| Perfusion-induced changes in cardiac O2 consumption and contractility are based on different mechanisms. | |
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MedLine Citation:
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PMID: 8853332 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Increased cardiac perfusion results in increased oxygen consumption (VO2) and increased contractility (Gregg phenomenon) in the isolated heart. We investigated whether these two aspects of the Gregg phenomenon are related to coronary flow or arterial pressure. Coronary flow and, thus, arterial pressure were changed in the reference state and during vasoconstriction (3 nM vasopressin) in the Langendorff-perfused rat heart contracting isovolumically (ventricular balloon) at 27 degrees C (n = 5). All hearts showed an increase in developed isovolumic left ventricular pressure (measure of contractility) and in VO2 with increased perfusion. Developed left ventricular pressure depended primarily on arterial pressure, so its relationship with coronary flow was shifted by vasoconstriction. Conversely, VO2 primarily depended on coronary flow, so its relationship with arterial pressure was shifted with vasoconstriction. By use of vasoconstriction (decreased vascular radii), the effects of arterial pressure and wall shear stress (proportional to arterial pressure x radius) should be separable, but the results did not reach significance. Thus contractility is related to arterial pressure or shear stress, whereas VO2 is related to coronary flow. We conclude that the two aspects of the Gregg phenomenon are based on different mechanisms. |
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Authors:
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M A Dijkman; J W Heslinga; P Sipkema; N Westerhof |
Publication Detail:
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Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: The American journal of physiology Volume: 271 ISSN: 0002-9513 ISO Abbreviation: Am. J. Physiol. Publication Date: 1996 Sep |
Date Detail:
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Created Date: 1996-12-05 Completed Date: 1996-12-05 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0370511 Medline TA: Am J Physiol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: H984-9 Citation Subset: IM |
Affiliation:
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Laboratory for Physiology, Vrije Universiteit, Amsterdam, The Netherlands. m.dijkman.physiol@med.vu.nl |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Biomechanics Coronary Circulation Male Myocardial Contraction* Myocardium / metabolism* Oxygen Consumption* Perfusion* Pressure Rats Rats, Wistar Vascular Resistance Vasoconstrictor Agents / pharmacology Vasopressins / pharmacology Ventricular Function, Left |
| Grant Support | |
ID/Acronym/Agency:
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HL-44399-01/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Vasoconstrictor Agents; 11000-17-2/Vasopressins |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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