1
40
4
-
Text
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URL Address
<a href="http://doi.org/10.1152/jappl.1999.87.2.611" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/jappl.1999.87.2.611</a>
Pages
611–618
Issue
2
Volume
87
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
Effect of epinephrine on alveolar liquid clearance in the rat.
Publisher
An entity responsible for making the resource available
Journal of applied physiology (Bethesda, Md. : 1985)
Date
A point or period of time associated with an event in the lifecycle of the resource
1999
1999-08
Subject
The topic of the resource
Adrenergic; Adrenergic beta-Agonists/*pharmacology; Amiloride/pharmacology; Animals; beta/metabolism; Bronchoalveolar Lavage Fluid/chemistry; Epinephrine/blood/*pharmacology; Male; Norepinephrine/blood; Propranolol/pharmacology; Pulmonary Alveoli/*drug effects; Rats; Receptors; Serum Albumin/metabolism; Sprague-Dawley; Time Factors
Creator
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Charron P D; Fawley J P; Maron M B
Description
An account of the resource
Endogenous epinephrine has been found to increase alveolar liquid clearance (ALC) in several pulmonary edema models. In this study, we infused epinephrine intravenously for 1 h in anesthetized rats to produce plasma epinephrine concentrations commonly observed in this species under stressful conditions and measured ALC by mass balance. Epinephrine increased ALC from 31.5 +/- 3.2 to 48.9 +/- 1.1 (SE)% of the instilled volume (P \textless 0.05). The increased ALC was prevented by either propranolol or amiloride. To determine whether ALC returns to normal after plasma epinephrine concentration normalizes, we measured ALC 2 h after stopping an initial 1-h epinephrine infusion and found ALC to be at baseline values. Finally, to determine whether desensitization of the liquid clearance response occurs, we evaluated the effects of both repeated 1-h infusions and a continuous 4-h infusion of epinephrine on ALC and found no reduction in ALC under either condition. We conclude that epinephrine increases ALC by stimulating beta-adrenoceptors and sodium transport, that the increase is reversible once plasma epinephrine concentration normalizes, and that desensitization of the ALC response does not appear to occur after 4 h of continuous epinephrine exposure.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/jappl.1999.87.2.611" target="_blank" rel="noreferrer noopener">10.1152/jappl.1999.87.2.611</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).
1999
Adrenergic
Adrenergic beta-Agonists/*pharmacology
Amiloride/pharmacology
Animals
beta/metabolism
Bronchoalveolar Lavage Fluid/chemistry
Charron P D
Epinephrine/blood/*pharmacology
Fawley J P
Journal of applied physiology (Bethesda, Md. : 1985)
Male
Maron M B
Norepinephrine/blood
Propranolol/pharmacology
Pulmonary Alveoli/*drug effects
Rats
Receptors
Serum Albumin/metabolism
Sprague-Dawley
Time Factors
-
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/ajplung.00381.2001" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajplung.00381.2001</a>
Pages
L666–674
Issue
4
Volume
282
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
Prolonged isoproterenol infusion impairs the ability of beta(2)-agonists to increase alveolar liquid clearance.
Publisher
An entity responsible for making the resource available
American journal of physiology. Lung cellular and molecular physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2002
2002-04
Subject
The topic of the resource
Adrenergic; Adrenergic beta-Agonists/*pharmacology; Animals; beta/metabolism; Down-Regulation/drug effects; Drug Interactions; Epithelial Cells/metabolism; Extravascular Lung Water/*metabolism; Isoproterenol/*pharmacology; Male; Pulmonary Alveoli/cytology/*metabolism; Pulmonary Circulation/physiology; Pulmonary Edema/metabolism; Rats; Receptors; Respiratory Mucosa/cytology/*metabolism; Sprague-Dawley; Terbutaline/pharmacology
Creator
An entity primarily responsible for making the resource
Morgan Eric E; Hodnichak Cheryl M; Stader Sonya M; Maender Kay C; Boja John W; Folkesson Hans G; Maron Michael B
Description
An account of the resource
We determined if prolonged isoproterenol (Iso) infusion in rats impaired the ability of the beta(2)-adrenergic agonist terbutaline to increase alveolar liquid clearance (ALC). We infused rats with Iso (at rates of 4, 40, or 400 microg.kg(-1).h(-1)) or vehicle (0.001 N HCl) for 48 h using subcutaneously implanted miniosmotic pumps. After this time, the rats were anesthetized, and ALC was determined (by mass-balance after instillation of Ringer lactate containing albumin into the lungs) under baseline conditions and after terbutaline administration. Baseline and terbutaline-stimulated ALC in vehicle-infused rats averaged, respectively, 19.6 +/- 1.2% (SE) and 44.7 +/- 1.5%/h. The ability of terbutaline to increase ALC was eliminated at 400 microg.kg(-1).h(-1)Iso, inhibited by 26% at 40 microg.kg(-1).h(-1) Iso, and was not affected by 4 microg.kg(-1).h(-1) Iso. beta-adrenergic receptor (betaAR) density of freshly isolated alveolar epithelial type II (ATII) cells from Iso-infused rats was reduced by the 40 and 400 microg.kg(-1).h(-1) infusion rates. These data demonstrate that prolonged exposure to beta-agonists can impair the ability of beta(2)-agonists to stimulate ALC and produce ATII cell betaAR downregulation.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajplung.00381.2001" target="_blank" rel="noreferrer noopener">10.1152/ajplung.00381.2001</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).
