DOCSLIB.ORG

Leukotriene Inhibition Prevents and Reverses Hypoxic Pulmonary Vasoconstriction in Newborn Lambs

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Leukotriene Inhibition Prevents and Reverses Hypoxic Pulmonary Vasoconstriction in Newborn Lambs LEUKOTRIENE INHIBITION AND HPV 437 003 1-3998/85/1905-0437$02.00/0 PEDIATRIC RESEARCH Vol. 19, No. 5, 1985 Copyright O 1985 International Pediatric Research Foundation, Inc. Printed in U.S.A. Leukotriene Inhibition Prevents and Reverses Hypoxic Pulmonary Vasoconstriction in Newborn Lambs MICHAEL D. SCHREIBER, MICHAEL A. HEYMANN, AND SCOTT J. SOIFER The Cardiovascular Research Institute and the Departments of Pediatrics, Physiology, and Obstetrics, Gynecology, and Reproductive Sciences, University of California, Sun Francisco, California 94143 ABSTRACT. The effects of the leukotriene antagonist have been isolated from the lung lavage fluid of newborn infants FPL 57231 on the circulation were studied in sponta- with persistent pulmonary hypertension syndrome but not from neously breathing normoxic and hypoxic newborn lambs in newborn infants with other lung diseases (14). These findings order to evaluate the role of leukotrienes in the perinatal suggest that leukotrienes may play a role in maintaining the control of hypoxic pulmonary vasoconstriction. Hypoxia elevated pulmonary vascular tone in the normal fetus in utero produced a 58% increase in pulmonary arterial pressure and also in the mediation of hypoxic pulmonary vasoconstriction (p < 0.05) and a 37% increase in pulmonary vascular after birth. The effects of the leukotriene antagonist FPL 5723 1 resistance (p < 0.05). Hypoxic pulmonary vasoconstriction on the circulation were therefore studied in normoxic and hy- was abolished by the prior infusion of FPL 57231. Pul- poxic spontaneously breathing newborn lambs. monary arterial pressure increased by only 8% and pul- monary vascular resistance decreased by 10% from nor- METHODS moxia. The infusion of FPL 57231 during hypoxia-induced pulmonary vasoconstriction reversed the increase in pul- Surgical procedure and drug preparation. Six mixed-breed monary arterial pressure (p e 0.05) and pulmonary vas- newborn lambs from 3-7 days old were operated on under local cular resistance (p < 0.05). The hypoxia-induced increase anesthesia with 1% lidocaine hydrochloride. Polyvinyl catheters in cardiac output was maintained during the infusion of were placed in both hind limb arteries and veins and advanced FPL 57231. Leukotrienes may play a significant role in to the descending aorta and inferior vena cava, respectively. A the mediation of hypoxic pulmonary vasoconstriction. Leu- no. 5 French flow-directed thermodilution catheter, with the kotriene inhibition with FPL 57231 may be useful in the proximal injection port 15 cm from the tip, was introduced into management of infants with persistent pulmonary hyper- the jugular vein and advanced into the pulmonary artery for tension syndrome. (Pediatr Res 19: 437-441,1985) measuring pulmonary arterial and pulmonary arterial wedge pressures. Right atrial pressure was measured through the prox- imal port. Cardiac output was determined by the thermodilution Abbreviations technique and calculated by computer (Electro-Catheter model PPHN, persistent pulmonary hypertension of the newborn 5000, Electro-Catheter Corp., Rahway, NJ). Three milliliters of PG, prostaglandin iced-saline was injected into the proximal port for each measure- PG12, prostacyclin ment. Each cardiac output value was taken as the average of three determinations. Following surgery, the lambs were placed in a sling under a radiant warmer to maintain body temperature. An intravenous infusion of dextrose in water was started. Two horns were allowed for recovery. The exact mechanisms by which hypoxia produces pulmonary FPL 5723 1 was prepared immediately before each experiment vasoconstriction remain unknown. The production and release as a 1% solution in sterile water. of the noncyclooxygenase products of arachidonic acid from the Experimental Protocol. FPL 57231 infusion prior to the onset lung may play an important role. Leukotrienes, the 5'-lipoxygen- of hypoxia. Following the recovery period, baseline vascular ase metabolites of arachidonic acid, are produced by mast cells pressures, cardiac output, and arterial blood gas measurements (1, 2), alveolar macrophages (3), and pulmonary vascular tissue were made in room air (NORMOXIA). Normocarbic hypoxia (4-6). Leukotrienes induce smooth muscle contraction in a was then