1
40
3
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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/10.1093/cvr/cvy286" target="_blank" rel="noreferrer noopener">http://doi.org/10.1093/cvr/cvy286</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1143-1155
Issue
7
Volume
115
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
coronary circulation in acute myocardial ischaemia/reperfusion injury: a target for cardioprotection.
Publisher
An entity responsible for making the resource available
Cardiovascular Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
1905-07
Subject
The topic of the resource
acute coronary syndromes; blood capillaries; cardiac myocytes; cardiac vasculature; Cardioprotection; Coronary circulation; Coronary circulation; CYTOLOGY; edema; endothelium; erythrocytes; HEMORRHAGE; infarction; Ischaemia; ischemia; ischemia; ISCHEMIC preconditioning; leukocytes; MEDICAL sciences; Microvascular obstruction; midventricular obstruction; MYOCARDIAL reperfusion; personal integrity; pharmacology; physiologic reperfusion; PRASUGREL; Reperfusion; reperfusion injury; reperfusion injury; reperfusion therapy
Creator
An entity primarily responsible for making the resource
Hausenloy Derek J; Chilian William; Crea Filippo; Davidson Sean M; Ferdinandy Peter; Garcia-Dorado David; van Royen Niels; Schulz Rainer; Heusch Gerd
Description
An account of the resource
The coronary circulation is both culprit and victim of acute myocardial infarction. The rupture of an epicardial atherosclerotic plaque with superimposed thrombosis causes coronary occlusion, and this occlusion must be removed to induce reperfusion. However, ischaemia and reperfusion cause damage not only in cardiomyocytes but also in the coronary circulation, including microembolization of debris and release of soluble factors from the culprit lesion, impairment of endothelial integrity with subsequently increased permeability and oedema formation, platelet activation and leucocyte adherence, erythrocyte stasis, a shift from vasodilation to vasoconstriction, and ultimately structural damage to the capillaries with eventual no-reflow, microvascular obstruction (MVO), and intramyocardial haemorrhage (IMH). Therefore, the coronary circulation is a valid target for cardioprotection, beyond protection of the cardiomyocyte. Virtually all of the above deleterious endpoints have been demonstrated to be favourably influenced by one or the other mechanical or pharmacological cardioprotective intervention. However, no-reflow is still a serious complication of reperfused myocardial infarction and carries, independently from infarct size, an unfavourable prognosis. MVO and IMH can be diagnosed by modern imaging technologies, but still await an effective therapy. The current review provides an overview of strategies to protect the coronary circulation from acute myocardial ischaemia/reperfusion injury. This article is part of a Cardiovascular Research Spotlight Issue entitled 'Cardioprotection Beyond the Cardiomyocyte', and emerged as part of the discussions of the European Union (EU)-CARDIOPROTECTION Cooperation in Science and Technology (COST) Action, CA16225.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1093/cvr/cvy286" target="_blank" rel="noreferrer noopener">10.1093/cvr/cvy286</a>
2019
acute coronary syndromes
blood capillaries
cardiac myocytes
cardiac vasculature
cardioprotection
Cardiovascular research
Chilian William
Coronary Circulation
Crea Filippo
CYTOLOGY
Davidson Sean M
Department of Integrative Medical Sciences
Edema
Endothelium
erythrocytes
Ferdinandy Peter
Garcia-Dorado David
Hausenloy Derek J
Hemorrhage
Heusch Gerd
Infarction
Ischaemia
ischemia
Ischemic Preconditioning
June 2019 Update
LEUKOCYTES
MEDICAL sciences
Microvascular obstruction
midventricular obstruction
Myocardial Reperfusion
NEOMED College of Medicine
personal integrity
pharmacology
physiologic reperfusion
PRASUGREL
Reperfusion
Reperfusion Injury
reperfusion therapy
Schulz Rainer
van Royen Niels
-
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/10.1152/ajpheart.00694.2010" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00694.2010</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
H1069-H1077
Issue
3
Volume
300
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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
Endothelial NOS activity and myocardial oxygen metabolism define the salvageable ischemic time window for ischemic postconditioning
Publisher
An entity responsible for making the resource available
American Journal of Physiology-Heart and Circulatory Physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-03
Subject
The topic of the resource
cardioprotection; mice; inhibition; Physiology; Cardiovascular System & Cardiology; activation; dysfunction; reperfusion injury; tissue oxygenation; consumption; blood flow; electron paramagnetic resonance; infarct size; ischemia and reperfusion; mitochondrial enzyme activity; mitochondrial permeability transition; rabbit hearts; regional
Creator
An entity primarily responsible for making the resource
Cai M; Li Y J; Xu Y; Swartz H M; Chen C L; Chen Y R; He G L
Description
An account of the resource
