Document Detail


The low oxygen-carrying capacity of Krebs buffer causes a doubling in ventricular wall thickness in the isolated heart.
MedLine Citation:
PMID:  15791291     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The buffer-perfused Langendorff heart is significantly vasodilated compared with the in vivo heart. In this study, we employed ultrasound to determine if this vasodilation translated into changes in left ventricular wall thickness (LVWT), and if this effect persisted when these hearts were switched to the "working" mode. To investigate the effects of perfusion pressure, vascular tone, and oxygen availability on cardiac dimensions, we perfused hearts (from male Wistar rats) in the Langendorff mode at 80, 60, and 40 cm H2O pressure, and infused further groups of hearts with either the vasoconstrictor endothelin-1 (ET-1) or the blood substitute FC-43. Buffer perfusion induced a doubling in diastolic LVWT compared with the same hearts in vivo (5.4 +/- 0.2 mm vs. 2.6 +/- 0.2 mm, p < 0.05) that was not reversed by switching hearts to "working" mode. Perfusion pressures of 60 and 40 cm H2O resulted in an increase in diastolic LVWT. ET-1 infusion caused a dose-dependent decrease in diastolic LVWT (6.6 +/- 0.4 to 4.8 +/- 0.4 mm at a concentration of 10(-9) mol/L, p < 0.05), with a concurrent decrease in coronary flow. FC-43 decreased diastolic LVWT from 6.7 +/- 0.5 to 3.8 +/- 0.7 mm (p < 0.05), with coronary flow falling from 16.1 +/- 0.4 to 8.1 +/- 0.4 mL/min (p < 0.05). We conclude that the increased diastolic LVWT observed in buffer-perfused hearts is due to vasodilation induced by the low oxygen-carrying capacity of buffer compared with blood in vivo, and that the inotropic effect of ET-1 in the Langendorff heart may be the result of a reversal of this wall thickening. The implications of these findings are discussed.
Authors:
R Southworth; S C Blackburn; K A B Davey; G K Sharland; P B Garlick
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Canadian journal of physiology and pharmacology     Volume:  83     ISSN:  0008-4212     ISO Abbreviation:  Can. J. Physiol. Pharmacol.     Publication Date:  2005 Feb 
Date Detail:
Created Date:  2005-03-25     Completed Date:  2005-07-12     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0372712     Medline TA:  Can J Physiol Pharmacol     Country:  Canada    
Other Details:
Languages:  eng     Pagination:  174-82     Citation Subset:  IM    
Affiliation:
NMR Laboratory, Division of Imaging Sciences, Guy's, King's and St Thomas' School of Medicine, Guy's Hospital, St. Thomas, London, UK. richard.southworth@kcl.ac.uk
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Substitutes / pharmacology
Buffers
Coronary Circulation
Echocardiography*
Endothelin-1 / pharmacology
Fluorocarbons / pharmacology
Heart / anatomy & histology*,  physiology*
Heart Ventricles / anatomy & histology
Isotonic Solutions*
Male
Models, Animal*
Myocardial Reperfusion
Oxygen / metabolism*
Perfusion
Rats
Vasodilation
Ventricular Function
Chemical
Reg. No./Substance:
0/Blood Substitutes; 0/Buffers; 0/Endothelin-1; 0/Fluorocarbons; 0/Isotonic Solutions; 0/Krebs-Ringer solution; 311-89-7/perfluorotributylamine; 7782-44-7/Oxygen

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


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