Cited by 462Cardiac Ischemia and ReperfusionNitric Oxide and Endothelin EffectsNeuroprotection in Cerebral Ischemia

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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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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 › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Life Sciences › Neuroscience › Neurology › Neuroprotection in Cerebral Ischemia
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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Nitric oxide in myocardial ischemia/reperfusion injury

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