Document Detail


The role of adrenergic stimulation in maintaining maximum cardiac performance in rainbow trout (Oncorhynchus mykiss) during hypoxia, hyperkalemia and acidosis at 10 degrees C.
MedLine Citation:
PMID:  16788027     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
As rainbow trout approach exhaustion during prolonged exercise, they maintain maximum cardiac output despite the fact their venous blood, which bathes the heart, becomes hypoxic, acidotic and hyperkalemic. Because these factors are individually recognized to have detrimental inotropic and chronotropic effects on cardiac performance, we hypothesized that adrenergic stimulation is critical in maintaining maximum cardiac performance under these collectively adverse conditions in vivo. To test this hypothesis, maximum cardiac performance in the presence and absence of maximal adrenergic stimulation was assessed with in situ rainbow trout hearts using relevant hyperkalemic (5.0 mmol l(-1) K+), acidotic (pH 7.5) and hypoxic challenges. With tonic adrenergic stimulation (5.0 nmol l(-1) adrenaline), hearts produced only 44.8+/-14.6% of their normal maximum cardiac output when exposed under normoxic conditions (20 kPa) to the hyperkalemic, acidotic perfusate, indicating that in vivo there was no refuge from cardiac impairment even if venous blood was fully oxygenated. By contrast, maximum adrenergic stimulation (500 nmol l(-1) adrenaline), fully protected maximum cardiac performance under hyperkalemic and acidotic conditions over a wide range of oxygen availability, from normoxia to 2.0 kPa, a venous oxygen tension close to routine values in vivo. Extending the level of hypoxia to 1.3 kPa resulted in a 43.6+/-2.8% decrease in maximum cardiac output, with hearts failing when tested at 1.0 kPa. Our results suggest that adrenergic stimulation of the trout heart is critical in maintaining maximum performance during prolonged swimming tests, and probably during all forms of exhaustive activity and recovery, when venous blood is hyperkalemic, acidotic and hypoxic.
Authors:
Linda M Hanson; Shannon Obradovich; Janet Mouniargi; Anthony P Farrell
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of experimental biology     Volume:  209     ISSN:  0022-0949     ISO Abbreviation:  J. Exp. Biol.     Publication Date:  2006 Jul 
Date Detail:
Created Date:  2006-06-21     Completed Date:  2006-09-01     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0243705     Medline TA:  J Exp Biol     Country:  England    
Other Details:
Languages:  eng     Pagination:  2442-51     Citation Subset:  IM    
Affiliation:
Department of Zoology, University of British Columbia, 6270 University Blvd., Vancouver, BC V6T 1Z4, Canada. hanson@zoology.ubc.ca
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MeSH Terms
Descriptor/Qualifier:
Acidosis / physiopathology,  veterinary*
Adrenergic Agonists / pharmacology
Animals
Anoxia / physiopathology,  veterinary*
Cardiac Output* / drug effects
Catecholamines / metabolism
Epinephrine / pharmacology*
Female
Fish Diseases / blood,  physiopathology*
Heart / drug effects
Hydrogen-Ion Concentration
Hyperkalemia / physiopathology,  veterinary*
Male
Oncorhynchus mykiss / blood,  physiology*
Oxygen / blood
Perfusion
Physical Exertion / physiology
Potassium / blood
Temperature
Chemical
Reg. No./Substance:
0/Adrenergic Agonists; 0/Catecholamines; 51-43-4/Epinephrine; 7440-09-7/Potassium; 7782-44-7/Oxygen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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