2002
Adrenergic
Adrenergic beta-Agonists/*pharmacology
American journal of physiology. Lung cellular and molecular physiology
Animals
beta/metabolism
Boja John W
Down-Regulation/drug effects
Drug Interactions
Epithelial Cells/metabolism
Extravascular Lung Water/*metabolism
Folkesson Hans G
Hodnichak Cheryl M
Isoproterenol/*pharmacology
Maender Kay C
Male
Maron Michael B
Morgan Eric E
Pulmonary Alveoli/cytology/*metabolism
Pulmonary Circulation/physiology
Pulmonary Edema/metabolism
Rats
Receptors
Respiratory Mucosa/cytology/*metabolism
Sprague-Dawley
Stader Sonya M
Terbutaline/pharmacology
-
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/ajplung.00339.2002" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajplung.00339.2002</a>
Pages
L578–583
Issue
3
Volume
285
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
Postreceptor defects in alveolar epithelial beta-adrenergic signaling after prolonged isoproterenol infusion.
Publisher
An entity responsible for making the resource available
American journal of physiology. Lung cellular and molecular physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2003
2003-09
Subject
The topic of the resource
8-Bromo Cyclic Adenosine Monophosphate/pharmacology; Adenylyl Cyclases/metabolism; Adrenergic; Adrenergic beta-Agonists/*pharmacology; Animals; beta/*metabolism; Colforsin/pharmacology; Cyclic AMP-Dependent Protein Kinase Type II; Cyclic AMP-Dependent Protein Kinases/metabolism; Cyclic AMP/metabolism; Extravascular Lung Water/metabolism; Isoproterenol/*pharmacology; Male; Pulmonary Alveoli/*drug effects/*metabolism; Pulmonary Edema/metabolism; Rats; Receptors; Respiratory Mucosa/drug effects/metabolism; Signal Transduction/drug effects; Sprague-Dawley
Creator
An entity primarily responsible for making the resource
Morgan Eric E; Stader Sonya M; Hodnichak Cheryl M; Mavrich Kate E; Folkesson Hans G; Maron Michael B
Description
An account of the resource
We previously found that prolonged isoproterenol (Iso) infusion in rats impaired the ability of beta-adrenoceptor (beta-AR) agonists to increase alveolar liquid clearance (ALC). Here, we determined if postreceptor defects in beta-AR signaling contribute to this impairment. Iso was infused using subcutaneous miniosmotic pumps (4, 40, or 400 microg. kg-1. h-1) in rats for 48 h. At this time, forskolin-stimulated ALC was measured by mass balance. Forskolin-stimulated ALC [33.4 +/- 2.1%/h (mean +/- SE) in vehicle-infused rats] was reduced by 25 and 38%, respectively, after the 40 and 400 microg. kg-1. h-1 Iso infusions. The ability of forskolin to increase cAMP was reduced by 70% in alveolar type II (ATII) cells isolated from rats infused with 400 microg. kg-1. h-1 Iso. Additionally, the ability of the stable cAMP analog 8-bromoadenosine-3',5'-cyclic monophosphorothioate, Sp-isomer, to increase ALC (48.7 +/- 3.0% in vehicle-infused rats) was reduced by 25 and 51%, respectively, after the 40 and 400 microg. kg-1. h-1 infusions. Finally, the ability of cAMP to increase protein kinase A activity was eliminated in ATII cells isolated from rats infused with Iso at 400 microg. kg-1. h-1. These data demonstrate that prolonged beta-AR agonist exposure can impair alveolar epithelial beta-AR signaling downstream of the beta-AR.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajplung.00339.2002" target="_blank" rel="noreferrer noopener">10.1152/ajplung.00339.2002</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).
