ArticleThe Journal of thoracic and cardiovascular surgery2010
Activation of A1, A2A, or A3 adenosine receptors attenuates lung ischemia-reperfusion injury.
Article in The Journal of thoracic and cardiovascular surgery, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 63 citations in OpenAlex.
- Lung Ischemia-Reperfusion Injury in Lung Transplant Surgery: Where Do We Stand?Antioxidants (Basel, Switzerland) · 2025Review
- Activating A1 adenosine receptor signaling boosts early pulmonary neutrophil recruitment in aged mice in response to Streptococcus pneumoniae infection.Immunity & ageing : I & A · 2024Article
- Effect of adenosine treatment on ionizing radiation toxicity in zebrafish early life stages.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Article
- Adenosine AExperimental and therapeutic medicine · 2023Article
- The role of adenosine AInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- The potential of ex vivo lung perfusion on improving organ quality and ameliorating ischemia reperfusion injury.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2021Review
- Adenosine and ATPγS protect against bacterial pneumonia-induced acute lung injury.Scientific reports · 2020Article
- Review 2: Primary graft dysfunction after lung transplant-pathophysiology, clinical considerations and therapeutic targets.Journal of anesthesia · 2020Review
- Extracellular nucleotide signaling in solid organ transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020Review
- Increasing circulating sphingosine-1-phosphate attenuates lung injury during ex vivo lung perfusion.The Journal of thoracic and cardiovascular surgery · 2018Article
- Purinergic Regulation of Neutrophil Function.Frontiers in immunology · 2018Review
- Oxidative and nitrosative stress during pulmonary ischemia-reperfusion injury: from the lab to the OR.Annals of translational medicine · 2017Review
- Lung injury pathways: Adenosine receptor 2B signaling limits development of ischemic bronchiolitis obliterans organizing pneumonia.Experimental lung research · 2017Article
- Protein phosphatase 2A activation attenuates inflammation in murine models of acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Attenuation of Pulmonary Ischemia-Reperfusion Injury by Adenosine A2B Receptor Antagonism.The Annals of thoracic surgery · 2016Article
- Purinergic regulation of the immune system.Nature reviews. Immunology · 2016Review
- Ex Vivo Perfusion With Adenosine A2A Receptor Agonist Enhances Rehabilitation of Murine Donor Lungs After Circulatory Death.Transplantation · 2015Article
- Adenosine 2A receptor modulates inflammation and phenotype in experimental abdominal aortic aneurysms.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Adenosine A1 receptor activation attenuates lung ischemia-reperfusion injury.The Journal of thoracic and cardiovascular surgery · 2013Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectiveAdenosine and the activation of specific adenosine receptors are implicated in the attenuation of inflammation and organ ischemia-reperfusion injury. We hypothesized that activation of A(1), A(2A), or A(3) adenosine receptors would provide protection against lung ischemia-reperfusion injury.
methodsWith the use of an isolated, ventilated, blood-perfused rabbit lung model, lungs underwent 18 hours of cold ischemia followed by 2 hours of reperfusion. Lungs were administered vehicle, adenosine, or selective A(1), A(2A), or A(3) receptor agonists (CCPA, ATL-313, or IB-MECA, respectively) alone or with their respective antagonists (DPCPX, ZM241385, or MRS1191) during reperfusion.
resultsCompared with the vehicle-treated control group, treatment with A(1), A(2A), or A(3) agonists significantly improved function (increased lung compliance and oxygenation and decreased pulmonary artery pressure), decreased neutrophil infiltration by myeloperoxidase activity, decreased edema, and reduced tumor necrosis factor-alpha production. Adenosine treatment was also protective, but not to the level of the agonists. When each agonist was paired with its respective antagonist, all protective effects were blocked. The A(2A) agonist reduced pulmonary artery pressure and myeloperoxidase activity and increased oxygenation to a greater degree than the A(1) or A(3) agonists.
conclusionSelective activation of A(1), A(2A), or A(3) adenosine receptors provides significant protection against lung ischemia-reperfusion injury. The decreased elaboration of the potent proinflammatory cytokine tumor necrosis factor-alpha and decreased neutrophil sequestration likely contribute to the overall improvement in pulmonary function. These results provide evidence for the therapeutic potential of specific adenosine receptor agonists in lung transplant recipients.
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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.