A structure-function analysis of the left ventricle

dc.contributor.authorSnelling, Edward P.
dc.contributor.authorSeymour, Roger S.
dc.contributor.authorGreen, J.E.F.
dc.contributor.authorMeyer, Leith Carl Rodney
dc.contributor.authorFuller, Andrea
dc.contributor.authorHaw, Anna
dc.contributor.authorMitchell, Duncan
dc.contributor.authorFarrell, Anthony P.
dc.contributor.authorCostello, Mary-Ann
dc.contributor.authorIzwan, Adian
dc.contributor.authorBadenhorst, Margaret
dc.contributor.authorMaloney, Shane K.
dc.date.accessioned2017-03-01T10:06:44Z
dc.date.issued2016-10
dc.description.abstractThis study presents a structure-function analysis of the mammalian left ventricle and examines the performance of the cardiac capillary network, mitochondria, and myofibrils at rest and during simulated heavy exercise. Left ventricular external mechanical work rate was calculated from cardiac output and systemic mean arterial blood pressure in resting sheep (Ovis aries; n = 4) and goats (Capra hircus; n = 4) under mild sedation, followed by perfusion-fixation of the left ventricle and quantification of the cardiac capillary-tissue geometry and cardiomyocyte ultrastructure. The investigation was then extended to heavy exercise by increasing cardiac work according to published hemodynamics of sheep and goats performing sustained treadmill exercise. Left ventricular work rate averaged 0.017 W/cm3 of tissue at rest and was estimated to increase to ∼0.060 W/cm3 during heavy exercise. According to an oxygen transport model we applied to the left ventricular tissue, we predicted that oxygen consumption increases from 195 nmol O2·s-1·cm-3 of tissue at rest to ∼600 nmol O2·s-1·cm-3 during heavy exercise, which is within 90% of the oxygen demand rate and consistent with work remaining predominantly aerobic. Mitochondria represent 21-22% of cardiomyocyte volume and consume oxygen at a rate of 1,150 nmol O2·s-1·cm-3 of mitochondria at rest and ∼3,600 nmol O2·s-1·cm-3 during heavy exercise, which is within 80% of maximum in vitro rates and consistent with mitochondria operating near their functional limits. Myofibrils represent 65-66% of cardiomyocyte volume, and according to a Laplacian model of the left ventricular chamber, generate peak fiber tensions in the range of 50 to 70 kPa at rest and during heavy exercise, which is less than maximum tension of isolated cardiac tissue (120-140 kPa) and is explained by an apparent reserve capacity for tension development built into the left ventricle.en_ZA
dc.description.departmentParaclinical Sciencesen_ZA
dc.description.embargo2017-10-31
dc.description.librarianhb2017en_ZA
dc.description.sponsorshipThis research was supported by an Australian Research Council Discovery Project Award to R. S. Seymour, S. K. Maloney, and A. P. Farrell (DP-120102081). E. P. Snelling holds a South African Claude Leon Foundation Postdoctoral Fellowship. J. E. F. Green is supported by an Australian Research Council Discovery Early Career Researcher Award (DE- 130100031). A. P. Farrell holds a Canada Research Chair and is supported by a Discovery Grant from the Natural Sciences and Engineering Research Council of Canada.en_ZA
dc.description.urihttp://jap.physiology.orgen_ZA
dc.identifier.citationSnelling, EP, Seymour, RS, Green, JEF, Meyer, LCR, Fuller, A, Haw, A, Mitchell, D, Farrell, AP, Costello, M-A, Izwan, A, Badenhorst, M & Maloney, SK 2016, 'A structure-function analysis of the left ventricle', Journal of Applied Physiology, vol. 121, no. 4, pp. 900-909.en_ZA
dc.identifier.issn8750-7587 (print)
dc.identifier.issn1522-1601 (online)
dc.identifier.other10.1152/japplphysiol.00435.2016
dc.identifier.urihttp://hdl.handle.net/2263/59211
dc.language.isoenen_ZA
dc.publisherAmerican Physiological Societyen_ZA
dc.rights© 2016 the American Physiological Societyen_ZA
dc.subjectCapillaryen_ZA
dc.subjectHearten_ZA
dc.subjectMitochondriaen_ZA
dc.subjectWorken_ZA
dc.subjectMammalian left ventricleen_ZA
dc.subjectCardiac capillary networken_ZA
dc.subjectMyofibrilsen_ZA
dc.subjectResten_ZA
dc.subjectSimulated heavy exerciseen_ZA
dc.titleA structure-function analysis of the left ventricleen_ZA
dc.typePostprint Articleen_ZA

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