DOCSLIB.ORG

Cardiac Pump Function

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Cardiac Pump Function Left Ventricular Pump Function Michael R. Pinsky, MD, Dr hc Department of Critical Care Medicine University of Pittsburgh Left Ventricular Pump Function • Maintain a constant and high organ input pressure • Eject Stroke Volume into a low compliance high resistance arterial circuit • Transfer all blood received with a minimal back pressure • Match cardiac output to venous return on a beat-to-beat basis Bedside Assessment of Ventricular Pump Function Assessing Left Ventricular Performance Commonly Used Measures of Cardiovascular Function: Heart Rate Blood Pressure Cardiac Output Stroke Volume LV ejection fraction Frank-Starling Relationship • Frank: Force of fiber contraction proportional to length prior to excitation • Frank. Z Biol 32:370-437, 1895 • Starling: Fiber length proportional to end-diastolic volume • Patterson & Starling. J Physiol (Lon) 48:465-513,1914 • Frank-Starling: Systolic function proportional to end- diastolic volume Primacy of Preload in Determining Systolic Performance Otto Frank Isometric contractions of a frog ventricle at increasing filling pressures Frank O, Z Biol 1895; 32:370 Ernest Starling Stroke volume increases with end-diastolic volume End-diastolic Volume Increased End-diastolic Volume Patterson & Starling. J Physiol 48:357-87, 1914 Starling versus Anrep Heterometric v. Homeometric autoregulation of the heart Increased Preload Starling EDV Preload Afterload Heart Rate Anrep Contractility ESV Increased Contractility Sudden increase and decrease in venous return Rosenblueth et al. Arch Int Physiol 67: 358, 1959 Frank-Starling Relationship LV Ejection Hyper-effective Phase Indies: Ejection Fraction Stroke Volume Stroke Work Hypo-effective LV dP/dt Vcf Preload (end-diastolic volume) Sarnoff & Berglund. Circulation 9:706-18, 1954 Frank-Starling Relationship Is heart A “better” than heart B? A B Stroke Volume Stroke Preload (end-diastolic volume) Arterial pressure increases with end-diastolic volume Patterson & Starling. J Physiol (London) 48:357-79, 1914 Inherent Weaknesses with Using Stroke Volume as a Measure of Cardiac Contractility • Stroke volume is altered by Ejection Pressure • Increasing arterial pressure decreases stroke volume • Decreasing arterial pressure increases stroke volume • Stroke volume is altered by Heart Rate • Tachycardia decreases stroke volume (less filling time) • Bradycardia increases stroke volume (more filling time) • Chronotropy For a constant end-diastolic volume: • Increasing heart rate increases stroke volume • Decreasing heart rate decreases stroke volume Ventricular Function Muscular Work LV ejection: volume under pressure Stroke Work = Developed Pressure x Stroke Volume Minute Work = Stroke Work x Heart Rate Frank-Starling Relationship A B Stroke Work Stroke Preload (end-diastolic volume) Wiggers CJ, Circulation 5:321-48, 1952 LV Pressure-Volume Loop End-systole Ejection (stroke volume) Aortic Valve Opening LV Isometric Isometric Pressure Relaxation Contraction (mm Hg) Mitral Valve End-diastole Opening Diastolic filling LV Volume (mL) Patterson & Starling. J Physiol 48:465-513,1914 Determinants of LV Function Preload End-diastolic volume Afterload Systolic wall stress Contractility Intrinsic myocardial performance Heart Rate Chronotropy Patterson & Starling. J Physiol 48:357-79, 1914 Frank-Starling Relation Primacy of PRELOAD in determining ventricular systolic performance Preload is determined by systemic venous return Preload is the primary determinant of cardiac output LV Preload equals LV end-diastolic volume Patterson & Starling. J Physiol 48:465-513,1914 LV Pressure-Volume Relations Diastolic Filling LV Diastolic Compliance = P/ V Pressure End-diastolic P/V Relation Increased (mm Hg) Stiffness P V LV Volume (mL) Pinsky Intensive Care Med 