induced by placing a loosely fitting bag over the lamb's variety of tissues (7-10). Leukotriene D4 infused into the pul- head and adding nitrogen with 5% C02to the gas mixture. The monary artery of young lambs produces pulmonary arterial F102 was varied to produce a Pao2 of 30-40 mm Hg in each hypertension (1 1). Leukotriene inhibition with FPL 57231 (Fi- animal. Measurements were made after 10 rnin of hypoxia and sons, plc, Loughborough, UK), a leukotriene receptor antagonist stable pulmonary hypertension (HYPOXIA). The lamb was re- (12), significantly increases pulmonary blood flow and decreases turned to room air. pulmonary vascular resistance in fetal lambs (13). Leukotrienes After the lambs resumed baseline values (NORMOXIA), an Received October 9, 1984; accepted December 27, 1984. intravenous infusion of FPL 5723 1 (1 mg. kg-'. min-I) for 20 Requests for reprints should be addressed to Dr. Scott J. Soifer, Cardiovascular rnin was started. Measurements were made after 10 rnin of the Research Institute M-342A, University of California, San Francisco, CA 94143. infusion (NORMOXIA + FPL 57231). Hypoxia was then in- Supported in part by grants from the American Lung Association and U.S. Public Health Service Program Project Grant HL 24056. M.D.S. is recipient of the duced as the drug infusion continued, and measurements were American Heart Association, California affiliate fellowship award. S.J.S. is recipient made after another 10 rnin (HYPOXIA + FPL 57231). The of New Investigator Award HL 29941 from the NHLBI. infusion was stopped as hypoxia continued, and measurements 438 SCHREIBER ET AL. were made after 15 min. The lambs were returned to room air. infusion of FPL 5723 1 (HYPOXIA + FPL 5723 1). Pulmonary Measurements were also made with an equivalent infusion of arterial pressure increased by only 8% and pulmonary vascular sterile water vehicle during normoxia and hypoxia. resistance decreased by 10% compared to NORMOXIA. Pul- FPL 57231 infusion started during hypoxia. Six to 24 hr were monary arterial pressure and pulmonary vascular resistance dur- allowed for recovery from the above experiment. In five lambs ing HYPOXIA + FPL 5723 1 were significantly lower than during baseline measurements were made in room air (NORMOXIA). HYPOXIA (p< 0.05). There were no significant changes in Normocarbic hypoxia was again induced producing hypoxemia systemic arterial pressure and systemic vascular resistance com- (Pao* 30-40 mm Hg) and stable pulmonary hypertension. After pared to HYPOXIA. The 24% increase in cardiac output during 10 min, measurements were repeated (HYPOXIA). Hypoxia was continued and an infusion of FPL 5723 1 (2 mgkg-'. min-') was started. Measurements were made after 10 min (HYPOXIA + FPL 5723 1). The drug infusion was then stopped, and the lambs I * ~<0.05vs NORMOXIA were returned to room air. Measurements and calculations. Pulmonary and systemic ar- terial and right atrial pressures were measured with Statham P23 Db pressure transducers and recorded continuously on a Beck- I- 5 5 E man multichannel direct-writing recorder. Mean pressures were >, E obtained by electrical integration. Heart rate was measured with a a cardiotachometer triggered from the systemic arterial pressure. zauw 20- Cardiac output, pulmonary arterial wedge pressure, and systemic .........:_:.:.:.:.:.:. ....................... arterial blood gases were measured during all normoxia and ............... .............................. hypoxia periods after a steady-state had been reached. The ab- - ............... 2 10 ........................ sence of intracardiac shunting was determined by indicator di- a .............. lution technique. The validity of the thermodilution method has W .............. I ................::. been reported previously ( 15, 16). Pulmonary vascular resistance .............. .............. was calculated as the mean pulmonary arterial pressure minus 0 - mean pulmonary arterial wedge pressure divided by cardiac NORMOXIA HYPOXlA NORMOXIA NORMOXIA HYPOXIA output per kilogram. Systemic vascular resistance was calculated + + as the mean systemic arterial pressure minus mean right atrial pressure divided by cardiac output per kilogram. The mean f SD was computed for the vascular pressures, resistances, cardiac output, heart rate, and arterial blood gases during all normoxic and hypoxic conditions. The differences in these variables were compared by two-way analysis of variance and the Newman-Keuls test for multiple comparisons (I 7). A p c 0.05 was considered statistically