1
40
4
-
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.1993.265.4.H1184" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.1993.265.4.H1184</a>
Pages
H1184–1188
Issue
4
Volume
265
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
Acute exercise enhances nitric oxide modulation of vascular response to phenylephrine.
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
1993
1993-10
Subject
The topic of the resource
*Physical Exertion; Animals; Arginine/analogs & derivatives/pharmacology; Blood Flow Velocity; Blood Pressure/drug effects; Blood Vessels/*drug effects; Dose-Response Relationship; Drug; Female; Heart Rate/drug effects; Iliac Artery/drug effects/physiology; Male; NG-Nitroarginine Methyl Ester; Nitric Oxide/antagonists & inhibitors/*physiology; Phenylephrine/*pharmacology; Rats; Sprague-Dawley; Time Factors; Vasoconstriction/drug effects/physiology
Creator
An entity primarily responsible for making the resource
Patil R D; DiCarlo S E; Collins H L
Description
An account of the resource
The influence of the release of endothelium-derived nitric oxide (NO) on the vasoconstrictor response to phenylephrine (PE) was evaluated before and after a single bout of dynamic exercise. Each rat ran on a motor-driven treadmill at
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.1993.265.4.H1184" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.1993.265.4.H1184</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).
*Physical Exertion
1993
Animals
Arginine/analogs & derivatives/pharmacology
Blood Flow Velocity
Blood Pressure/drug effects
Blood Vessels/*drug effects
Collins H L
DiCarlo S E
Dose-Response Relationship
Drug
Female
Heart Rate/drug effects
Iliac Artery/drug effects/physiology
Male
NG-Nitroarginine Methyl Ester
Nitric Oxide/antagonists & inhibitors/*physiology
Patil R D
Phenylephrine/*pharmacology
Rats
Sprague-Dawley
The American journal of physiology
Time Factors
Vasoconstriction/drug effects/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/10.1152/ajpheart.01330.2006" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.01330.2006</a>
Pages
H2729–2736
Issue
6
Volume
292
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
Optimal reactive oxygen species concentration and p38 MAP kinase are required for coronary collateral growth.
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
2007
2007-06
Subject
The topic of the resource
*Collateral Circulation/drug effects; *Coronary Circulation/drug effects; *MAP Kinase Signaling System/drug effects; Acetophenones/pharmacology; Animal; Animals; Blood Flow Velocity; Cells; Coronary Vessels/surgery; Cultured; Disease Models; Ditiocarb/pharmacology; Endothelial Cells/drug effects/enzymology/*metabolism; Enzyme Inhibitors/pharmacology; Humans; Imidazoles/pharmacology; Inbred WKY; Ligation; Male; Myocardial Reperfusion Injury/enzymology/metabolism/*physiopathology; NADPH Oxidases/antagonists & inhibitors/metabolism; Neovascularization; Onium Compounds/pharmacology; Oxygenases/antagonists & inhibitors/metabolism; p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/*metabolism; Physiologic; Pyridines/pharmacology; Rats; Reactive Oxygen Species/*metabolism; Superoxide Dismutase/antagonists & inhibitors/metabolism; Vascular Endothelial Growth Factor A/metabolism
Creator
An entity primarily responsible for making the resource
Rocic Petra; Kolz Christopher; Reed Ryan; Potter Barry; Chilian William M
Description
An account of the resource
Reactive oxygen species (ROS) are implicated in coronary collateral growth (CCG). We evaluated the requirement for ROS in human coronary artery endothelial cell (HCAEC) tube formation, CCG in vivo, and signaling (p38 MAP kinase) by which ROS may stimulate vascular growth. The flavin-containing oxidase inhibitor diphenyleneiodonium (DPI) or the superoxide dismutase inhibitor diethyldithiocarbamate (DETC) blocked vascular endothelial growth factor-induced HCAEC tube formation in Matrigel. We assessed the effect of DPI and DETC on CCG in a rat model of repetitive ischemia (RI) (40 s left anterior descending coronary artery occlusion every 20 min for 2 h 20 min, 3 times/day, 10 days). DPI or DETC was given intraperitoneally, or the NAD(P)H oxidase inhibitor apocynin was given in drinking water. Collateral-dependent flow (measured by using microspheres) was expressed as a ratio of normal and ischemic zone flows. In sham-operated rats, collateral flow in the ischemic zone was 18 +/- 6% of normal zone; in the RI group, collateral flow in the ischemic zone was 83 +/- 5% of normal zone. DPI prevented the increase in collateral flow after RI (25 +/- 4% of normal zone). Similar results were obtained with apocynin following RI (32 +/- 7% of that in the normal zone). DETC achieved similar results (collateral flow after RI was 21 +/- 2% of normal zone). DPI and DETC blocked RI-induced p38 MAP kinase activation in response to vascular endothelial growth factor and RI. These results demonstrate a requirement for optimal ROS concentration in HCAEC tube formation, CCG, and p38 MAP kinase activation. p38 MAP kinase inhibition prevented HCAEC tube formation and partially blocked RI-induced CCG (42 +/- 7% of normal zone flow), indicating that p38 MAP kinase is a critical signaling mediator of CCG.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.01330.2006" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.01330.2006</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).