29:175-8, 2003 Isometric LV Ejection End-Systolic Developed Pressure LV Pressure (mm Hg) A B C LV Volume (mL) Suga et al. Circ Res 32:314-322, 1973 Isometric LV Ejection End-Systolic Pressure- Volume Relationship LV Pressure (mm Hg) A B C LV Volume (mL) Suga et al. Circ Res 32:314-322, 1973 LV Ejection from a Common EDV End-Systolic Pressure- C Volume Relationship LV B Pressure (mm Hg) A LV Volume (mL) Suga et al. Circ Res 32:314-322, 1973 Isometric LV Contraction or Ejection Suga et al. Circ Res 32:314-322, 1973 The Slope of the End-Systolic Pressure-Volume Relationship (ESPVR) is proportional to contractility • The ESPVR is relatively insensitive to loading conditions • Independent of prior end-diastolic volume • Independent of subsequent ejection pressure • Increasing ESPVR is increased contractility • Decreasing ESPVR is decreased contractility Suga et al. Circ Res 32:314-322, 1973 LV Pressure-Volume loops at variable venous return before and after epinephrine Suga et al. Circ Res 32:314-322, 1973 Effect of Changes in Contractility on the End-Systolic Pressure-Volume Relationship Decreased Contractility Increased Contractility Augmented Normal LV Pressure Failure (mm Hg) LV Volume (mL) Suga et al. Circ Res 32:314-322, 1973 The Functional Basis for Left Ventricular Contraction and ESPVR LV pressure-volume histories at differing preloads and afterloads LV Pressure LV Volume On the Nature of LV Contraction Sequential P/V Loops during IVC Occlusion IVC LV Occlusion Pressure LV Volume End-Systolic Pressure Volume Relationship (generated by IVC occlusion) Ees IVC Occlusion Ejection Diastolic compliance On the Nature of LV Contraction Iso-chronic lines at 20 ms intervals 200 140 100 80 ESPVR 60 LV 40 Pressure 20 LV Volume Suga et al. Circ Res 32:314-322, 1973 On the Nature of LV Contraction Iso-chronic lines at 20 ms intervals Baseline Increased Inotrophy (Epinephrine infusion) 100 80 60 200 140100 40 80 60 P P 40 20 20 Volume Volume Suga et al. Circ Res 32:314-322, 1973 Time-Varying Elastance (Et) Instantaneous LV Pressure/Volume Relations Increased Contractility (Epinephrine) (mmHg/ml) Normal LV P/V LV Contractility (Baseline) Time (sec) Suga et al. Circ Res 32:314-322, 1973 On the Nature of LV Contraction Time-Varying Elastance (Et) • Shortening proceeds uniformly from start to end of systole independent of either pressure or volume • Time post-initiation of systole defines a pressure- volume domain which is independent of history • Increased contractility increases Et throughout systole • Increased contractility decreases the time to end- systole Suga et al. Circ Res 32:314-322, 1973 Time-varying Elastance (Et) • All events characterized by the Frank- Starling Relationship can be explained completely by the concept of Et • Preload “appears” to be determining systolic function because Et has an increasing slope over time Suga et al. Circ Res 32:314-22, 1973 On the Nature of LV Contraction Time varying Elastance and the Frank-Starling Relationship 200 140 100 80 60 40 20 Pressure Ejection Indices Volume A B A B EDV Stroke volume, ejection fraction, dP/dt All increase with increasing EDV Cardiac Contractility Contractility proportional to the rate and amount of Ca+2 flux into the sarcolema of the contracting myocytes All known positive inotropes increase Ca+2 flux All known negative inotropes decrease Ca+2 flux Cardiac Contractility Since Ca+2 is essential for contraction, is Ca+2 a positive inotrope? Yes and No Where the Ca+2 goes is as important as how much Ca+ there is available Cardiac Contractility Changes in contractility reflect LONG TERM adaptations to external stress (Anrep effect) Cardiac Contractility • Autonomic Tone Exercise, Stress; Diabetes • Coronary Blood Flow • Kojima et al. Am J Physiol 264:H183-9, 1993 • Serum ionic Ca+2 • Marquez et al. Anesthesiology 65:457-61, 1986 • Local Catecholamine Stores Chronic stress • Catecholamine Receptors Sepsis • Extrinsic Catecholamine Supplements Assessing LV Contractility at the Bedside • LV dP/dt at 20 or 30 mmHg • Prior to aortic value opening • Preload, heart rate and afterload dependent • Can radial arterial dP/dtmax reflect LV contractility? • Reflected pressure waves distort arterial pressure • Compliance and inertance alter peripheral pressure • Compared LV dP/dtmax with femoral and radial arterial dP/dtmax as contractility, preload and afterload systematically altered in pigs Monge Garcia et al. Crit Care 22 325, 2018 Changes in Radial Artery dP/dtmax Tracks Changes in Ees DVasomotor D Volume D Contractility Monge Garcia et al. Crit Care 22 325, 2018 Determinants of Afterload LaPlace’s Law LV Wall Stress Tension = Px r r P Maximal tension at maximal P x r which usually occurs at the opening of the aortic value: EDV, diastolic pressure Chronotropy Increases in heart rate increase Ca+2 influx into the sarcolema of the myocytes increasing force of contraction Bers. Nature 415:198-205, 1998 Optimal heart rate? > 60 but < 120 Effect of Changes in Heart Rate on Contractility Force-Frequency Relationship Liu et al. Circulation 88:1893-906, 1993 Effect of Changes in Heart Rate on Contractility Force-Frequency Relationship 70 min-1 100 min-1 70 min-1 100 min-1 Chronotropy Diastolic Dysfunction 130 min-1 160 min-1 120 min-1 150 min-1 Liu et al. Circulation 88:1893-906, 1993 What is heart failure? Heart failure as a state in which the heart is unable to meet the demands for blood flow without excessive use of the Frank-Starling mechanism, that is the increase in stroke volume associated with increased preload. Sagawa, Maughan, Suga, Sunagawa. Cardiac Contraction and the Pressure- Volume Relationship. Oxford University Press, 1988 Heart failure Type 1: increased loading Type 2: altered inotropic state Type 3: altered lusitropic state Type I: Heart failure because of
Load more

Recommended publications
  • S41467-021-21178-4.Pdf
    ARTICLE https://doi.org/10.1038/s41467-021-21178-4 OPEN The mechanosensitive Piezo1 channel mediates heart mechano-chemo transduction Fan Jiang1, Kunlun Yin2, Kun Wu 1,5, Mingmin Zhang1, Shiqiang Wang3, Heping Cheng 4, Zhou Zhou2 & ✉ Bailong Xiao 1 The beating heart possesses the intrinsic ability to adapt cardiac output to changes in mechanical load. The century-old Frank–Starling law and Anrep effect have documented that 1234567890():,; stretching the heart during diastolic filling increases its contractile force. However, the molecular mechanotransduction mechanism and its impact on cardiac health and disease remain elusive. Here we show that the mechanically activated Piezo1 channel converts mechanical stretch of cardiomyocytes into Ca2+ and reactive oxygen species (ROS) sig- naling, which critically determines the mechanical activity of the heart. Either cardiac-specific knockout or overexpression of Piezo1 in mice results in defective Ca2+ and ROS signaling and the development of cardiomyopathy, demonstrating a homeostatic role of Piezo1. Piezo1 is pathologically upregulated in both mouse and human diseased hearts via an autonomic response of cardiomyocytes. Thus, Piezo1 serves as a key cardiac mechanotransducer for initiating mechano-chemo transduction and consequently maintaining normal heart function, and might represent a novel therapeutic target for treating human heart diseases. 1 State Key Laboratory of Membrane Biology, Tsinghua-Peking Center for Life Sciences, Beijing Advanced Innovation Center for Structural Biology, IDG/ McGovern Institute for Brain Research, School of Pharmaceutical Sciences, Tsinghua University, Beijing 100084, China. 2 State Key Laboratory of Cardiovascular Disease, Beijing Key Laboratory for Molecular Diagnostics of Cardiovascular Diseases, Center of Laboratory Medicine, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China.
