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      In vivo Mechanisms of Myocardial Functional Stability during Physiological Interventions

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          Abstract

          Metabolic regulatory mechanisms are designed to maintain stable myocardial function during extremes in physiological insult; they can now be studied in vivo and may provide insight into mechanisms of altered myocardial functional decompensation during disease processes. To determine mechanisms of myocardial stability during hypoxia and acute pressure loading, creatine kinase (CK) kinetics (forward rate constant, K<sub>f</sub>, and flux of phosphocreatine, PCr, to adenosine triphosphate, ATP), and nicotinamide adenine dinucleotide (NADH) redox state were determined with <sup>31</sup>P nuclear magnetic resonance (NMR) and NADH fluorometry, respectively, and correlated with heart work (heart rate × systolic blood pressure, HR × SBP), cardiac output (CO) and O<sub>2</sub> consumption (MVO<sub>2</sub>) in 15 anesthetized open chest dogs. Hypoxia (Pa<sub>o2</sub> of 30-35 mm Hg) was produced in 6 dogs with an inspired O<sub>2</sub>/N<sub>2</sub> of 200/3,000. Cardiac loading was produced in 9 dogs by administration of norepinephrine (NE, 1 µg/kg/min). Each dog acted as its own control. Baseline NADH fluorometry, <sup>31</sup>P-NMR saturation transfer and cardiac function measurements were performed simultaneously in each dog, after which the experimental interventions were made. Similar increases in HR × SBP, CO, and MVO2 which occurred during both interventions were associated with different bioenergetic responses. During NE infusion, the K<sub>f</sub> of CK increased from control; during hypoxia, the K<sub>f</sub> decreased from control (p < 0.05). Flux of PCr → ATP was significantly lower during hypoxia than during NE infusion (p < 0.05). PCr was decreased significantly during NE infusion (p < 0.05). In addition, NADH redox state increased (from baseline of 100%) during hypoxia (140 ± 10%) and decreased during NE infusion (78 ± 6%). These data indicate that the myocardial response to demand is not universally regulated by adenosine diphosphate (ADP) or redox state. In addition, metabolic regulators can induce changes related to the type of intervention irrespective of similarity of workload.

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          Author and article information

          Journal
          CRD
          Cardiology
          10.1159/issn.0008-6312
          Cardiology
          S. Karger AG
          0008-6312
          1421-9751
          1991
          1991
          12 November 2008
          : 79
          : 1
          : 1-13
          Affiliations
          Department of aMedicine (Cardiology), bAnesthesia, cBiochemistry/Biophysics, University of Pennsylvania, Philadelphia, Pa., USA
          Article
          174851 Cardiology 1991;79:1–13
          10.1159/000174851
          1777909
          © 1991 S. Karger AG, Basel

          Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

          Page count
          Pages: 13
          Categories
          General Cardiology

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