significant. RESULTS FPL 57231 inxusion prior to the onset of hypoxia (Table I, Fig. 1). Normocarbic hypoxia (HYPOXIA) produced a 58% increase in pulmonary arterial pressure from 18.1 f 2.7 to 28.6 k 3.2 mm Hg (pc 0.05) and a 37% increase in pulmonary vascular resistance from 44.0 * 6.6 to 60.4 f 6.8 mm Hg.1-I. min-I .kg-' (p< 0.05) compared to normoxia. Systemic arterial pressure was unchanged. Systemic vascular resistance decreased - by 16% during HYPOXIA (pc 0.05), as cardiac output in- NORMOXIA HYPOXIA NORMOXIA NORMOXIA HYPOXIA creased by 1 %. + + 9 FPL5723I FPL57231 Infusing FPL 5723 1 during normoxia (NORMOXIA + FPL 5723 1) produced no significant changes in the hemodynamic Fig. 1. The effects of an infusion of FPL 5723 1 prior to
Load more

Recommended publications
  • Pathophysiology of the Cardiovascular System and Neonatal Hypotension
    Pathophysiology of the Cardiovascular System and Neonatal Hypotension Sandra L. Shead, RNC-NIC, MSN, CNS, NNP-BC Continuing Nursing Education BSTRACT (CNE) Credit A A total of 2.5 contact Hypotension is common in low birth weight neonates and less common in term newborns and is hours may be earned as CNE credit associated with significant morbidity and mortality. Determining an adequate blood pressure in for reading the articles in this issue neonates remains challenging for the neonatal nurse because of the lack of agreed-upon norms. Values identified as CNE and for completing an online posttest and evaluation. for determining norms for blood pressure at varying gestational and postnatal ages are based on To be successful the learner must empirical data. Understanding cardiovascular pathophysiology, potential causes of hypotension, and obtain a grade of at least 80% on assessment of adequate perfusion in the neonatal population is important and can assist the neonatal the test. Test expires three (3) years from publication date. Disclosure: nurse in the evaluation of effective blood pressure. This article reviews cardiovascular pathophysiology The author/planning committee as it relates to blood pressure and discusses potential causes of hypotension in the term and preterm has no relevant financial interest or affiliations with any commercial neonate. Variation in management of hypotension across centers is discussed. Underlying causes and interests related to the subjects pathophysiology of hypotension in the neonate are described. discussed within this article. No commercial support or sponsorship was provided for this educational Keywords: neonatal hypotension; definition; physiology; cardiovascular system; preterm; management; activity. ANN/ANCC does not assessment; cerebral; autoregulation; blood pressure endorse any commercial products discussed/displayed in conjunction with this educational activity.
    [Show full text]
  • Arterial System Lecture Block 10 Vascular Structure/Function
    Arterial System Lecture Block 10 Arterial System Bioengineering 6000 CV Physiology Vascular Structure/Function Arterial System Bioengineering 6000 CV Physiology Functional Overview Arterial System Bioengineering 6000 CV Physiology Vessel Structure Aorta Artery Vein Vena Cava Arteriole Capillary Venule Diameter 25 mm 4 mm 5 mm 30 mm 30 µm 8 µm 20 µm Wall 2 mm 1 mm 0.5 mm 1.5 mm 6 µm 0.5 µm 1 µm thickness Endothelium Elastic tissue Smooth Muscle Fibrous Tissue Arterial System Bioengineering 6000 CV Physiology Aortic Compliance • Factors: – age 20--24 yrs – athersclerosis 300 • Effects – more pulsatile flow 200 dV 30--40 yrs C = – more cardiac work dP 50-60 yrs – not hypertension Laplace’s Law 100 70--75 yrs (thin-walled cylinder): [%] Volume Blood T = wall tension P = pressure T = Pr r = radius For thick wall cylinder 100 150 200 P = pressure Pr Pressure [mm Hg] σ = wall stress r = radius σ = Tension Wall Stress w = wall thickness w [dyne/cm] [dyne/cm2] Aorta 2 x 105 10 x 105 Capillary 15-70 1.5 x 105 Arterial System Bioengineering 6000 CV Physiology Arterial Hydraulic Filter Arterial System Bioengineering 6000 CV Physiology Arterial System as Hydraulic Filter Arterial Cardiac Pressure • Pulsatile --> Output t Physiological smooth flow t Ideal • Cardiac energy conversion Cardiac • Reduces total Output Arterial cardiac work Pressure t Pulsatile t Challenge Cardiac Output Arterial Pressure t Filtered t Reality Arterial System Bioengineering 6000 CV Physiology Elastic Recoil in Arteries Arterial System Bioengineering 6000 CV Physiology Effects of Vascular Resistance and Compliance Arterial System Bioengineering 6000 CV Physiology Cardiac Output vs.