    [Show full text]
  • Mechanical Model of the Left Ventricle of the Heart Approximated by Axisymmetric Geometry
    pp. 1–14 (2017) Mechanical model of the left ventricle of the heart approximated by axisymmetric geometry F. A. Syomin∗ and A. K. Tsaturyan∗ Abstract — An axisymmetric model is suggested to simulate mechanical performance of the left vent- ricle of the heart. Cardiac muscle is treated as incompressible anisotropic material with active tension directed along muscle fibres. This tension depends on kinetic variables that characterize interaction of contractile proteins and regulation of muscle contraction by calcium ions. For numerical simulation of heartbeats the finite element method was implemented. The model reproduces well changes in vent- ricle geometry between systole and diastole, ejection fraction, pulse wave of ventricular and arterial pressure typical for normal human heart. The model also reproduces well the dependence of the stroke volume on end-diastolic and arterial pressures (the Frank–Starling law of the heart and Anrep effect). The results demonstrate that our model of cardiac muscle can be successfully applied to multiscale 3D simulation of the heart. Keywords: Heart, cardiac muscle, muscle contraction, mathematical model, finite elements. MSC 2010: 74L15, 92C10, 92C30, 74S05 Computer modelling of the heart mechanics is a fast developing field of computa- tional physiology. During the last two decades a number of electromechanical mod- els of the whole heart or its left ventricle has been developed [26]. Such multiscale models usually combine several models that describe electrical and chemical pro- cesses at the level of a single cell with mechanical properties of cardiac muscle tissue. Generally, a model of the heart consists of a model of ionic currents in the cardiomyocytes, model of myocardial mechanics, model of blood circulation (hae- modynamics model), and a geometrical approximation of the heart.
    [Show full text]
  • Heart Failure Therapy: Potential Lessons Heart: First Published As 10.1136/Heartjnl-2015-309110 on 23 December 2016
    Heart Online First, published on December 23, 2016 as 10.1136/heartjnl-2015-309110 Review ‘End-stage’ heart failure therapy: potential lessons Heart: first published as 10.1136/heartjnl-2015-309110 on 23 December 2016. Downloaded from from congenital heart disease: from pulmonary artery banding and interatrial communication to parallel circulation Dietmar Schranz, Hakan Akintuerk, Norbert F Voelkel ▸ Additional material is ABSTRACT reflected by the calculated transpulmonary gradient published online only. To view The final therapy of ‘end-stage heart failure’ is (TPG=mean PAP−LAP) and in particular the dia- please visit the journal online (http://dx.doi.org/10.1136/ orthotopic heart, lung or heart-lung transplantation. stolic PAP to LAP difference, the so-called diastolic heartjnl-2015-309110). However, these options are not available for many pressure gradient (DPG=diastolic PAP−LAP). Both patients worldwide. Therefore, novel therapeutical parameters become even more important in the Pediatric Heart Center, Justus Liebig University Giessen, strategies are needed. Based on pathophysiological setting of heart failure: pulmonary hypertension Virginia Commonwealth insights regarding (1) the long-term impact of an (PH) associated with an increased LAP, but normal University, School of Pharmacy, obstructive pulmonary outflow tract in neonates with TPG (<12 mm Hg) and in particular DPG Richmond, Virginia, USA congenitally corrected transposition of the great arteries, (<7 mm Hg)—labelled isolated postcapillary pul- — Correspondence to (2) the importance of a restrictive versus a non-restrictive monary hypertension may increase RV afterload Professor Dietmar Schranz, atrial septum in neonates born with a borderline left and negatively affect right (subpulmonary) ven- Pediatric Heart Center, Justus ventricle and (3) the significance of both, a patent tricular function.
