Document Detail


Perfusion-induced changes in cardiac contractility and oxygen consumption are not endothelium-dependent.
MedLine Citation:
PMID:  9093529     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Are substances released from rat coronary endothelial cells responsible for the increase in contractility and oxygen consumption (Gregg phenomenon) seen with an increase in cardiac perfusion? METHODS: In an isovolumically contracting, Langendorff, crystalloid perfused rat heart (n = 6) at 27 degrees C, coronary flow was changed (from 4.4 to 15.4 ml.min-1.gww(-1)) before and after the endothelium was made dysfunctional by Triton X-100. Vascular endothelium and smooth muscle function were tested with bradykinin (BK, 1 microM, an endothelium-dependent dilator) and papaverine (PAP, 1 microM, an endothelium-independent dilator) in a preconstricted vascular bed (vasopressin, VP, 3 nM). RESULTS: Before Triton X-100, coronary resistance (at constant flow) decreased significantly in response to BK and to PAP. After Triton X-100 treatment the dilatory response to BK was abolished while the PAP response was still present, suggesting endothelial dysfunction with intact smooth muscle function. Due to Triton X-100 treatment, coronary resistance increased significantly. Therefore coronary flow changes were also applied during a similar increase in coronary resistance induced by VP infusion (3 nM) before Triton X-100 treatment. During control, developed left ventricular pressure (dev Plv) increased with 68 +/- 21% and oxygen consumption (VO2) increased with 122 +/- 25% in response to the maximal increase in coronary flow. During increased coronary resistance with and without functional endothelium, dev Plv increased by 57 +/- 16 and 64 +/- 22%, respectively, and VO2 increased by 126 +/- 21 and 103 +/- 20%, respectively, in response to the maximal increase in flow. These changes were not significantly different from control. CONCLUSION: The results suggest that the arterial endothelium is not involved in the Gregg phenomenon.
Authors:
M A Dijkman; J W Heslinga; P Sipkema; N Westerhof
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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:  Cardiovascular research     Volume:  33     ISSN:  0008-6363     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  1997 Mar 
Date Detail:
Created Date:  1997-06-09     Completed Date:  1997-06-09     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  593-600     Citation Subset:  IM    
Affiliation:
Laboratory for Physiology, ICaR-VU, Free University of Amsterdam, Netherlands. m.dijkman.physiol@med.vu.nl
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MeSH Terms
Descriptor/Qualifier:
Animals
Bradykinin / pharmacology
Endothelium, Vascular / drug effects,  physiology*
Male
Muscle, Smooth, Vascular / drug effects,  physiology
Myocardial Contraction*
Octoxynol / pharmacology
Oxygen Consumption*
Papaverine / pharmacology
Perfusion*
Rats
Rats, Wistar
Regional Blood Flow / drug effects
Vascular Resistance / drug effects
Vasodilator Agents / pharmacology
Vasopressins / pharmacology
Grant Support
ID/Acronym/Agency:
HL-44399-01/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Vasodilator Agents; 11000-17-2/Vasopressins; 58-74-2/Papaverine; 58-82-2/Bradykinin; 9002-93-1/Octoxynol

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


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