosine Triphosphate – Metabolism
Adenosine Triphosphate/*metabolism
Ammi Azzdine Y
Animal Studies
Animals
Belcik J Todd
Chilian William M
Chon Chae Ryung
Circulation
contrast echocardiography
Davidson Brian P
Department of Integrative Medical Sciences
Equipment and Supplies
Field Joshua
Harmann Leanne
Hemodynamics
Humans
Inbred C57BL
Liang Sherry
Linden Joel
Lindner Jonathan R
Male
Mice
Microbubbles
Microcirculation
Muscle
NEOMED College of Medicine
Neurotransmitter Agents – Metabolism
Perfusion
Purinergic Agents/*metabolism
Qi Yue
Signal Transduction
Skeletal – Blood Supply
Skeletal/*blood supply
Ultrasonography – Methods
Ultrasonography/*methods
Wu Melinda D
Xie Aris
Yadava Mrinal
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/CIRCRESAHA.115.306642" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCRESAHA.115.306642</a>
Pages
612–621
Issue
7
Volume
117
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Requisite Role of Kv1.5 Channels in Coronary Metabolic Dilation.
Publisher
An entity responsible for making the resource available
Circulation research
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-09
Subject
The topic of the resource
129 Strain; Animals; cardiac function; contrast echocardiography; Coronary Circulation/*physiology; Coronary Vessels/*metabolism; hydrogen peroxide; Inbred C57BL; ion channel; Knockout; Kv1.5 Potassium Channel/*physiology; Mice; Muscle; Smooth; Transgenic; transgenic mice; Vascular/*metabolism; vasodilation; Vasodilation/*physiology; voltage-gated potassium channels
Creator
An entity primarily responsible for making the resource
Ohanyan Vahagn; Yin Liya; Bardakjian Raffi; Kolz Christopher; Enrick Molly; Hakobyan Tatevik; Kmetz John; Bratz Ian; Luli Jordan; Nagane Masaki; Khan Nadeem; Hou Huagang; Kuppusamy Periannan; Graham Jacqueline; Fu Frances Kwan; Janota Danielle; Oyewumi Moses O; Logan Suzanna; Lindner Jonathan R; Chilian William M
Description
An account of the resource
RATIONALE: In the working heart, coronary blood flow is linked to the production of metabolites, which modulate tone of smooth muscle in a redox-dependent manner. Voltage-gated potassium channels (Kv), which play a role in controlling membrane potential in vascular smooth muscle, have certain members that are redox-sensitive. OBJECTIVE: To determine the role of redox-sensitive Kv1.5 channels in coronary metabolic flow regulation. METHODS AND RESULTS: In mice (wild-type [WT], Kv1.5 null [Kv1.5(-/-)], and Kv1.5(-/-) and WT with inducible, smooth muscle-specific expression of Kv1.5 channels), we measured mean arterial pressure, myocardial blood flow, myocardial tissue oxygen tension, and ejection fraction before and after inducing cardiac stress with norepinephrine. Cardiac work was estimated as the product of mean arterial pressure and heart rate. Isolated arteries were studied to establish whether genetic alterations modified vascular reactivity. Despite higher levels of cardiac work in the Kv1.5(-/-) mice (versus WT mice at baseline and all doses of norepinephrine), myocardial blood flow was lower in Kv1.5(-/-) mice than in WT mice. At high levels of cardiac work, tissue oxygen tension dropped significantly along with ejection fraction. Expression of Kv1.5 channels in smooth muscle in the null background rescued this phenotype of impaired metabolic dilation. In isolated vessels from Kv1.5(-/-) mice, relaxation to H2O2 was impaired, but responses to adenosine and acetylcholine were normal compared with those from WT mice. CONCLUSIONS: Kv1.5 channels in vascular smooth muscle play a critical role in coupling myocardial blood flow to cardiac metabolism. Absence of these channels disassociates metabolism from flow, resulting in cardiac pump dysfunction and tissue hypoxia.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/CIRCRESAHA.115.306642" target="_blank" rel="noreferrer noopener">10.1161/CIRCRESAHA.115.306642</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
129 Strain
2015
Animals
Bardakjian Raffi
Bratz Ian
Cardiac function
Chilian William M
Circulation research
contrast echocardiography
Coronary Circulation/*physiology
Coronary Vessels/*metabolism
Department of Integrative Medical Sciences
Department of Pharmaceutical Sciences
Enrick Molly
Fu Frances Kwan
Graham Jacqueline
Hakobyan Tatevik
Hou Huagang
Hydrogen peroxide
Inbred C57BL
ion channel
Janota Danielle
Khan Nadeem
Kmetz John
Knockout
Kolz Christopher
Kuppusamy Periannan
Kv1.5 Potassium Channel/*physiology
Lindner Jonathan R
Logan Suzanna
Luli Jordan
Mice
Muscle
Nagane Masaki
NEOMED College of Medicine
NEOMED College of Pharmacy
Ohanyan Vahagn
Oyewumi Moses O
Smooth
Transgenic
Transgenic mice
Vascular/*metabolism
vasodilation
Vasodilation/*physiology
voltage-gated potassium channels
Yin Liya