    [Show full text]
  • Vascular Peripheral Resistance and Compliance in the Lobster Homarus Americanus
    The Journal of Experimental Biology 200, 477–485 (1997) 477 Printed in Great Britain © The Company of Biologists Limited 1997 JEB0437 VASCULAR PERIPHERAL RESISTANCE AND COMPLIANCE IN THE LOBSTER HOMARUS AMERICANUS JERREL L. WILKENS*,1, GLEN W. DAVIDSON†,1 AND MICHAEL J. CAVEY1,2 1Department of Biological Sciences, The University of Calgary, 2500 University Drive NW, Calgary, Alberta, Canada T2N 1N4 and 2Department of Anatomy, The University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, Canada T2N 4N1 Accepted 24 October 1996 Summary The peripheral resistance to flow through each arterial become stiffer at pressures greater than peak systolic bed (in actuality, the entire pathway from the heart back pressure and at radii greater than twice the unpressurized to the pericardial sinus) and the mechanical properties of radius. The dorsal abdominal artery possesses striated the seven arteries leaving the lobster heart are measured muscle in the lateral walls. This artery remains compliant and compared. Resistance is inversely proportional to over the entire range of hemolymph pressures expected in artery radius and, for each pathway, the resistance falls lobsters. These trends are illustrated when the non-linearly as flow rate increases. The resistance of the incremental modulus of elasticity is compared among hepatic arterial system is lower than that predicted on the arteries. All arteries should function as Windkessels to basis of its radius. Body-part posture and movement may damp the pulsatile pressures and flows generated by the affect the resistance to perfusion of that region. The total heart. The dorsal abdominal artery may also actively vascular resistance placed on the heart when each artery regulate its flow.
    [Show full text]
  • Pathophysiology of the Right Ventricle And€Of the Pulmonary Circulation In
    SERIES | WORLD SYMPOSIUM ON PULMONARY HYPERTENSION Pathophysiology of the right ventricle and of the pulmonary circulation in pulmonary hypertension: an update Anton Vonk Noordegraaf1, Kelly Marie Chin2, François Haddad3, Paul M. Hassoun4, Anna R. Hemnes5, Susan Roberta Hopkins6, Steven Mark Kawut7, David Langleben8, Joost Lumens9,10 and Robert Naeije11,12 Number 3 in the series “Proceedings of the 6th World Symposium on Pulmonary Hypertension” Edited by N. Galiè, V.V. McLaughlin, L.J. Rubin and G. Simonneau Affiliations: 1Amsterdam UMC, Vrije Universiteit Amsterdam, Pulmonary Medicine, Amsterdam Cardiovascular Sciences, Amsterdam, The Netherlands. 2Division of Pulmonary and Critical Care Medicine, University of Texas Southwestern, Dallas, TX, USA. 3Division of Cardiovascular Medicine, Stanford University and Stanford Cardiovascular Institute, Palo Alto, CA, USA. 4Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, MD, USA. 5Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN, USA. 6Dept of Medicine, University of California, San Diego, La Jolla, CA, USA. 7Penn Cardiovascular Institute, Dept of Medicine, and Center for Clinical Epidemiology and Biostatistics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. 8Center for Pulmonary Vascular Disease, Cardiology Division, Jewish General Hospital and McGill University, Montreal, QC, Canada. 9Maastricht University Medical Center, CARIM School for Cardiovascular Diseases, Maastricht, The Netherlands. 10Université de Bordeaux, LIRYC (L’Institut de Rythmologie et Modélisation Cardiaque), Bordeaux, France. 11Dept of Cardiology, Erasme University Hospital, Brussels, Belgium. 12Laboratory of Cardiorespiratory Exercise Physiology, Faculty of Motor Sciences, Université Libre de Bruxelles, Brussels, Belgium. Correspondence: Anton Vonk Noordegraaf, Amsterdam UMC, Vrije Universiteit Amsterdam, Pulmonary Medicine, Amsterdam Cardiovascular Sciences, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands.
