1
40
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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/10.1152/ajpheart.1990.258.3.H748" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.1990.258.3.H748</a>
Pages
H748–753
Issue
3
Volume
258
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
Macromolecular transport in canine coronary microvasculature.
Publisher
An entity responsible for making the resource available
The American journal of physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
1990
1990-03
Subject
The topic of the resource
*Coronary Circulation; Animals; Biological Transport; Blood Proteins/metabolism; Coronary Disease/metabolism; Dogs; Female; Immunoglobulin G/*metabolism; Immunoglobulin M/*metabolism; Lymph/metabolism; Macromolecular Substances; Male; Microcirculation; Myocardial Reperfusion; Myocardium/metabolism; Osmolar Concentration; Permeability; Reference Values; Serum Albumin/*metabolism
Creator
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Pilati C F
Description
An account of the resource
Coronary vascular osmotic reflection coefficients (sigma dS) for total protein, albumin (Alb), immunoglobulin (Ig)G, and IgM were determined in the anesthetized dog. Myocardial lymph was collected from the anterior interventricular lymphatic trunk, and the sigma dS estimated from filtration rate-independent lymph-to-plasma protein concentration ratios (CL/CPS). Lymph flows of at least 12 times base line were needed to produce filtration rate-independent CL/CPS, and these were achieved in 9 of 12 experiments. In these nine experiments, sigma dS for total protein, Alb, IgG, and IgM were, respectively, 0.67 +/- 0.02 (SE), 0.59 +/- 0.05, 0.70 +/- 0.03, and 0.87 +/- 0.01. The data were fitted to a model that showed that transvascular fluid and solute flux could be described by two populations of pores. A large pore system with an equivalent radius of 235 A was responsible for 39% of the transvascular volume flow. A small pore system less than 53 A accounted for the remaining flow. In a second group of experiments (n = 8), 60 min of ischemia decreased the sigma dS to 0.27 +/- 0.03, 0.07 +/- 0.05, 0.22 +/- 0.03, and 0.69 +/- 0.04 for total protein, Alb, IgG, and IgM, respectively. A single population of pores of 220 A could describe the entire transvascular volume flow. These results indicate that coronary vascular protein permeability is moderately high and can be increased significantly by ischemia.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.1990.258.3.H748" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.1990.258.3.H748</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).
*Coronary Circulation
1990
Animals
Biological Transport
Blood Proteins/metabolism
Coronary Disease/metabolism
Dogs
Female
Immunoglobulin G/*metabolism
Immunoglobulin M/*metabolism
Lymph/metabolism
Macromolecular Substances
Male
Microcirculation
Myocardial Reperfusion
Myocardium/metabolism
Osmolar Concentration
Permeability
Pilati C F
Reference Values
Serum Albumin/*metabolism
The American journal of physiology
-
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
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coronary circulation in acute myocardial ischaemia/reperfusion injury: a target for cardioprotection.
Publisher
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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.
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<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