Nitric oxide in myocardial ischemia/reperfusion injury

Schulz, R

doi:10.1016/j.cardiores.2003.09.019

Cited by 462Cardiac Ischemia and ReperfusionNitric Oxide and Endothelin EffectsNeurological Disorders and Treatments

Nitric oxide in myocardial ischemia/reperfusion injury

Schulz, R·2004·Cardiovascular Research

DOI 10.1016/j.cardiores.2003.09.019

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Abstract

Administration of nitric oxide (NO), NO donors or drugs that enhance NO release (statins, calcium antagonists, ACE-inhibitors, dexamethasone) prior to ischemia protects the myocardium against ischemia/reperfusion injury. While this exogenous administration of NO prior to ischemia can initiate a preconditioning-like phenomenon, endogenous NO-synthase (NOS)-derived NO is not involved in triggering or mediating the early phase of ischemic preconditioning's protection, but does play a pivotal role for initiating and mediating the delayed phase of ischemic preconditioning's protection. The present review now summarizes the importance of endogenous and exogenous NO when given at the time of reperfusion for vascular and myocardial function and morphological outcome following ischemia/reperfusion. Given the inconsistency of the published data, potential confounding factors that might affect experimental results on the role of NO in myocardial ischemia/reperfusion were identified, such as (1) the lack of characterization of the involved NOS isoforms in myocardial ischemia/reperfusion injury in different animal species, (2) the lack of direct measurements of myocardial NO concentration and/or NOS activity to assure sufficient NOS inhibition, (3) the lack of consideration of nonenzymatic NO production as a potential source of NO, and (4) the absence of plasma or blood components in in vitro studies influencing NO delivery and metabolism. Future research on the importance of NO in ischemia/reperfusion injury will have to focus more precisely on the identification and standardization of potential confounding experimental factors that influence synthesis, transport, and interaction of NO with various targets in blood and tissue.

