Literature DB >> 1951729

Cardiac contraction affects deep myocardial vessels predominantly.

M Goto1, A E Flynn, J W Doucette, C M Jansen, M M Stork, D L Coggins, D D Muehrcke, W K Husseini, J I Hoffman.   

Abstract

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.

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Year:  1991        PMID: 1951729     DOI: 10.1152/ajpheart.1991.261.5.H1417

Source DB:  PubMed          Journal:  Am J Physiol        ISSN: 0002-9513


  18 in total

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Review 2.  Theoretical models for coronary vascular biomechanics: progress & challenges.

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3.  Phasic changes in arterial blood volume is influenced by collateral blood flow: implications for the quantification of coronary stenosis at rest.

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5.  Wall thickness of coronary vessels varies transmurally in the LV but not the RV: implications for local stress distribution.

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6.  Changes in regional myocardial volume during the cardiac cycle: implications for transmural blood flow and cardiac structure.

Authors:  Hiroshi Ashikaga; Benjamin A Coppola; Katrina G Yamazaki; Francisco J Villarreal; Jeffrey H Omens; James W Covell
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7.  Mechanisms of myocardium-coronary vessel interaction.

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8.  Transmural variation and anisotropy of microvascular flow conductivity in the rat myocardium.

Authors:  Amy F Smith; Rebecca J Shipley; Jack Lee; Gregory B Sands; Ian J LeGrice; Nicolas P Smith
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Review 9.  Heterogeneity of myocardial blood flow.

Authors:  J I Hoffman
Journal:  Basic Res Cardiol       Date:  1995 Mar-Apr       Impact factor: 17.165

10.  Cyclic tensile strain triggers a sequence of autocrine and paracrine signaling to regulate angiogenic sprouting in human vascular cells.

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Journal:  Proc Natl Acad Sci U S A       Date:  2009-08-24       Impact factor: 11.205

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