    [Show full text]
  • Effects of Vasodilation and Arterial Resistance on Cardiac Output Aliya Siddiqui Department of Biotechnology, Chaitanya P.G
    & Experim l e ca n i t in a l l C Aliya, J Clinic Experiment Cardiol 2011, 2:11 C f a Journal of Clinical & Experimental o r d l DOI: 10.4172/2155-9880.1000170 i a o n l o r g u y o J Cardiology ISSN: 2155-9880 Review Article Open Access Effects of Vasodilation and Arterial Resistance on Cardiac Output Aliya Siddiqui Department of Biotechnology, Chaitanya P.G. College, Kakatiya University, Warangal, India Abstract Heart is one of the most important organs present in human body which pumps blood throughout the body using blood vessels. With each heartbeat, blood is sent throughout the body, carrying oxygen and nutrients to all the cells in body. The cardiac cycle is the sequence of events that occurs when the heart beats. Blood pressure is maximum during systole, when the heart is pushing and minimum during diastole, when the heart is relaxed. Vasodilation caused by relaxation of smooth muscle cells in arteries causes an increase in blood flow. When blood vessels dilate, the blood flow is increased due to a decrease in vascular resistance. Therefore, dilation of arteries and arterioles leads to an immediate decrease in arterial blood pressure and heart rate. Cardiac output is the amount of blood ejected by the left ventricle in one minute. Cardiac output (CO) is the volume of blood being pumped by the heart, by left ventricle in the time interval of one minute. The effects of vasodilation, how the blood quantity increases and decreases along with the blood flow and the arterial blood flow and resistance on cardiac output is discussed in this reviewArticle.
    [Show full text]
  • Pulmonary Vascular Resistance and Compliance Relationship in Pulmonary Hypertension
    SERIES PHYSIOLOGY IN RESPIRATORY MEDICINE Pulmonary vascular resistance and compliance relationship in pulmonary hypertension Denis Chemla1,2, Edmund M.T. Lau1,2,3, Yves Papelier2, Pierre Attal4 and Philippe Hervé5 Number 10 in the series “Physiology in respiratory medicine” Edited by R. Naeije, D. Chemla, A. Vonk-Noordegraaf and A.T. Dinh-Xuan Affiliations: 1Univ. Paris-Sud, Faculté de Médecine, Inserm U_999, Le Kremlin Bicêtre, France. 2AP-HP, Services des Explorations Fonctionnelles, Hôpital de Bicêtre, Le Kremlin Bicêtre, France. 3Dept of Respiratory Medicine, Royal Prince Alfred Hospital, University of Sydney, Camperdown, Australia. 4Dept of Otolaryngology-Head and Neck Surgery, Shaare-Zedek Medical Center and Hebrew University Medical School, Jerusalem, Israel. 5Centre Chirurgical Marie Lannelongue, Le Plessis-Robinson, France. Correspondence: Denis Chemla, Service des Explorations Fonctionnelles - Broca 7, Hôpital de Bicêtre, 78 rue du Général Leclerc, 94 275 Le Kremlin Bicêtre, France. E-mail: [email protected] ABSTRACT Right ventricular adaptation to the increased pulmonary arterial load is a key determinant of outcomes in pulmonary hypertension (PH). Pulmonary vascular resistance (PVR) and total arterial compliance (C) quantify resistive and elastic properties of pulmonary arteries that modulate the steady and pulsatile components of pulmonary arterial load, respectively. PVR is commonly calculated as transpulmonary pressure gradient over pulmonary flow and total arterial compliance as stroke volume over pulmonary arterial pulse pressure (SV/PApp). Assuming that there is an inverse, hyperbolic relationship between PVR and C, recent studies have popularised the concept that their product (RC-time of the pulmonary circulation, in seconds) is “constant” in health and diseases. However, emerging evidence suggests that this concept should be challenged, with shortened RC-times documented in post-capillary PH and normotensive subjects.
