Cited by 302Nitric Oxide and Endothelin EffectsCardiovascular Function and Risk FactorsCardiac Fibrosis and Remodeling

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Reduced Nitric Oxide Production and Altered Myocardial Metabolism During the Decompensation of Pacing-Induced Heart Failure in the Conscious Dog

Recchia, Fabio A., McConnell, Patrick I., Bernstein, Robert D., Vogel, Traci R., Xu, Xiaobin, Hintze, Thomas H.·1998·Circulation Research

DOI 10.1161/01.res.83.10.969

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Abstract

Abstract —The aim of the present study was to determine whether cardiac nitric oxide (NO) production changes during the progression of pacing-induced heart failure and whether this occurs in association with alterations in myocardial metabolism. Dogs (n=8) were instrumented and the heart paced until left ventricular end-diastolic pressure reached 25 mm Hg and clinical signs of severe failure were evident. Every week, hemodynamic measurements were recorded and blood samples were withdrawn from the aorta and the coronary sinus for measurement of NO metabolites, O 2 content, free fatty acids (FFAs), and lactate and glucose concentrations. Cardiac production of NO metabolites or consumption of O 2 or utilization of substrates was calculated as coronary sinus-arterial difference times coronary flow. In end-stage failure, occurring at 29±1.6 days, left ventricular end-diastolic pressure was 25±1 mm Hg, left ventricular systolic pressure was 92±3 mm Hg, mean arterial pressure was 75±2.5 mm Hg, and dP/dt max was 1219±73 mm Hg/s (all P <0.05). These changes in hemodynamics were associated with a fall of cardiac NO metabolite production from 0.37±0.16 to −0.28±0.13 nmol/beat ( P <0.05). O 2 consumption and lactate uptake did not change significantly from control, while FFA uptake decreased from 0.16±0.03 to 0.05±0.01 μEq/beat and glucose uptake increased from −2.3±7.0 to 41±10 μg/beat ( P <0.05). The cardiac respiratory quotient also increased significantly by 28%. In 14 normal dogs the same measurements were performed at control and 1 hour after we injected 30 mg/kg of nitro- l -arginine, a competitive inhibitor of NO synthase. O 2 consumption increased from 0.05±0.002 mL/beat at control to 0.071±0.003 mL/beat after nitro- l -arginine, while FFA uptake decreased from 0.1±0.01 to 0.06±0.01 μEq/beat, lactate uptake increased from 0.15±0.04 to 0.31±0.03 μmol/beat, glucose uptake increased from 8.2±5.0 to 35.4±9.5 μg/beat, and RQ increased by 23% (all P <0.05). Our results indicate that basal cardiac production of NO falls below normal levels during cardiac decompensation and that there are shifts in substrate utilization. This switch in myocardial substrate utilization also occurs after acute pharmacological blockade of NO production in normal dogs.

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Self-citation

Authors: Recchia, F. A., McConnell, P. I., Bernstein, R. D., Vogel, T. R., Xu, X., & Hintze, T. H.
Affiliations: New York Medical College (US)
ORCID: Recchia, Fabio A.
McConnell, Patrick I.
Xu, Xiaobin
Venue: Circulation Research
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 1998-11-16
Volume: 83
Issue: 10
Pages: 969-979
ISSN: 0009-7330 (ISSN-L)
1524-4571
DOI: 10.1161/01.res.83.10.969
OpenAlex: W2033767220
Cited by: 302
References: 59
Citations by year: 2026: 5 · 2025: 3 · 2024: 1 · 2023: 5 · 2022: 5 · 2021: 4 · 2020: 3 · 2019: 4 · 2018: 8 · 2017: 5 · 2016: 4 · 2015: 10 · 2014: 5 · 2013: 10 · 2012: 6
FWCI: 12.70
Type: journal article
Language: en
Open access: closed
Locations: Circulation Research (publishedVersion)
PubMed (publishedVersion)
CINECA IRIS Institutional Research Information System (Sant'Anna School of Advanced Studies) (submittedVersion)
Funders: Sarnoff Cardiovascular Research Foundation
National Heart, Lung, and Blood Institute (R01 HL 50142, P01 HL 43023)
Topics: Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Keywords: nitric oxide production, pacing-induced heart failure, myocardial metabolism, oxygen consumption, free fatty acid uptake, glucose uptake, lactate utilization, respiratory quotient, nitro-L-arginine, nitric oxide synthase inhibition, left ventricular end-diastolic pressure, coronary sinus blood flow, conscious dogs, heart failure decompensation, substrate utilization
MeSH terms: Animals, Blood Pressure, Carbon Dioxide, Consciousness, Diastole, Dogs, Fatty Acids, Nonesterified, Glucose, Heart Failure, Male, Myocardium, Nitric Oxide, Oxygen Consumption, Pacemaker, Artificial, Respiration, Systole, Muscle Fibers, Skeletal, Ventricular Dysfunction, Left, Nitric Oxide Synthase, Nitroarginine, Lactic Acid, Nitric Oxide Synthase Type II

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Reduced Nitric Oxide Production and Altered Myocardial Metabolism During the Decompensation of Pacing-Induced Heart Failure in the Conscious Dog

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