The DOI matches its Crossref record; 137 of the 139 references it cites were found in a registry or an index.
Nitric oxide in myocardial ischemia/reperfusion injury
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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“In these studies, oxygen cost was also reduced during maximal performance, and time-to-exhaustion was significantly extended after beetroot juice.”
From Nitrate-Nitrite-Nitric Oxide Pathway: Implications for Anesthesiology and Intensive Care (2010) · cites this paper as [130]
In the citing paper
“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]
In the citing paper
“There were no effects of any of the interventions on DBP.”
From The effects of dietary nitrate on blood pressure and endothelial function: a review of human intervention studies (2013) · cites this paper as [92]
In the citing paper
“The study showed a significant reduction in SBP with 200 g spinach containing 3 mmol nitrate, but not when spinach and apple interventions were given simultaneously (92) .”
From The effects of dietary nitrate on blood pressure and endothelial function: a review of human intervention studies (2013) · cites this paper as [92]
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Metadata
- 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)
- 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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