2003
8-Bromo Cyclic Adenosine Monophosphate/pharmacology
Adenylyl Cyclases/metabolism
Adrenergic
Adrenergic beta-Agonists/*pharmacology
American journal of physiology. Lung cellular and molecular physiology
Animals
beta/*metabolism
Colforsin/pharmacology
Cyclic AMP-Dependent Protein Kinase Type II
Cyclic AMP-Dependent Protein Kinases/metabolism
Cyclic AMP/metabolism
Extravascular Lung Water/metabolism
Folkesson Hans G
Hodnichak Cheryl M
Isoproterenol/*pharmacology
Male
Maron Michael B
Mavrich Kate E
Morgan Eric E
Pulmonary Alveoli/*drug effects/*metabolism
Pulmonary Edema/metabolism
Rats
Receptors
Respiratory Mucosa/drug effects/metabolism
Signal Transduction/drug effects
Sprague-Dawley
Stader Sonya M
-
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/ajplung.00134.2004" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajplung.00134.2004</a>
Pages
L349–354
Issue
2
Volume
289
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
PKA delivery to the distal lung air spaces increases alveolar liquid clearance after isoproterenol-induced alveolar epithelial PKA desensitization.
Publisher
An entity responsible for making the resource available
American journal of physiology. Lung cellular and molecular physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2005
2005-08
Subject
The topic of the resource
Adrenergic beta-Agonists/*pharmacology; Animals; Body Fluids/physiology; Cyclic AMP-Dependent Protein Kinases/*administration & dosage; Desensitization; Extravascular Lung Water/metabolism; Immunologic; Isoproterenol/*pharmacology; Male; Pulmonary Alveoli/cytology/*drug effects/*metabolism; Pulmonary Circulation/physiology; Pulmonary Edema/metabolism; Rats; Respiratory Mucosa/cytology/drug effects/metabolism; Sprague-Dawley
Creator
An entity primarily responsible for making the resource
Maron Michael B; Folkesson Hans G; Stader Sonya M; Walro Jon M
Description
An account of the resource
Isoproterenol (Iso) infusion for 48 h in rats decreases the ability of beta-adrenoceptor (beta-AR) agonists to increase alveolar liquid clearance (ALC). An impairment in protein kinase A (PKA) function appears to be critical in producing the desensitized ALC response. To test this hypothesis, we used a novel protein delivery reagent (Chariot, Active Motif) to deliver either the PKA catalytic subunit or the PKA holoenzyme to the distal lung epithelium of Iso-infused rats (400 microg.kg(-1).h(-1), 48 h). After this infusion, ALC was measured by mass balance over 2 h. ALC in Iso-infused rats was 27.9% (SD 5.8) of instilled volume absorbed. Delivery of the catalytic PKA subunit to Iso-infused rats increased ALC to 47.7% (SD 8.9) (P \textless 0.05). ALC in Iso-infused rats delivered the inactive PKA holoenzyme [29.6% (SD 2.5)] was not increased above baseline values. Subsequent holoenzyme activation by intravenous infusion of the stable cAMP analog Sp-8-Bromo-cAMPS increased ALC to 41.7% (SD 8.8) (P \textless 0.05). Immunohistochemical localization of Chariot-delivered PKA revealed staining in the alveolar and distal airway epithelium. These data indicate that protein delivery reagents can be used to rapidly deliver biologically active proteins to the distal lung epithelium and that PKA desensitization may be an important rate-limiting event in the development of Iso-induced desensitization of the alveolar epithelial beta-AR signaling pathway.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajplung.00134.2004" target="_blank" rel="noreferrer noopener">10.1152/ajplung.00134.2004</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).
2005
Adrenergic beta-Agonists/*pharmacology
American journal of physiology. Lung cellular and molecular physiology
Animals
Body Fluids/physiology
Cyclic AMP-Dependent Protein Kinases/*administration & dosage
Desensitization
Extravascular Lung Water/metabolism
Folkesson Hans G
Immunologic
Isoproterenol/*pharmacology
Male
Maron Michael B
Pulmonary Alveoli/cytology/*drug effects/*metabolism
Pulmonary Circulation/physiology
Pulmonary Edema/metabolism
Rats
Respiratory Mucosa/cytology/drug effects/metabolism
Sprague-Dawley
Stader Sonya M
Walro Jon M