Trial reportBritish journal of clinical pharmacology2007
Nitroglycerin protects the endothelium from ischaemia and reperfusion: human mechanistic insight.
Trial report in British journal of clinical pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Protective role of nitric oxide donors on endothelium in ischemia-reperfusion injury: a meta-analysis of randomized controlled trials.BMC anesthesiology · 2023Pooled it
- Passive heat therapy protects against endothelial cell hypoxia-reoxygenation via effects of elevations in temperature and circulating factors.The Journal of physiology · 2018Trial
- Acute (but not chronic) smoking paradoxically protects the endothelium from ischemia and reperfusion: insight into the "smoking paradox".Clinical research in cardiology : official journal of the German Cardiac Society · 2013Trial
- Daily ischemic preconditioning provides sustained protection from ischemia-reperfusion induced endothelial dysfunction: a human study.Journal of the American Heart Association · 2013Trial
- Chronic protection against ischemia and reperfusion-induced endothelial dysfunction during therapy with different organic nitrates.Clinical research in cardiology : official journal of the German Cardiac Society · 2012Trial
- Remote ischaemic preconditioning - translating cardiovascular benefits to humans.The Journal of physiology · 2022Review
- The Role of Nitroglycerin and Other Nitrogen Oxides in Cardiovascular Therapeutics.Journal of the American College of Cardiology · 2017Review
- Vasodilator Therapy: Nitrates and Nicorandil.Cardiovascular drugs and therapy · 2016Review
- Redox Roles of Reactive Oxygen Species in Cardiovascular Diseases.International journal of molecular sciences · 2015Review
- The use of regional cerebral oximetry monitoring during controlled hypotension: a case series.Journal of clinical monitoring and computing · 2014Article
- Reactive oxygen species and the cardiovascular system.Oxidative medicine and cellular longevity · 2013Review
- Model-based analysis of flow-mediated dilation and intima-media thickness.International journal of biomedical imaging · 2008Article
- Nitroglycerine causes mitochondrial reactive oxygen species production: in vitro mechanistic insights.The Canadian journal of cardiology · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsNitroglycerin (GTN) modulates tissue damage induced by ischaemia and reperfusion (IR) in a mechanism that is similar to ischaemic preconditioning. We set out to study, using a human model of endothelial IR injury, whether GTN-induced endothelial preconditioning is mediated by reactive oxygen species (ROS) formation and/or opening of mitochondrial permeability transition pores (mPTP).
methodsIn two double-blind, randomized, parallel studies, a total of 66 volunteers underwent measurement of radial artery endothelium-dependent, flow-mediated dilation (FMD) before and after local IR. Subjects were treated, 24 h before IR, with different drugs in order to test the mechanism of GTN-induced endothelial protection.
resultsTransdermal GTN (0.6 mg h(-1) for 2 h, administered 24 h before IR) significantly reduced the impairment of FMD caused by IR (placebo group: FMD after IR, 1.3 +/- 0.8%; GTN group: FMD after IR, 5.3 +/- 0.9%, P < 0.01 compared with placebo). This protective effect was lost when vitamin C (2 g i.v. at the time of GTN administration) or ciclosporin (an inhibitor of mPTP, 100 mg 2 h prior to GTN administration) were coadministered (FMD after IR: vit C + GTN group, 2.1 +/- 1.0%; ciclosporin + GTN group, 1.7 +/- 0.8%; both P < 0.05 compared with GTN alone).
conclusionsWe demonstrate that GTN protects the endothelium against IR-induced endothelial dysfunction, in an effect similar to delayed ischaemic preconditioning. Using a human model, we provide evidence supporting the concept that this protective effect is mediated by ROS release and mPTP opening upon GTN administration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.