*Collateral Circulation/drug effects
*Coronary Circulation/drug effects
*MAP Kinase Signaling System/drug effects
2007
Acetophenones/pharmacology
American journal of physiology. Heart and circulatory physiology
Animal
Animals
Blood Flow Velocity
Cells
Chilian William M
Coronary Vessels/surgery
Cultured
Department of Integrative Medical Sciences
Disease Models
Ditiocarb/pharmacology
Endothelial Cells/drug effects/enzymology/*metabolism
Enzyme Inhibitors/pharmacology
Humans
Imidazoles/pharmacology
Inbred WKY
Kolz Christopher
Ligation
Male
Myocardial Reperfusion Injury/enzymology/metabolism/*physiopathology
NADPH Oxidases/antagonists & inhibitors/metabolism
NEOMED College of Medicine
Neovascularization
Onium Compounds/pharmacology
Oxygenases/antagonists & inhibitors/metabolism
p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/*metabolism
Physiologic
Potter Barry
Pyridines/pharmacology
Rats
Reactive Oxygen Species/*metabolism
Reed Ryan
Rocic Petra
Superoxide Dismutase/antagonists & inhibitors/metabolism
Vascular Endothelial Growth Factor A/metabolism
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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/10.1097/RUQ.0b013e31814fb469" target="_blank" rel="noreferrer noopener">http://doi.org/10.1097/RUQ.0b013e31814fb469</a>
Pages
199–202
Issue
3
Volume
23
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
Duplex Doppler sonography of the carotid artery: velocity measurements in an artery with contralateral stenosis.
Publisher
An entity responsible for making the resource available
Ultrasound quarterly
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
2007-09
Subject
The topic of the resource
*Ultrasonography; Adult; Angiography; Blood Flow Velocity; Carotid Stenosis – Physiopathology; Carotid Stenosis – Radiography; Carotid Stenosis – Ultrasonography; Carotid Stenosis/*diagnostic imaging/physiopathology; Doppler; Duplex; Female; Human; Humans; Male; Retrospective Design; Retrospective Studies; Ultrasonography
Creator
An entity primarily responsible for making the resource
Grajo Joseph R; Barr Richard G
Description
An account of the resource
To determine if a significant contralateral stenosis affects interpretation tables of the ipsilateral internal carotid artery's degree of stenosis in duplex Doppler ultrasound, the records of 307 patients with carotid duplex ultrasound studies with an angiogram performed within 3 months without intervening intervention were retrospectively reviewed for peak systolic velocity, end-diastolic velocity, internal carotid artery-common carotid artery ratio, and angiographic degree of stenosis. Data were grouped into categories of degree of contralateral stenosis, and Pearson r correlation was used to determine significance of ipsilateral Doppler parameters to angiographic data. As the degree of contralateral stenosis increases, the correlation of ultrasound parameters becomes less significant. At a contralateral stenosis of less than 40%, the P value for peak systolic velocity was 0.0006; at a contralateral stenosis between 40% and 59%, the P value was 0.133; at a contralateral stenosis between 60% and 79%, the P value was 0.241; and at a contralateral stenosis between 80% and 99%, the P value was 0.439. Therefore, correlations are no longer significant at levels above 40% contralateral stenosis. The Doppler parameters were scattered in patients with greater than 40%contralateral stenosis, and "corrected" correlation tables could not be derived. As stenosis increases in the contralateral internal carotid artery, Doppler values become inaccurate in determining the degree of stenosis in the ipsilateral internal carotid artery, with the occurrence of both the overestimation and underestimation of the degree of stenosis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1097/RUQ.0b013e31814fb469" target="_blank" rel="noreferrer noopener">10.1097/RUQ.0b013e31814fb469</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).