    [Show full text]
  • Core Topics in Cardiac Anesthesia, Second Edition
    Cambridge University Press 978-0-521-19685-7 - Core Topics in Cardiac Anesthesia: Second Edition Edited by Jonathan H. Mackay and Joseph E. Arrowsmith Index More information Index abciximab 465–6 airway management, postoperative endocarditis therapy 449 abdominal arteries 79 resuscitation 416 multi-resistant bacteria 450–2 accessory conducting pathways aldosterone 31–2 surgical prophylaxis 246, 342, 362, 9–10 alfentanil 36–7 447–8 acetylcholine (ACh) 25 allograft vasculopathy 280 anticoagulation acid-base management 391, 403–4, allostasis 29 atrial fibrillation 412 441 alpha-1-microalbumin 435 CPB 64–7, 175 actin 13–15 alpha-adrenergic receptors (a-ARs) ECMO 364 action potentials (APs), cardiac 8–11 25, 41, 48 endogenous 367–8 activated clotting time (ACT) 64, 67, alpha-stat blood-gas management 391, intra-aortic balloon pump 357 175, 370 403–4, 441 monitoring 67, 175 activated partial thromboplastin time e-aminocaproic acid (EACA) 68, 69, off-pump coronary surgery (APPT) 67 175, 368 190–1 acute coronary syndromes (ACS) amiodarone 57, 60 preoperative cessation 169 257–60 amitriptyline 463 prosthetic valve recipients 127, anesthetic management 258 Amplatzer muscular VSD 129–30 pathogenesis 257 occluder 264 antidepressants 463 acute kidney injury (AKI) 431–6 Amplatzer septal occluder 262–3 antidiuretic hormone (ADH) 31–2 acute lung injury (ALI) 421 analgesia anti-dysrhythmic drugs 57–62, 256, acute normovolemic hemodilution chronic pain 463 409 (ANH) 372, 468 postoperative 182, 191, 238–9, antifibrinolytics 68–9, 368–9 acute renal failure
    [Show full text]
  • The Role of Heart Rate on Functional Capacity In
    The role of heart rate on functional capacity in chronic heart failure: association or contribution? Haqeel Ahmed Jamil Submitted in accordance with the requirements for the degree of Doctor of Philosophy The University of Leeds Leeds Institute for Cardiovascular and Metabolic Medicine School of Medicine September 2015 - ii - Intellectual Property and Publication Statements: The candidate confirms that the work submitted is his own and that appropriate credit has been given where reference has been made to the work of others. This copy has been supplied on the understanding that it is copyright material and that no quotation from the thesis may be published without proper acknowledgement. The right of Haqeel Ahmed Jamil to be identified as Author of this work has been asserted by him in accordance with the Copyright, Designs and Patents Act 1988. © 2015 The University of Leeds and Haqeel Ahmed Jamil - iii - Dedication This thesis is affectionately dedicated to my parents, Mohammed and Azra Jamil for their unremitting love and wisdom, and without whom none of my career would have been possible; to my brothers, Adeel and Nabeel for always providing a mixture of encouragement and welcome distractions; to my wife Sana for her selfless support and understanding throughout: and to my son Zackaria, for the joy he brings to all of our lives. - iv - Acknowledgements I would like to start by thanking my supervisors, Klaus Witte and Mark Kearney for recognising my potential, constantly inspiring me and allowing me the opportunity to undertake research at the Leeds Institute for Cardiovascular and Metabolic Medicine (LICAMM). I would also like to sincerely thank the LICAMM research team and all the staff at the Leeds Cardiac Investigations Unit, for their assistance and support.
    [Show full text]
  • Thrombospondin-4 Is Required for Stretch-Mediated Contractility Augmentation in Cardiac Muscle Oscar H
    Thrombospondin-4 Is Required for Stretch-Mediated Contractility Augmentation in Cardiac Muscle Oscar H. Cingolani, Jonathan A. Kirk, Kinya Seo, Norimichi Koitabashi, Dong-ik Lee, Genaro Ramirez-Correa, Djahida Bedja, Andreas S. Barth, An L. Moens and David A. Kass Circ Res. 2011;109:1410-1414; originally published online October 27, 2011; doi: 10.1161/CIRCRESAHA.111.256743 Circulation Research is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 2011 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7330. Online ISSN: 1524-4571 The online version of this article, along with updated information and services, is located on the World Wide Web at: http://circres.ahajournals.org/content/109/12/1410 Data Supplement (unedited) at: http://circres.ahajournals.org/content/suppl/2011/10/27/CIRCRESAHA.111.256743.DC1.html Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Circulation Research can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. Once the online version of the published article for which permission is being requested is located, click Request Permissions in the middle column of the Web page under Services. Further information about this process is available in the Permissions and Rights Question and Answer document. Reprints: Information about reprints can be found online at: http://www.lww.com/reprints Subscriptions: Information about subscribing to Circulation Research is online at: http://circres.ahajournals.org//subscriptions/ Downloaded from http://circres.ahajournals.org/ at SWETS SUBSCRIPTION SERVICE on November 25, 2013 Integrative Physiology Thrombospondin-4 Is Required for Stretch-Mediated Contractility Augmentation in Cardiac Muscle Short Communication Oscar H.