    [Show full text]
  • Cardiovascular Physiology
    Dr Matthew Ho BSc(Med) MBBS(Hons) FANZCA Cardiovascular Physiology Electrical Properties of the Heart Physiol-02A2/95B4 Draw a labelled diagram of a cardiac action potential highlighting the sequence of changes in ionic conductance. Explain the terms 'threshold', 'excitability', and 'irritability' with the aid of a diagram. 1. Cardiac muscle contraction is electrically activated by an action potential, which is a wave of electrical discharge that travels along the cell membrane. Under normal circumstances, it is created by the SA node, and propagated to the cardiac myocytes through gap junctions (intercalated discs). 2. Cardiac action potential: a. Phase 4 – resting membrane potential: i. Usually -90mV ii. Dependent mostly on potassium permeability, and gradient formed from Na-K ATPase pump b. Phase 0 - -90mV-+20mV i. Generated by the opening of fast Na channels Na into cell potential inside rises > 65mV (threshold potential) positive feedback further Na channel opening action potential ii. Threshold potential also triggers opening Ca channels (L type) at -10mV iii. Reduced K permeability c. Phase 1 – starts + 20mV i. The positive AP causes rapid closure of fast Na channels transient drop in potential d. Phase 2 – plateau i. Maximum permeability of Ca through L type channels ii. Rising K permeability iii. Maintenance of depolarisation e. Phase 3 – repolarisation i. Na, Ca and K conductance returns to normal ii. Ca. Na channels close, K channels open 3. Threshold: the membrane potential at which an AP occurs a. Usually-65mV in the cardiac cell b. AP generated via positive feedback Na channel opening 4. Excitability: the ease with which a myocardial cell can respond to a stimulus by depolarising.
    [Show full text]
  • Pulmonary Artery Catheter Learning Package
    2016 Pulmonary Artery Catheter Learning Package Paula Nekic, CNE Liverpool ICU SWSLHD, Liverpool ICU 1/12/2016 Liverpool Hospital Intensive Care: Learning Packages Intensive Care Unit Pulmonary Artery Catheter Learning Package CONTENTS 1. Objectives 3 2. Pulmonary Artery Catheter 4 . Indications . Contraindications . Complications 3. Sheath 6 4. Lumens 7 5. Insertion 8 6. Waveforms 13 7. Wedging 21 8. Cardiac output studies 23 9. Nursing management 33 10. Learning Questions 35 11. Reference List 36 LH_ICU2016_Learning_Package_Pulmonary-Artery_Catheter_Learning_Package 2 | P a g e Liverpool Hospital Intensive Care: Learning Packages Intensive Care Unit Pulmonary Artery Catheter Learning Package OBJECTIVES The aim of this package is to provide the nurse with a learning tool which can be used in conjunction with clinical practice under supervision of a CNE and or resource person for the management of a pulmonary artery catheter. After completion of the package the RN will be able to: 1. State the indications, contraindications and complications of a PA catheter 2. Identify the lumens and their uses 3. Identify normal and abnormal waveforms 4. Perform all routine and safety checks 5. Identify normal ranges for haemodynamic values measured from a PA catheter 6. Identify the position and waveforms of PA catheter 7. Perform a wedge procedure safely 8. Perform cardiac output studies 9. Interpret cardiac output studies 10. Identify the risks and complications associated with the insertion and management of a PA catheter 11. Discuss nursing management of a PA catheter LH_ICU2016_Learning_Package_Pulmonary-Artery_Catheter_Learning_Package 3 | P a g e Liverpool Hospital Intensive Care: Learning Packages Intensive Care Unit Pulmonary Artery Catheter Learning Package Pulmonary Artery Catheter History The first introduction of a catheter into a human pulmonary artery was in 1929 by Forsmann.
