Document Detail


Cardiac contraction affects deep myocardial vessels predominantly.
MedLine Citation:
PMID:  1951729     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To evaluate the roles of intramyocardial forces and systolic ventricular pressure in myocardial flow in the different layers separately, we measured myocardial flow in rabbit hearts during stable systolic contracture with left ventricular pressures of 60 (n = 5) and 0 mmHg (n = 5) and during stable diastolic arrest (n = 5). We also measured the number and size of the intramyocardial vessels after perfusion fixation (systolic arrest, n = 5; diastolic arrest, n = 5). In 25 rabbits, hearts were excised and perfused from the aortic root. Systolic arrest was achieved by perfusion of a low-Ca2+ Tyrode solution containing 2.0 mM Ba2+. Diastolic arrest was achieved by intraventricular injection of 700-1,000 mg pentobarbital sodium and was maintained by perfusion with St. Thomas cardioplegic solution. At perfusion pressure of 100 mmHg, subendocardial flow was lower than subepicardial flow during systolic arrest regardless of left ventricular pressure, whereas during diastolic arrest, subendocardial flow was higher than subepicardial flow. Subendocardial-to-subepicardial flow ratios for a physiological range of perfusion pressures were lower during systolic arrest with low rather than with high left ventricular pressure. Small arteriolar and capillary densities showed no difference between subendocardium and subepicardium. During systolic arrest, diameters of subendocardial terminal arterioles (4.6 +/- 1.3 microns) and capillaries (4.0 +/- 1.3 microns) were smaller than those in the subepicardium (8.8 +/- 1.7 and 7.1 +/- 1.6 microns, respectively; P less than 0.0001), whereas during diastolic arrest, diameters of subendocardial terminal arterioles (10.1 +/- 2.0 microns) and capillaries (7.6 +/- 1.8 microns) were slightly larger than those in the subepicardium (9.5 +/- 1.5 and 6.7 +/- 1.0 microns, respectively; P less than 0.01). We conclude that cardiac contraction predominantly affects subendocardial vessels and impedes subendocardial flow more than subepicardial flow regardless of left ventricular pressure.
Authors:
M Goto; A E Flynn; J W Doucette; C M Jansen; M M Stork; D L Coggins; D D Muehrcke; W K Husseini; J I Hoffman
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Publication Detail:
Type:  In Vitro; 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:  261     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1991 Nov 
Date Detail:
Created Date:  1991-12-23     Completed Date:  1991-12-23     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H1417-29     Citation Subset:  IM    
Affiliation:
Cardiovascular Research Institute, University of California, San Francisco 94143.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arterioles / physiology
Barium / pharmacology
Blood Pressure*
Calcium / pharmacology
Coronary Circulation
Coronary Vessels / drug effects,  physiology*
Endocardium / cytology,  physiology
Muscle, Smooth, Vascular / drug effects,  physiology*
Myocardial Contraction*
Myocardium / cytology
Rabbits
Systole
Grant Support
ID/Acronym/Agency:
HL-07192/HL/NHLBI NIH HHS; HL-25847/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
7440-39-3/Barium; 7440-70-2/Calcium

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


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