    [Show full text]
  • The Anrep Effect Reconsidered
    The Anrep Effect Reconsidered R. G. Monroe, … , C. Phornphutkul, M. Davis J Clin Invest. 1972;51(10):2573-2583. https://doi.org/10.1172/JCI107074. Research Article Evidence is presented supporting the hypothesis that the positive inotropic effect after an abrupt increase in systolic pressure (Anrep effect) is the recovery from subendocardial ischemia induced by the increase and subsequently corrected by vascular autoregulation of the coronary bed. Major evidence consists of data obtained from an isolated heart preparation showing that the Anrep effect can be abolished with coronary vasodilation, and that with an abrupt increase in systolic pressure there is a significant reduction in the distribution of coronary flow to subendocardial layers of the ventricle. Furthermore, the intracardiac electrocardiogram shows S-T segment and T wave changes after an abrupt increase in ventricular pressure similar to that noted after coronary constriction. Major implications are that normally there may be ischemia of the subendocardial layers tending to reduce myocardial contractility which may account, in part, for the positive inotropic effect of various coronary vasodilators; that with an abrupt increase in ventricular pressure the subendocardium is rendered temporarily ischemic, placing the heart in jeopardy from arrhythmias until this is corrected; and that end-diastolic pressure and the intracardiac electrocardiogram may provide a means of evaluating the adequacy of circulation to subendocardial layers in diseased ventricles when systolic pressure is abruptly increased. Find the latest version: https://jci.me/107074/pdf rhe Anrep Effect Reconsidered R. G. MONROE, W. J. GAMBLE, C. G. LAFARGE, A. E. KUMAR, J. STARK, G. L. SANDERS, C.
    [Show full text]
  • Emergence of Mechano-Sensitive Contraction Autoregulation in Cardiomyocytes
    life Article Emergence of Mechano-Sensitive Contraction Autoregulation in Cardiomyocytes Leighton Izu 1,*, Rafael Shimkunas 1, Zhong Jian 1, Bence Hegyi 1 , Mohammad Kazemi-Lari 1 , Anthony Baker 2, John Shaw 3 , Tamas Banyasz 1,4 and Ye Chen-Izu 1,5,6 1 Department of Pharmacology, University of California, Davis, CA 95616, USA; [email protected] (R.S.); [email protected] (Z.J.); [email protected] (B.H.); [email protected] (M.K.-L.); [email protected] (T.B.); [email protected] (Y.C.-I.) 2 Department of Medicine, University of California, San Francisco, CA 94121, USA; [email protected] 3 Department of Aerospace Engineering, University of Michigan, Ann Arbor, MI 48109, USA; [email protected] 4 Department of Physiology, University of Debrecen, 4032 Debrecen, Hungary 5 Department of Biomedical Engineering, University of California, Davis, CA 95616, USA 6 Department of Internal Medicine, Division of Cardiology, University of California, Davis, CA 95616, USA * Correspondence: [email protected] Abstract: The heart has two intrinsic mechanisms to enhance contractile strength that compensate for increased mechanical load to help maintain cardiac output. When vascular resistance increases the ventricular chamber initially expands causing an immediate length-dependent increase of contraction force via the Frank-Starling mechanism. Additionally, the stress-dependent Anrep effect slowly increases contraction force that results in the recovery of the chamber volume towards its initial state. The Anrep effect poses a paradox: how can the cardiomyocyte maintain higher contractility Citation: Izu, L.; Shimkunas, R.; Jian, even after the cell length has recovered its initial length? Here we propose a surface mechanosensor Z.; Hegyi, B.; Kazemi-Lari, M.; Baker, model that enables the cardiomyocyte to sense different mechanical stresses at the same mechanical A.; Shaw, J.; Banyasz, T.; Chen-Izu, Y.