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Subsequent studies with beetroot juice as the nitrate source, as well as sodium nitrate salt, confirmed and extended these results.
“Subsequent studies have confirmed and extended these results with beetroot juice as the nitrate source, as well as sodium nitrate salt.120,129 -131”
From Nitrate-Nitrite-Nitric Oxide Pathway: Implications for Anesthesiology and Intensive Care (2010) · cites this paper as [130]
There were no effects of any of the interventions on diastolic BP in the spinach/apple study.
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Ingestion of 200 g spinach containing 3 mmol nitrate significantly reduced systolic BP, but not when spinach and apple interventions were given simultaneously.
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Endogenous nitric oxide (NO) protects against ischaemia-reperfusion injury in the rabbit
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Inhibition of nitric oxide synthesis does not affect ischemic preconditioning in isolated perfused rat hearts
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No Involvement of Endogenous Nitric Oxide In Classical Ischemic Preconditioning in Swine
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The cardioprotective and mitochondrial depolarising properties of exogenous nitric oxide in mouse heart
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Intra-coronary administration of ?-arginine aggravates myocardial stunning through production of peroxynitrite in dogs
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Expression of an endothelial-type nitric oxide synthase isoform in human neutrophils: modification by tumor necrosis factor-alpha and during acute myocardial infarction
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Transcription activator protein 1 (AP‐1) mediates NO‐induced apoptosis of adult cardiomyocytes
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Kinin-Mediated Coronary Nitric Oxide Production Contributes to the Therapeutic Action of Angiotensin-Converting Enzyme and Neutral Endopeptidase Inhibitors and Amlodipine in the Treatment in Heart Failure
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L-Arginine reverses low coronary reflow and enhances postischaemic recovery of cardiac mechanical function
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Inhibition of nitric oxide synthesis protects the isolated working rabbit heart from ischaemia-reperfusion injury*1
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TNF-α antibodies are as effective as ischemic preconditioning in reducing infarct size in rabbits
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Delayed Enhanced Nitric Oxide–Mediated Coronary Vasodilation Following Brief Ischemia and Prolonged Reperfusion in Conscious Dogs
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Experimental hypothermia and rewarming: changes in mechanical function and metabolism of rat hearts
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Adenosine production and its interaction with protection of ischemic and reperfusion injury of the myocardium
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The protective effect of L-arginine on myocardial injury and endothelial function following ischaemia and reperfusion in the pig
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Nitric oxide synthase inhibitors decrease coronary sinus-free radical concentration and ameliorate myocardial stunning in an ischemia-reperfusion model
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Effects of l-Arginine and l-nitro-arginine methyl ester on recovery of neonatal lamb hearts after cold ischemia
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Bradykinin Protects Against Infarction but Does not Mediate Ischemic Preconditioning in the Isolated Rat Heart
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Intracoronary nitric oxide improves postischemic coronary blood flow and myocardial contractile function
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Effect of nitrovasodilators and inhibitors of nitric oxide synthase on ischaemic and reperfusion function of rat isolated hearts
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Effect of Endogenous Nitric Oxide on Cardiac Systolic and Diastolic Function During Ischemia and Reperfusion in the Rat Isolated Perfused Heart
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Endogenous Protection Against Reperfusion-induced Ventricular Fibrillation: Role of Neuronal versus Non-neuronal Sources of Nitric Oxide and Species Dependence in the Rat versus Rabbit Isolated Heart
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Deletion of Endothelial Nitric Oxide Synthase Exacerbates Myocardial Stunning in an Isolated Mouse Heart Model
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Comparison of tumor necrosis factor-α effect on the expression of iNOS in macrophage and cardiac myocytes
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Prostacyclin rather than endogenous nitric oxide is a tissue protective factor in myocardial ischemia
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Cardioprotective activity of endogenous and exogenous nitric oxide on ischaemia reperfusion injury in isolated guinea pig hearts
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Role of Cellular Acidosis in Production of Nitric Oxide in Canine Ischemic Myocardium
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Cholinergic and alpha-adrenergic coronary vasomotion [corrected] with increasing ischemia-reperfusion injury
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Effect of endogenous nitric oxide on energy metabolism of rat heart mitochondria during ischemia and reperfusion
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Nitrous Oxide Impairs Functional Recovery of Stunned Myocardium in Barbiturate-Anesthetized, Acutely Instrumented Dogs
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No involvement of nitric oxide in the limitation of β-adrenergic inotropic responsiveness during ischemia
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Inhibition of apoptotic responses after ischemic stress in isolated hearts and cardiomyocytes
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Nifedipine limits infarct size via NO-dependent mechanisms in dogs
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Intra-coronary administration of L-arginine aggravates myocardial stunning through production of peroxynitrite in dogs
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Sodium Nitroprusside Exacerbates Myocardial Ischemia–Reperfusion Injury
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INHIBITION OF NITRIC OXIDE DOES NOT AFFECT REPERFUSION-INDUCED MYOCARDIAL INJURY, BUT IT PREVENTS LIPID PEROXIDATION IN THE ISOLATED RAT HEART
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Activation of myocardial constitutive nitric oxide synthase during coronary artery surgery
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Positive inotropy due to lowering cyclic GMP is also mediated by increases in cyclic AMP in control and hypertrophic hearts
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Cyclic GMP Reduces Ventricular Myocyte Stunning after Simulated Ischemia–Reperfusion
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Intracoronary SIN-1C During Reperfusion Reduces Infarct Size in Dog
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Simultaneous manipulation of the nitric oxide and prostanoid pathways reduces myocardial reperfusion injury
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Reperfusion injury and reactive oxygen species: The evolution of a concept
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Myocardial ischaemia–reperfusion injury and cardioprotection in perspective
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Nitric oxide signaling in health and disease
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Sepsis and the Heart
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Nitrite is a signaling molecule and regulator of gene expression in mammalian tissues
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High-Density Lipoproteins and Their Constituent, Sphingosine-1-Phosphate, Directly Protect the Heart Against Ischemia/Reperfusion Injury In Vivo via the S1P 3 Lysophospholipid Receptor
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The role of the mitochondrial permeability transition pore in heart disease
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The Role of Oxidative Stress in Myocardial Ischemia and Reperfusion Injury and Remodeling: Revisited
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Proanthocyanidins, anthocyanins and cardiovascular diseases
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Ischemia reperfusion injury, ischemic conditioning and diabetes mellitus
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Nitric oxide-releasing vehicles for biomedical applications
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Nitric oxide and cardiac function
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Recent developments of fluorescent probes for the detection of gasotransmitters (NO, CO and H2S)
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Self-citation
Molecular Characterization of Reactive Oxygen Species in Myocardial Ischemia-Reperfusion Injury
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Near-Infrared Photoactivatable Nitric Oxide Donors with Integrated Photoacoustic Monitoring
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Role of the anion nitrite in ischemia-reperfusion cytoprotection and therapeutics
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Role of the nitric oxide pathway in AMPK-mediated glucose uptake and GLUT4 translocation in heart muscle
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Endogenous hydrogen sulfide contributes to the cardioprotection by metabolic inhibition preconditioning in the rat ventricular myocytes
Pan, T., Feng, Z.-N., Lee, S. W., Moore, P. K., & Bian, J. (2005) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2005.10.003 · Cited by 196 · see citing works
Nitric Oxide Mechanism of Protection in Ischemia and Reperfusion Injury
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Therapeutic effects of inorganic nitrate and nitrite in cardiovascular and metabolic diseases
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Insulin says NO to cardiovascular disease
Yu, Q., Gao, F., & Ma, X. L. (2011) · Cardiovascular Research · doi:10.1093/cvr/cvq349 · Cited by 172 · see citing works
The cellular mechanisms of the antiemetic action of dexamethasone and related glucocorticoids against vomiting
Chu, C., Hsing, C., Shieh, J., Chien, C.-C., Ho, C., & Wang, J.-J. (2013) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2013.10.008 · Cited by 172 · see citing works
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Authors: Schulz, R.
Affiliations: Essen University Hospital (DE)
Corresponding author: Schulz, R
ORCID: Schulz, R
Venue: Cardiovascular Research
Publisher: Oxford University Press (OUP)
Published: 2004-02-15
Volume: 61
Issue: 3
Pages: 402-413
ISSN: 0008-6363 (ISSN-L)
DOI: 10.1016/j.cardiores.2003.09.019
OpenAlex: W2119416582
Cited by: 462
References: 139
Citations by year: 2026: 10 · 2025: 10 · 2024: 12 · 2023: 19 · 2022: 11 · 2021: 17 · 2020: 16 · 2019: 19 · 2018: 24 · 2017: 16 · 2016: 20 · 2015: 24 · 2014: 20 · 2013: 28 · 2012: 20
FWCI: 10.71
Type: journal article
Language: en
Open access: closed
Locations: Cardiovascular Research (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
Keywords: nitric oxide, myocardial ischemia-reperfusion injury, ischemic preconditioning, nitric oxide synthase isoforms, statins, calcium channel blockers, ACE inhibitors, dexamethasone, nitric oxide synthase inhibition
MeSH terms: Animals, Hypoxia, Endothelium, Vascular, Humans, Mammals, Myocardial Contraction, Nitric Oxide, Myocardial Reperfusion Injury, Apoptosis, Nitric Oxide Synthase, Nitric Oxide Donors, Models, Animal, Myocytes, Cardiac

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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.

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Nitric oxide in myocardial ischemia/reperfusion injury

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