CoChat
Sign Up
Cited by 59Cardiac Ischemia and ReperfusionCardiac Imaging and DiagnosticsCardiovascular Function and Risk Factors

Glutamate degradation in the ischemic dog heart — contribution to anaerobic energy-production

Wiesner, R·1989·Journal of Molecular and Cellular Cardiology
DOI 10.1016/0022-2828(89)91492-2
Open this paper in CoChat — free account

Abstract

The present study investigated the conversion of amino acids to succinate and the contribution of this pathway to anaerobic energy production during regional ischemia in the dog heart in situ. The relation between regional myocardial blood flow, estimated by the tracer microsphere technique, and myocardial contents of metabolites (glutamate, alanine, succinate, lactate) as well as their local arterio-venous differences (A-V) were determined. During 30 min of coronary artery occlusion, myocardial glutamate decreased from 2.3 mumol/g wet wt in control tissue to 1.2 mumol/g wet wt in severely ischemic areas, while aspartate was unaffected. Myocardial alanine increased in a 1: 1 stoichiometry compared to glutamate, and succinate accumulated. During control perfusion (118 mmHg), A-V of lactate, succinate and glutamate were +470, -0.7 and -3.9 nmol/ml, respectively. Stepwise reduction of perfusion pressure led to the release of lactate and succinate from the underperfused area; extraction of glutamate occurred at the lowest perfusion pressure investigated (34 mmHg; A-V: -500, -10.4 and +4.2 nmol/ml, respectively). The data indicate that during regional ischemia in vivo, succinate is synthetized exclusively from glutamate via 2-oxo-glutarate, following transamination with glycolytic pyruvate yielding alanine, while the contribution of aspartate is negligible. Using tissue levels of glutamate and lactate together with the local arterio-venous concentration differences of these compounds, it can be estimated that degradation of glutamate delivers 20% of the ATP generated by substrate level phosphorylation reactions. Thus energy production by the glutamate degradation pathway is significant in vivo under conditions of flow deprivation.

Integrity signals

Registry

Crossref · 10.1016/0022-2828(89)91492-2

Cites

24 of 24 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

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?

  • The increased succinate pool under hypoxia may come from glutamate via alpha-ketoglutarate by transamination or from partial reversal of the TCA cycle from malate through fumarate, which would require complex II to act as a fumarate reductase.

    “This increased succinate pool under hypoxia might be supplied either from glutamate through α-ketoglutarate by transamination [76,77] or by a partial reversal of the TCA cycle from malate through fumarate, which requires that complex II would become a fumarate reductase under hypoxia [36,79].”

    From Differential effects of complex II on mitochondrial ROS production and their relation to cardioprotective pre- and postconditioning (2013) · cites this paper as [77]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Related

Authors
Wiesner, R.
Affiliations
Heinrich Heine University Düsseldorf (DE)
Corresponding author
Wiesner, R
ORCID
Wiesner, R
Venue
Journal of Molecular and Cellular Cardiology
Publisher
Elsevier BV
Published
1989-01
Volume
21
Issue
1
Pages
49-59
ISSN
0022-2828 (ISSN-L)
DOI
10.1016/0022-2828(89)91492-2
OpenAlex
W1998193909
Cited by
59
References
24
Citations by year
2026: 1 · 2025: 2 · 2020: 2 · 2018: 1 · 2017: 1 · 2016: 3 · 2015: 1 · 2014: 2 · 2013: 2 · 2012: 2
FWCI
2.54
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Journal of Molecular and Cellular Cardiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
  • Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Cardiac Imaging and Diagnostics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
Keywords
glutamate degradation, myocardial ischemia, anaerobic energy production, alpha-ketoglutarate, alanine, aspartic acid, lactate, substrate-level phosphorylation, coronary artery occlusion, myocardial blood flow, arteriovenous differences, myocardial metabolism, perfusion pressure
MeSH terms
Adenosine Triphosphate, Anaerobiosis, Animals, Coronary Disease, Dogs, Energy Metabolism, Glutamates, Lactates, Myocardium, Oxygen Consumption, Glutamic Acid, Lactic Acid

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