    [Show full text]
  • Mechanisms of Functional Tricuspid Valve Regurgitation in Ischemic Cardiomyopathy
    University of Montana ScholarWorks at University of Montana Graduate Student Theses, Dissertations, & Professional Papers Graduate School 2005 Mechanisms of functional tricuspid valve regurgitation in ischemic cardiomyopathy Thomas M. Joudinaud The University of Montana Follow this and additional works at: https://scholarworks.umt.edu/etd Let us know how access to this document benefits ou.y Recommended Citation Joudinaud, Thomas M., "Mechanisms of functional tricuspid valve regurgitation in ischemic cardiomyopathy" (2005). Graduate Student Theses, Dissertations, & Professional Papers. 9567. https://scholarworks.umt.edu/etd/9567 This Dissertation is brought to you for free and open access by the Graduate School at ScholarWorks at University of Montana. It has been accepted for inclusion in Graduate Student Theses, Dissertations, & Professional Papers by an authorized administrator of ScholarWorks at University of Montana. For more information, please contact [email protected]. NOTE TO USERS This reproduction is the best copy available. UMI Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Maureen and Mike MANSFIELD LIBRARY The University of Montana Permission is granted by the author to reproduce this material in its entirety, provided that this material is used for scholarly purposes and is properly cited in published works and reports. '*Please check "Yes" or "No" and provide signature Yes, I grant permission K No, I do not grant permission _________ Author's Signature: -------- Date :_______ 03 wA oS Any copying for commercial purposes or financial gain may be undertaken only with the author's explicit consent. 8/98 Reproduced with permission of the copyright owner.
    [Show full text]
  • Modulations of Cardiac Functions and Pathogenesis by Reactive Oxygen Species and Natural Antioxidants
    antioxidants Review Modulations of Cardiac Functions and Pathogenesis by Reactive Oxygen Species and Natural Antioxidants Sun-Hee Woo 1,*, Joon-Chul Kim 2 , Nipa Eslenur 1, Tran Nguyet Trinh 1 and Long Nguyen Hoàng Do 1 1 College of Pharmacy, Chungnam National University, 99 Daehak-ro, Yuseong-gu, Daejeon 34134, Korea; [email protected] (N.E.); [email protected] (T.N.T.); [email protected] (L.N.H.D.) 2 NEXEL Co., 8F 55 Magokdong-ro, Gangseo-gu, Seoul 07802, Korea; [email protected] * Correspondence: [email protected]; Tel.: +82-42-821-5924; Fax: +82-42-823-6566 Abstract: Homeostasis in the level of reactive oxygen species (ROS) in cardiac myocytes plays a critical role in regulating their physiological functions. Disturbance of balance between generation and removal of ROS is a major cause of cardiac myocyte remodeling, dysfunction, and failure. Cardiac myocytes possess several ROS-producing pathways, such as mitochondrial electron transport chain, NADPH oxidases, and nitric oxide synthases, and have endogenous antioxidation mechanisms. Cardiac Ca2+-signaling toolkit proteins, as well as mitochondrial functions, are largely modulated by ROS under physiological and pathological conditions, thereby producing alterations in contraction, membrane conductivity, cell metabolism and cell growth and death. Mechanical stresses under hypertension, post-myocardial infarction, heart failure, and valve diseases are the main causes for stress-induced cardiac remodeling and functional failure, which are associated with ROS-induced pathogenesis. Experimental evidence demonstrates that many cardioprotective natural antioxidants, enriched in foods or herbs, exert beneficial effects on cardiac functions (Ca2+ signal, contractility and rhythm), myocytes remodeling, inflammation and death in pathological hearts.
