Document Detail


Altered muscle metaboreflex control of coronary blood flow and ventricular function in heart failure.
MedLine Citation:
PMID:  15528224     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We investigated the effect of muscle metaboreflex activation on left circumflex coronary blood flow (CBF), coronary vascular conductance (CVC), and regional left ventricular performance in conscious, chronically instrumented dogs during treadmill exercise before and after the induction of heart failure (HF). In control experiments, muscle metaboreflex activation during mild exercise elicited significant reflex increases in mean arterial pressure, heart rate, and cardiac output. CBF increased significantly, whereas no significant change in CVC occurred. There was no significant change in the minimal rate of myocardial shortening (-dl/dt(min)) with muscle metaboreflex activation during mild exercise (15.5 +/- 1.3 to 16.8 +/- 2.4 mm/s, P > 0.05); however, the maximal rate of myocardial relaxation (+dl/dt(max)) increased (from 26.3 +/- 4.0 to 33.7 +/- 5.7 mm/s, P < 0.05). Similar hemodynamic responses were observed with metaboreflex activation during moderate exercise, except there were significant changes in both -dl/dt(min) and dl/dt(max). In contrast, during mild exercise with metaboreflex activation during HF, no significant increase in cardiac output occurred, despite a significant increase in heart rate, inasmuch as a significant decrease in stroke volume occurred as well. The increases in mean arterial pressure and CBF were attenuated, and a significant reduction in CVC was observed (0.74 +/- 0.14 vs. 0.62 +/- 0.12 ml x min(-1) x mmHg(-1); P < 0.05). Similar results were observed during moderate exercise in HF. Muscle metaboreflex activation did not elicit significant changes in either -dl/dt(min) or +dl/dt(max) during mild exercise in HF. We conclude that during HF the elevated muscle metaboreflex-induced increases in sympathetic tone to the heart functionally vasoconstrict the coronary vasculature, which may limit increases in myocardial performance.
Authors:
Eric J Ansorge; Robert A Augustyniak; Mariana L Perinot; Robert L Hammond; Jong-Kyung Kim; Javier A Sala-Mercado; Jaime Rodriguez; Noreen F Rossi; Donal S O'Leary
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.     Date:  2004-11-04
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  288     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2005 Mar 
Date Detail:
Created Date:  2005-02-11     Completed Date:  2005-03-22     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1381-8     Citation Subset:  IM    
Affiliation:
Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Pressure / physiology
Coronary Circulation / physiology*
Dogs
Female
Heart Failure / physiopathology*
Ischemia / physiopathology
Male
Muscle Contraction / physiology
Muscle, Skeletal / blood supply,  physiology
Myocardial Contraction / physiology
Reflex / physiology*
Vasoconstriction / physiology
Ventricular Function, Left / physiology*
Grant Support
ID/Acronym/Agency:
HL-55473/HL/NHLBI NIH HHS

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


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