Document Detail


O2 consumption during exercise in dogs--roles of splenic contraction and alpha-adrenergic vasoconstriction.
MedLine Citation:
PMID:  2875657     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To examine the influence of alpha-adrenergic vasoconstriction on the aerobic capacity of dogs, we calculated O2 consumption (VO2) by the Fick method during submaximal and maximal exertion before and during alpha-adrenergic blockade with phentolamine. Regional blood flow was measured with radioactive microspheres. alpha-Adrenergic receptor blockade reduced VO2 by 12.9% during submaximal and 17.9% during maximal exercise. Arterial and venous lactic acid approximately doubled during both levels of stress in the presence of alpha-adrenergic receptor blockade. Calculated VO2 decreased because arteriovenous O2 (A-V)O2 extraction was reduced by 11.6% during submaximal exercise. During maximal exercise a 16.7% decrease in (A-V)O2 extraction and a 5.7% decrease in cardiac output contributed to the decrease in maximal VO2. During both levels of stress, (A-V)O2 extraction was reduced because arterial O2 content was decreased. Since circulating hematocrits during exercise were reduced by alpha-adrenergic receptor blockade (43-38%), we postulate that splenic contraction likely was inhibited. Additionally, distribution of blood flow to skeletal muscle and visceral organs was unaltered by alpha-blockade. To examine the importance of splenic contraction during maximal exercise, we examined hemodynamic and metabolic responses before and after splenectomy. Compared with the spleen-intact condition, splenectomized dogs demonstrated a 12.6% reduction in VO2 as a result of 7.7 and 5.5% reductions in (A-V)O2 extraction and cardiac output, respectively. (A-V)O2 extraction was reduced because arterial O2 content and circulating hematocrit during exercise were decreased. Therefore, in the exercising dog, alpha-adrenergic receptor blockade reduces O2 consumption and causes a shift to anaerobic metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)
Authors:
J C Longhurst; T I Musch; G A Ordway
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  251     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1986 Sep 
Date Detail:
Created Date:  1986-10-21     Completed Date:  1986-10-21     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H502-9     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Adrenergic alpha-Antagonists / pharmacology*
Animals
Dogs
Hemodynamics / drug effects
Lactates / blood
Lactic Acid
Oxygen Consumption*
Phentolamine / pharmacology*
Physical Exertion*
Regional Blood Flow / drug effects
Rest
Spleen / physiology*
Splenectomy
Vasoconstriction*
Grant Support
ID/Acronym/Agency:
HL-06296/HL/NHLBI NIH HHS; HL-07360/HL/NHLBI NIH HHS; HL-30222/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Adrenergic alpha-Antagonists; 0/Lactates; 50-21-5/Lactic Acid; 50-60-2/Phentolamine

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


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