    [Show full text]
  • The Lack of Slow Force Response in Failing Rat Myocardium: Role of Stretch‑Induced Modulation of Ca–Tnc Kinetics
    The Journal of Physiological Sciences (2019) 69:345–357 https://doi.org/10.1007/s12576-018-0651-3 ORIGINAL PAPER The lack of slow force response in failing rat myocardium: role of stretch‑induced modulation of Ca–TnC kinetics Oleg Lookin1,2 · Yuri Protsenko1 Received: 20 September 2018 / Accepted: 8 December 2018 / Published online: 18 December 2018 © The Physiological Society of Japan and Springer Japan KK, part of Springer Nature 2018 Abstract The slow force response (SFR) to stretch is an important adaptive mechanism of the heart. The SFR may result in ~ 20–30% extra force but it is substantially attenuated in heart failure. We investigated the relation of SFR magnitude with Ca­ 2+ tran- sient decay in healthy (CONT) and monocrotaline-treated rats with heart failure (MCT). Right ventricular trabeculae were stretched from 85 to 95% of optimal length and held stretched for 10 min at 30 °C and 1 Hz. Isometric twitches and ­Ca2+ transients were collected on 2, 4, 6, 8, 10 min after stretch. The changes in peak tension and ­Ca2+ transient decay charac- teristics during SFR were evaluated as a percentage of the value measured immediately after stretch. The amount of Ca­ 2+ utilized by TnC was indirectly evaluated using the methods of Ca­ 2+ transient “bump” and “diference curve.” The muscles of CONT rats produced positive SFR and they showed prominent functional relation between SFR magnitude and the magni- tude (amplitude, integral intensity) of Ca­ 2+ transient “bump” and “diference curve.” The myocardium of MCT rats showed negative SFR to stretch (force decreased in time) which was not correlated well with the characteristics of ­Ca2+ transient decay, evaluated by the methods of “bump” and “diference curve.” We conclude that the intracellular mechanisms of Ca­ 2+ balancing during stretch-induced slow adaptation of myocardial contractility are disrupted in failing rat myocardium.
    [Show full text]
  • N 1912, Anrep1) As Well As Knowlton and Starling2) Reported That An
    Afterloading Increases the Left Ventricular End- Systolic Force-Length Relation Slope in Dogs Ryutaro KADOTA, M.D., Kouichi TAKEDA, M.D., Takahiko SHIMIZU, M.D., Yasuyuki NAKAMURA, M.D., and Shigeru YAGI, M.D. SUMMARY We evaluated the effects of pressure loading produced by gradual aortic occlusion on left ventricular (LV) myocardial contractility by as- sessing changes in the slope of the LV end-systolic force-diameter (Fes- Des) relation. Eleven adult mongrel dogs were prepared with ultra- sonic crystals for measuring LV diameter and a micromanometer for measuring LV pressure. Preload was decreased by vena caval occlusion (VCO), and afterload was increased by aortic occlusion (AOO). The slopes (Ec) and extrapolated diameter intercepts (Do) of the LV Fes-Des relation were determined for each dog from the end-systolic data obtained during VCO and AOO. During VCO and also AOO, the heart rate showed little change (134•}18 vs. 134•}16bpm in VCO, 135•}16 vs. 132 •} 17bpm in AOO). The values of Ec and Do during VCO were 62.8•} 15.6g/cm and 1.20•}0.36cm, respectively, while during AOO the respec- tive values were 122.6•}18.6g/cm and 1.66•}0.38cm. Ec and Do were both significantly increased during AOO in comparison with VCO (p< 0.001). These results suggest that gradual aortic occlusion increases LV myocardial contractility in anesthetized, open-chest dogs under autonomic blockade. This phenomenon might be related to length-dependent cal- cium activation. Key Words: Cylinder model Myocardial contractility Loading intervention Anrep effect Length-dependent calcium activation N 1912, Anrep1) as well as Knowlton and Starling2) reported that an abrupt increase in left ventricular (LV) pressure had a delayed positive inotropic effect on the LV myocardium of the isolated heart.
    [Show full text]