ArticleBritish journal of pharmacology2003
Mechanisms of endothelial dysfunction after ionized radiation: selective impairment of the nitric oxide component of endothelium-dependent vasodilation.
Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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.
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Who cites it
29 citing papers in PubMed, 78 citations in OpenAlex.
- Review
- Vascular Toxicities of Cancer Therapies: 2025 Update.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Radiation-Induced Macrovessel/Microvessel Disease.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Oxidative and Nitrous Stress Underlies Vascular Malfunction Induced by Ionizing Radiation and Diabetes.Cardiovascular toxicology · 2024Review
- Short-Term Statin Treatment Reduces, and Long-Term Statin Treatment Abolishes, Chronic Vascular Injury by Radiation Therapy.Journal of the American Heart Association · 2024Article
- Luteolin target HSPB1 regulates endothelial cell ferroptosis to protect against radiation vascular injury.PloS one · 2024Article
- Radiation-induced skin reactions: oxidative damage mechanism and antioxidant protection.Frontiers in cell and developmental biology · 2024Review
- Mechanisms of Myocardial Ischemia in Cancer Patients: A State-of-the-Art Review of Obstructive Versus Non-Obstructive Causes.Reviews in cardiovascular medicine · 2022Review
- Lower endothelium-dependent microvascular function in adult breast cancer patients receiving radiation therapy.Cardio-oncology (London, England) · 2021Article
- A derivative of vitamin BScientific reports · 2021Article
- Vascular toxic effects of cancer therapies.Nature reviews. Cardiology · 2020Review
- The Role of NLRP3 Inflammasome in Radiation-Induced Cardiovascular Injury.Frontiers in cell and developmental biology · 2020Review
- Gene Activation as a Cell Protection Mechanism Against Gamma-Ray radiation.Journal of lasers in medical sciences · 2020Article
- Cancer and Coronary Artery Disease: Common Associations, Diagnosis and Management Challenges.Current treatment options in oncology · 2019Review
- Pathological effects of ionizing radiation: endothelial activation and dysfunction.Cellular and molecular life sciences : CMLS · 2019Review
- Radiation-Induced Cardiovascular Disease: Mechanisms and Importance of Linear Energy Transfer.Frontiers in cardiovascular medicine · 2018Review
- Flow Induced Microvascular Network Formation of Therapeutic Relevant Arteriovenous (AV) Loop-Based Constructs in Response to Ionizing Radiation.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- Altered Blood Flow Response to Small Muscle Mass Exercise in Cancer Survivors Treated With Adjuvant Therapy.Journal of the American Heart Association · 2017Article
- The Vitamin E Analog Gamma-Tocotrienol (GT3) Suppresses Radiation-Induced Cytogenetic Damage.Pharmaceutical research · 2016Article
- A Review of Radiation-Induced Coagulopathy and New Findings to Support Potential Prevention Strategies and Treatments.Radiation research · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
(1) Gamma radiation impairs vascular function, leading to the depression of endothelium-dependent vasodilatation. Loss of the nitric oxide (NO) pathway has been implicated, but little is known about radiation effects on other endothelial mediators. (2) This study investigated the mechanisms of endothelial dysfunction in rabbits subjected to whole-body irradiation from a cobalt(60) source. (3) The endothelium-dependent relaxation of rabbit aorta evoked by acetylcholine (ACh) or A23187 was impaired in a dose-dependent manner by irradiation at 2 Gy or above. Inhibition was evident 9 days post-irradiation and persisted over the 30 day experimental period. (4) Endothelium-independent responses to glyceryl trinitrate (GTN), sodium nitroprusside (SNP) and 3-morpholino-sydnonimine (SIN-1) were suppressed over a similar dose range at 7-9 days post-irradiation, but recovered fully by 30 days post-irradiation. (5) In healthy vessels, ACh-induced relaxation was inhibited by L-N(omega)-nitroarginine (L-NA; 3 x 10(-4) M) and charybdotoxin (10(-8) M) plus apamin (10(-6) M) but resistant to indomethacin, indicating the involvement of NO and endothelium-derived hyperpolarizing factor (EDHF). Supporting this, ACh caused smooth muscle hyperpolarization that was reduced by L-NA and charybdotoxin plus apamin. (6) In irradiated vessels, responses to ACh were insensitive to L-NA but abolished by charybdotoxin plus apamin, indicating selective loss of NO-mediated relaxation. (7) In animals treated shortly after irradiation with the antioxidant, alpha-tocopherol acetate, the NO-dependent relaxation was restored without effect on the EDHF-dependent component. (8) The results imply that radiation selectively impairs the NO pathway as a consequence of oxidative stress, while EDHF is able to maintain endothelium-dependent relaxation at a reduced level.
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Registered trials
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