    [Show full text]
  • Is Vasomotion in Cerebral Arteries Impaired in Alzheimer's
    Journal of Alzheimer’s Disease 46 (2015) 35–53 35 DOI 10.3233/JAD-142976 IOS Press Review CORE Metadata, citation and similar papers at core.ac.uk Provided by SZTE Publicatio Repozitórium - SZTE - Repository of Publications Is Vasomotion in Cerebral Arteries Impaired in Alzheimer’s Disease? Luigi Yuri Di Marcoa,∗, Eszter Farkasb, Chris Martinc, Annalena Vennerid,e and Alejandro F. Frangia aCentre for Computational Imaging and Simulation Technologies in Biomedicine (CISTIB), Department of Electronic and Electrical Engineering, University of Sheffield, Sheffield, UK bDepartment of Medical Physics and Informatics, Faculty of Medicine and Faculty of Science and Informatics, University of Szeged, Szeged, Hungary cDepartment of Psychology, University of Sheffield, Sheffield, UK dDepartment of Neuroscience, University of Sheffield, Sheffield, UK eIRCCS, Fondazione Ospedale S. Camillo, Venice, Italy Handling Associate Editor: Mauro Silvestrini Accepted 11 February 2015 Abstract. A substantial body of evidence supports the hypothesis of a vascular component in the pathogenesis of Alzheimer’s disease (AD). Cerebral hypoperfusion and blood-brain barrier dysfunction have been indicated as key elements of this path- way. Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder, frequent in AD, characterized by the accumulation of amyloid-␤ (A␤) peptide in cerebral blood vessel walls. CAA is associated with loss of vascular integrity, resulting in impaired regulation of cerebral circulation, and increased susceptibility to cerebral ischemia, microhemorrhages, and white matter dam- age. Vasomotion—the spontaneous rhythmic modulation of arterial diameter, typically observed in arteries/arterioles in various vascular beds including the brain—is thought to participate in tissue perfusion and oxygen delivery regulation. Vasomotion is impaired in adverse conditions such as hypoperfusion and hypoxia.
    [Show full text]
  • INDE 221 Spring 2010 Syllabus Part 2
    Human Health & Disease Mondays, Tuesdays, Thursdays and Fridays 9:00 - 11:50 AM Lectures: Room M-112, Labs: Fleischmann IINNDDEE 222211 SSpprriinngg 22001100 Syllabus SSyyllllaabbuuss PPaarrtt 22 (2010) Year's Last Syllabus (2010) Year's Last Human Health & Disease Inde 221 Spring 2010 Table of Contents CARDIOVASCULAR BLOCK SYLLABUS SCHEDULE 7 SYLLABUS PREFACE 11 CARDIAC MUSCLE AND FHC 15 EXCITATION-CONTRACTION COUPLING Syllabus27 NERNST POTENTIAL AND OSMOSIS 43 EXCITABILITY AND CONDUCTION 51 CIRCULATORY VESSEL HISTOLOGY LAB 63 CARDIAC ACTION POTENTIAL 71 CONTROL OF HEART RHYTHM (2010) 85 AUTONOMIC DRUGS OVERVIEW I 97 ELECTROCARDIOGRAM (ECG) 99 LESIONS OF BLOOD VESSELS 109 THROMBOEMBOLIC DISEASE 117 CARDIAC REFLEXESYear's 123 AUTONOMIC DRUGS OVERVIEW II 141 ECG SMALL GROUPS 143 LastAUTONOMIC DRUGS: CHOLINERGICS 147 CARDIAC MUSCLE MECHANICS 149 AUTONOMIC DRUGS: ANTICHOLINERGICS 175 ARRHYTHMIAS 177 AUTONOMIC DRUGS: SYMPATHOMIMETICS I 203 VENTRICULAR PHYSIOLOGY 205 AUTONOMIC DRUGS: SYMPATHOMIMETICS II 235 STARLING CURVE AND VENOUS RETURN 237 CARDIAC OUTPUT AND CATHETERIZATION 245 AUTONOMIC DRUGS: ADRENOCEPTOR BLOCKERS 267 PHYSICS OF CIRCULATION Syllabus269 CASE DISCUSSIONS: AUTONOMIC DRUGS 289 SMOOTH MUSCLE 291 ISCHEMIC AND VALVULAR HEART DISEASE 303 RENAL CIRCULATION (2010) 323 HYPERTENSION 333 CARDIOMYOPATHY, MYOCARDITIS AND ATRIAL MYXOMA 351 ENDOTHELIUM AND CORONARY CIRCULATION 369 ANGINA PECTORIS 389 DRUGS USEDYear's IN HYPERTENSION 397 SHOCK 399 ADULT CARDIAC LAB 413 CARDIAC ANESTHESIA & BYPASS 421 LastEXERCISE PHYSIOLOGY 431 ISCHEMIC
