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

The DOI matches its Crossref record; 59 of the 59 references it cites were found in a registry or an index.

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
Open this paper in CoChat — free account

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 Every week, hemodynamic measurements were recorded and blood samples were withdrawn from the aorta and the coronary sinus for measurement of NO metabolites, O 2 content, free fatty acids (FFAs), and lactate and glucose concentrations.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.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1161/01.res.83.10.969

Cites

59 of 59 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 59 references

Research works printed but not linked: 21

  1. 10.1161/circ.92.8.2198 · DOI
  2. 10.1161/res.75.4.7923615 · DOI
  3. 10.1161/hyp.30.1.50 · DOI
  4. 10.1161/circ.94.1.44 · DOI
  5. 10.1161/res.78.1.58 · DOI
  6. 10.1161/res.79.3.381 · DOI
  7. 10.1161/res.79.4.840 · DOI
  8. 10.1161/circ.91.12.2982 · DOI
  9. Oser BL. Hawks Physiological Chemistry. 14th ed. New York NY: McGraw-Hill Publishing Co; 1965:900–905.
  10. 10.1161/circ.93.6.1223 · DOI
  11. 10.1161/circ.88.1.8391403 · DOI
  12. Rose CP Goresky CA. Interactions between capillary exchange cellular entry and metabolic sequestration processes in the heart. In: Renkin EM Michel CC eds. Handbook of Physiology: The Cardiovascular System Microcirculation. Bethesda Md: American Physiological Society; 1984:781–798.
  13. 10.1161/res.74.5.8156644 · DOI
  14. 10.1161/circ.96.4.1320 · DOI
  15. 10.1161/circ.89.5.7910117 · DOI
  16. 10.1161/circ.95.1.176 · DOI
  17. 10.1161/res.70.3.1311222 · DOI
  18. 10.1161/circ.93.5.932 · DOI
  19. 10.1161/res.77.1.88 · DOI
  20. Stone CK, Holden J, Stanley WC, Perlman SB. Effect of substrate availability upon cardiac glucose uptake. J Nucl Med. 1995;36:996–1002.
  21. 10.1161/circ.94.11.2837 · DOI

Cited by

Sorted by citations

Items 201–300 of 301

Related

See all

Metadata

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
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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review