*Ultrasonography
2007
Adult
Angiography
Barr Richard G
Blood Flow Velocity
Carotid Stenosis – Physiopathology
Carotid Stenosis – Radiography
Carotid Stenosis – Ultrasonography
Carotid Stenosis/*diagnostic imaging/physiopathology
Doppler
Duplex
Female
Grajo Joseph R
Human
Humans
Male
Retrospective Design
Retrospective Studies
Ultrasonography
Ultrasound quarterly
-
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.freeradbiomed.2016.09.021" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2016.09.021</a>
Pages
10–19
Volume
101
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
4-Hydroxynonenal dependent alteration of TRPV1-mediated coronary microvascular signaling.
Publisher
An entity responsible for making the resource available
Free radical biology & medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-12
Subject
The topic of the resource
*4-Hydroxynonenal; *Coronary regulation; *Lipid peroxidation; *Post-translational modification; *Protein Processing; *Reactive oxygen species; *Signal Transduction; *TRPV1; Action Potentials/drug effects; Aldehydes/antagonists & inhibitors/metabolism/*pharmacology; Animal; Animals; Blood Flow Velocity; Calcium Signaling/drug effects; Capsaicin/*pharmacology; Cardiovascular Agents/*pharmacology; Coronary Circulation/drug effects; Coronary Vessels/metabolism/physiopathology; Cysteine/genetics/metabolism; Diabetes Mellitus/drug therapy/*metabolism/physiopathology; Disease Models; Femoral Artery/metabolism/physiopathology; HEK293 Cells; Humans; Inbred C57BL; Lipid Peroxidation; Male; Mice; Patch-Clamp Techniques; Post-Translational; TRPV Cation Channels/genetics/*metabolism; Vasodilation/drug effects
Creator
An entity primarily responsible for making the resource
DelloStritto Daniel J; Sinharoy Pritam; Connell Patrick J; Fahmy Joseph N; Cappelli Holly C; Thodeti Charles K; Geldenhuys Werner J; Damron Derek S; Bratz Ian N
Description
An account of the resource
We demonstrated previously that TRPV1-dependent regulation of coronary blood flow (CBF) is disrupted in diabetes. Further, we have shown that endothelial TRPV1 is differentially regulated, ultimately leading to the inactivation of TRPV1, when exposed to a prolonged pathophysiological oxidative environment. This environment has been shown to increase lipid peroxidation byproducts including
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2016.09.021" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2016.09.021</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).
*4-Hydroxynonenal
*Coronary regulation
*Lipid peroxidation
*Post-translational modification
*Protein Processing
*Reactive oxygen species
*Signal Transduction
*TRPV1
2016
Action Potentials/drug effects
Aldehydes/antagonists & inhibitors/metabolism/*pharmacology
Animal
Animals
Blood Flow Velocity
Bratz Ian N
Calcium Signaling/drug effects
Cappelli Holly C
Capsaicin/*pharmacology
Cardiovascular Agents/*pharmacology
Connell Patrick J
Coronary Circulation/drug effects
Coronary Vessels/metabolism/physiopathology
Cysteine/genetics/metabolism
Damron Derek S
DelloStritto Daniel J
Department of Integrative Medical Sciences
Diabetes Mellitus/drug therapy/*metabolism/physiopathology
Disease Models
Fahmy Joseph N
Femoral Artery/metabolism/physiopathology
Free radical biology & medicine
Geldenhuys Werner J
HEK293 Cells
Humans
Inbred C57BL
Lipid Peroxidation
Male
Mice
NEOMED College of Medicine
Patch-Clamp Techniques
Post-Translational
Sinharoy Pritam
Thodeti Charles K
TRPV Cation Channels/genetics/*metabolism
Vasodilation/drug effects