    [Show full text]
  • Cardiovascular System: Vessels Blood Vessel Anatomy: Per Human Body (Branch / Diverge / Fork)
    Over 60,000 Cardiovascular System – Vessels miles of vessels Cardiovascular System: Vessels Blood Vessel Anatomy: per human body (branch / diverge / fork) Elastic Muscular Arterioles Arteries Arteries Vessel Types: Heart (nutrient 1) Arteries (away from heart) exchange) 2) Capillaries Capillaries 3) Veins (toward heart) Veins Venules (join / merge / converge) Cardiovascular System – Vessels Cardiovascular System – Vessels Blood Vessel Anatomy: Blood Vessel Anatomy: Only tunic present in capillaries Vessels composed of distinct tunics : O2-rich; CO2-poor 1) Tunica intima Pulmonary circuit Tunica intima • Endothelium (simple squamous epithelium) (short, low pressure loop) • Connective tissue ( elastic fibers) O2-poor; CO2-rich (long, high pressure loop) 2) Tunica media Systemic circuit • Smooth muscle / elastic fibers • Regulates pressure / circulation • Sympathetic innervation Lumen O2-poor; O2-rich; Vasa CO2-rich CO2-poor 3) Tunica externa vasorum • Loose collagen fibers • Nerves / lymph & blood vessels • Protects / anchors vessel % / volume not fixed: Function: • Alteration of arteriole size 1) Circulate nutrients / waste • Alteration of cardiac output Vasomotor stimulation = vasoconstriction Tunica media 2) Regulate blood pressure • Combination of two above Vasomotor relaxation = vasodilation Tunica externa Costanzo (Physiology, 4th ed.) – Figure 4.1 Cardiovascular System – Vessels Relative tissue Cardiovascular System – Vessels Relative tissue makeup makeup Blood Vessel Anatomy: Blood Vessel Anatomy: Arteriosclerosis: Arteries: Hardening
    [Show full text]
  • CHAPTER 7 — Cardiovascular Physiology
    © Jones & Bartlett Learning, LLC. NOT FOR SALE OR DISTRIBUTION © Sebastian Kaulitzki/ShutterStock, Inc. 7 Cardiovascular Physiology Case 1 Introduction The Anatomy of the Cardiovascular System: The Heart Cardiac Muscle: Cellular Level of Organization Anatomy: The Vasculature Nutrient Exchange How Does Blood Return to the Heart? Blood: What Is Flowing Through These Vessels? What Causes the Heart to Beat? What Is an ECG and What Information Does It Provide? What Is Cardiac Output and How Is It Regulated? Metabolism, O2 Consumption, and Cardiac Work Blood Vessels Carry Blood to Tissues—The End Users Blood Flow: Behavior of Fluids Summary Key Concepts Key Terms Application: Pharmacology Cardiovascular Clinical Case: Type 2 Diabetes Mellitus 143 9781284030341_CH07.indd 143 11/4/2013 8:03:32 PM © Jones & Bartlett Learning, LLC. NOT FOR SALE OR DISTRIBUTION Case 1 You generally go for a 3-mile run in the morning, and today is no exception. Within the first minute, you feel your heart rate increase, and before long you can feel the pounding of your heart. As your run continues, you think about the blood coursing through your arteries and veins and wonder at the workings of the cardiovascular system. What caused your heart rate to increase? What makes your heart beat harder? What makes you flush by the end of the run? How is all this regulated, so that it returns to “normal” at the end of your run? Introduction The cardiovascular system consists of the heart and the connecting vasculature, from aorta to arterioles to capillaries to veins to vena cavae. It functions as the distributor of molecules to the billions of cells in the body.
    [Show full text]