Cai M, Li Y, Xu Y, Swartz HM, Chen C, Chen Y, He G. Endothelial NOS activity and myocardial oxygen metabolism define the salvageable ischemic time window for ischemic postconditioning. Am J Physiol Heart Circ Physiol 300: H1069-H1077, 2011. First published January 7, 2011; doi: 10.1152/ajpheart.00694.2010.-Ischemic postconditioning (IPOC) could be ineffective or even detrimental if the index ischemic duration is either too short or too long. The present study is to demonstrate that oxygen supply and metabolism defines a salvageable ischemic time window of IPOC in mice. C57BL/6 mice underwent coronary artery occlusion followed by reperfusion (I/R), with or without IPOC by three cycles of 10 s/10 s R/I. In vivo myocardial tissue oxygenation was monitored with electron paramagnetic resonance oximetry. Regional blood flow (RBF) was measured with a laser Doppler monitor. At the end of 60 min reperfusion, tissue from the risk area was collected, and mitochondrial enzyme activities were assayed. Tissue oximetry demonstrated that I/R induced a reperfusion hyperoxygenation state in the 30- and 45-min but not 15- and 60-min ischemia groups. IPOC attenuated the hyperoxygenation with 45 but not 30 min ischemia. RBF, eNOS phosphorylation, and mitochondrial enzyme activities were suppressed after I/R with different ischemic time, and IPOC afforded protection with 30 and 45 but not 60 min ischemia. Infarct size measurement indicated that IPOC reduced infarction with 30 and 45 min but not 60 min ischemia. Clearly, IPOC protected mouse heart with a defined ischemic time window between 30 and 45 min. This salvageable time window was accompanied by the improvement of RBF due to increased phosphorylated eNOS and the preservation of mitochondrial oxygen consumption due to conserved mitochondrial enzyme activities. Interestingly, this salvageable ischemic time window was mirrored by tissue hyperoxygenation status in the postischemic heart.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00694.2010" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00694.2010</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2011
activation
American Journal of Physiology-Heart and Circulatory Physiology
blood flow
Cai M
cardioprotection
Cardiovascular System & Cardiology
Chen C L
Chen Y R
consumption
dysfunction
electron paramagnetic resonance
He G L
infarct size
inhibition
ischemia and reperfusion
Journal Article or Conference Abstract Publication
Li Y J
Mice
mitochondrial enzyme activity
mitochondrial permeability transition
Physiology
rabbit hearts
regional
Reperfusion Injury
Swartz H M
tissue oxygenation
Xu Y
-
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/10.1016/j.bbabio.2011.03.001" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.bbabio.2011.03.001</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
491-502
Issue
5
Volume
1807
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
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
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Excess no predisposes mitochondrial succinate-cytochrome c reductase to produce hydroxyl radical
Publisher
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Biochimica Et Biophysica Acta-Bioenergetics
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-05
Subject
The topic of the resource
Mitochondria; Biophysics; oxygen; Biochemistry & Molecular Biology; nitric-oxide synthase; reactive; smooth-muscle-cells; endothelial-cells; reperfusion injury; EPR; postischemic heart; complex-ii; Electron transport chain; electron-transport; Hydroxyl radical; NO; oxygen-free radicals; SCR; spin trapping; superoxide generation
Creator
An entity primarily responsible for making the resource
Chen J F; Chen C L; Alevriadou B R; Zweier J L; Chen Y R
Description
An account of the resource
Mitochondria-derived oxygen-free radical(s) are important mediators of oxidative cellular injury. It is widely hypothesized that excess NO enhances O(2)(center dot-) generated by mitochondria under certain pathological conditions. In the mitochondrial electron transport chain, succinate-cytochrome c reductase (SCR) catalyzes the electron transfer reaction from succinate to cytochrome c. To gain the insights into the molecular mechanism of how NO overproduction may mediate the oxygen-free radical generation by SCR, we employed isolated SCR, cardiac myoblast H9c2, and endothelial cells to study the interaction of NO with SCR in vitro and ex vivo. Under the conditions of enzyme turnover in the presence of NO donor (DEANO), SCR gained pro-oxidant function for generating hydroxyl radical as detected by EPR spin trapping using DEPMPO. The EPR signal associated with DEPMPO/(center dot)OH adduct was nearly completely abolished in the presence of catalase or an iron chelator and partially inhibited by SOD, suggesting the involvement of the iron-H(2)O(2)-dependent Fenton reaction or O(2)(center dot-)-dependent Haber-Weiss mechanism. Direct EPR measurement of SCR at 77 K indicated the formation of a nonheme iron-NO complex, implying that electron leakage to molecular oxygen was enhanced at the FAD cofactor, and that excess NO predisposed SCR to produce (center dot)OH. In H9c2 cells, SCR-dependent oxygen-free radical generation was stimulated by NO released from DEANO or produced by the cells following exposure to hypoxia/reoxygenation. With shear exposure that led to overproduction of NO by the endothelium, SCR-mediated oxygen-free radical production was also detected in cultured vascular endothelial cells. (C) 2011 Elsevier B.V. All rights reserved.
Identifier
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<a href="http://doi.org/10.1016/j.bbabio.2011.03.001" target="_blank" rel="noreferrer noopener">10.1016/j.bbabio.2011.03.001</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2011
Alevriadou B R
Biochemistry & Molecular Biology
Biochimica Et Biophysica Acta-Bioenergetics
Biophysics
Chen C L
Chen J F
Chen Y R
complex-ii
Electron transport chain
electron-transport
endothelial-cells
EPR
Hydroxyl radical
Journal Article or Conference Abstract Publication
Mitochondria
nitric-oxide synthase
NO
Oxygen
oxygen-free radicals
postischemic heart
reactive
Reperfusion Injury
SCR
smooth-muscle-cells
spin trapping
superoxide generation
Zweier J L