ArticleTheoretical biology & medical modelling2014
Beneficial effects of inhaled NO on apoptotic pneumocytes in pulmonary thromboembolism model.
Article in Theoretical biology & medical modelling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Role of PKM2 Tetramer in Modulating Endothelial Mitochondrial Dysfunction in a Rat Model of Chronic Thromboembolic Pulmonary Hypertension.Physiological research · 2026Article
- Non-mechanical haemodynamic support in acute pulmonary thromboembolism: a scoping review.Intensive care medicine experimental · 2025Review
- Inhaled pulmonary vasodilators: a narrative review.Annals of translational medicine · 2021Review
- Association between ACE2/ACE balance and pneumocyte apoptosis in a porcine model of acute pulmonary thromboembolism with cardiac arrest.Molecular medicine reports · 2018Article
- Role of FoxO1 and apoptosis in pulmonary vascular remolding in a rat model of chronic thromboembolic pulmonary hypertension.Scientific reports · 2017Article
- Article
- Expression of tissue factor and forkhead box transcription factor O-1 in a rat model for chronic thromboembolic pulmonary hypertension.Journal of thrombosis and thrombolysis · 2016Article
- The role of tissue factor and autophagy in pulmonary vascular remodeling in a rat model for chronic thromboembolic pulmonary hypertension.Respiratory research · 2016Article
- Close concordance between pulmonary angiography and pathology in a canine model with chronic pulmonary thromboembolism and pathological mechanisms after lung ischemia reperfusion injury.Journal of thrombosis and thrombolysis · 2016Article
- Inflammatory response and pneumocyte apoptosis during lung ischemia-reperfusion injury in an experimental pulmonary thromboembolism model.Journal of thrombosis and thrombolysis · 2015Article
- Pulmonary vasodilation in acute pulmonary embolism - a systematic review.Pulmonary circulationReview
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLung ischemia-reperfusion injury (LIRI) may occur in the region of the affected lung after reperfusion therapy. Inhaled NO may be useful in treating acute and chronic pulmonary thromboembolism (PTE) due to the biological effect property of NO.
methodsA PTE canine model was established through selectively embolizing blood clots to an intended right lower lobar pulmonary artery. PaO2/FiO2, the mPAP and PVR were investigated at the time points of 2, 4, 6 hours after inhaled NO. Masson's trichrome stain, apoptotic pneumocytes and lung sample ultrastructure were also investigated among different groups.
resultsThe PaO2/FiO2 in the Inhaled NO group increased significantly when compared with the Reperfusion group at time points of 4 and 6 hours after reperfusion, mPAP decreased significantly at point of 2 hours and the PVR decreased significantly at point of 6 hours after reperfusion. The amounts of apoptotic type II pneumocytes in the lower lobar lung have negative correlation trend with the arterial blood PaO2/FiO2 in Reperfusion group and Inhaled NO group. Inhaled nitric oxide given at 20 ppm for 6 hours can significantly alleviate the LIRI in the model.
conclusionsDramatic physiological improvements are seen during the therapeutic use of inhaled NO in pulmonary thromboembolism canine model. Inhaled NO may be useful in treating LIRI in acute or chronic PTE by alleviating apoptotic type II pneumocytes. This potential application warrants further investigation.
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