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The doctor touching the human lung system on blurred background

<a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Luis+Michel+Alonso+Martinez&amp;sort=date&amp;sort_order=desc" href="https://pubmed.ncbi.nlm.nih.gov/?term=Luis+Michel+Alonso+Martinez&amp;sort=date&amp;sort_order=desc" target="_blank" rel="noopener">Luis Michel Alonso Martinez</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Harel+F&amp;cauthor_id=38097449" href="https://pubmed.ncbi.nlm.nih.gov/?term=Harel+F&amp;cauthor_id=38097449" target="_blank" rel="noopener">François Harel</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Nguyen+QT&amp;cauthor_id=30388434" href="https://pubmed.ncbi.nlm.nih.gov/?term=Nguyen+QT&amp;cauthor_id=30388434" target="_blank" rel="noopener">Quang T. Nguyen</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=L%C3%A9tourneau+M&amp;cauthor_id=30388434" href="https://pubmed.ncbi.nlm.nih.gov/?term=L%C3%A9tourneau+M&amp;cauthor_id=30388434" target="_blank" rel="noopener">Myriam Létourneau</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=D%27Oliviera-Sousa+C&amp;cauthor_id=30388434" href="https://pubmed.ncbi.nlm.nih.gov/?term=D%27Oliviera-Sousa+C&amp;cauthor_id=30388434" target="_blank" rel="noopener">Caroline D'Oliviera-Sousa</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Meloche+B&amp;cauthor_id=30388434" href="https://pubmed.ncbi.nlm.nih.gov/?term=Meloche+B&amp;cauthor_id=30388434" target="_blank" rel="noopener">Bernard Meloche</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Finnerty+V&amp;cauthor_id=30388434" href="https://pubmed.ncbi.nlm.nih.gov/?term=Finnerty+V&amp;cauthor_id=30388434" target="_blank" rel="noopener">Vincent Finnerty</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Fournier+A&amp;cauthor_id=30388434" href="https://pubmed.ncbi.nlm.nih.gov/?term=Fournier+A&amp;cauthor_id=30388434" target="_blank" rel="noopener">Alain Fournier</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Dupuis+J&amp;cauthor_id=30388434" href="https://pubmed.ncbi.nlm.nih.gov/?term=Dupuis+J&amp;cauthor_id=30388434" target="_blank" rel="noopener">Jocelyn Dupuis</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=DaSilva+JN&amp;cauthor_id=30388434" href="https://pubmed.ncbi.nlm.nih.gov/?term=DaSilva+JN&amp;cauthor_id=30388434" target="_blank" rel="noopener">Jean N. DaSilva</a>.PMID: 30388434 DOI: <a data-mce-href="https://doi.org/10.1016/j.nucmedbio.2018.10.003" href="https://doi.org/10.1016/j.nucmedbio.2018.10.003" target="_blank" rel="noopener">10.1016/j.nucmedbio.2018.10.003</a><h3>Abstract</h3>Introduction Adrenomedullin receptors are highly expressed in human alveolar capillaries and provide a molecular target for imaging the integrity of pulmonary microcirculation. In this work, we aimed to develop a NOTA-derivatized adrenomedullin analog (DFH17), radiolabeled with [18F]AlF, for PET imaging of pulmonary microcirculation.Methods Highly concentrated [18F](AlF)2+ (15 μL) was produced from purified fluorine-18 in NaCl 0.9%. Various complexation experiments were carried out at Al-to-NOTA molar ratios ranging from 1:1 to 1:40 to assess optimal radiolabeling conditions before using the peptide. DFH17 peptide (2 mM, pH 4) was radiolabeled with [18F](AlF)2+ for 15 min at 100 °C in a total volume of 60 μL. As part of the radiolabeling process, parameters such as fluorine-18 activity (~37 and 1480 MBq), concentration of AlCl3 (0.75, 2, 3, 6 or 10 mM) and the effects of hydrophilic organic solvent (aqueous vs ethanol 50%) were studied. The final formulation was tested for purity, identity and stability in saline. Initial in vivo evaluation of [18F]AlF-DFH17 was performed in normal rats by PET/CT.Results The scaled-up production of [18F]AlF-DFH17 was performed in high radiochemical and chemical purities in an overall radiochemical yield of 22–38% (at end-of-synthesis) within 60 min. The final formulation was stable in saline at different radioactive concentrations for 8 h. PET evaluation in rats revealed high lung-to-background ratios and no defluorination in vivo up to 1 h post-injection.Conclusion The novel radioconjugate [18F]AlF-DFH17 appears to be a promising PET ligand for pulmonary microcirculation imaging. <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/30388434/" href="https://pubmed.ncbi.nlm.nih.gov/30388434/" target="_blank" rel="noopener">Full article</a>

Al[18F]F-complexation of DFH17, a NOTA-conjugated adrenomedullin analog, for PET imaging of pulmonary circulation

Doctor use stethoscope checkup lung health,respiratory disease,lung cancer,bronchitis,Bronchial Asthma,Tuberculosis,pneumonia,asthma,air pollution pm2.5.insurance and hospital.world no tobacco day

<a data-mce-href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Nguyen%20Q" href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Nguyen%20Q" target="_blank" rel="noopener">Quang T Nguyen</a>, <a data-mce-href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Nsaibia%20M" href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Nsaibia%20M" target="_blank" rel="noopener">Mohamed J Nsaibia</a>, <a data-mce-href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Sirois%20M" href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Sirois%20M" target="_blank" rel="noopener">Martin G Sirois</a>, <a data-mce-href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Calderone%20A" href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Calderone%20A" target="_blank" rel="noopener">Angelino Calderone</a>, <a data-mce-href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Tardif%20J" href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Tardif%20J" target="_blank" rel="noopener">Jean-Claude Tardif</a>, <a data-mce-href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Fen%20Shi%20Y" href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Fen%20Shi%20Y" target="_blank" rel="noopener">Yan Fen Shi</a>, <a data-mce-href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Ruiz%20M" href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Ruiz%20M" target="_blank" rel="noopener">Matthieu Ruiz</a>, <a data-mce-href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Daneault%20C" href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Daneault%20C" target="_blank" rel="noopener">Caroline Daneault</a>, <a data-mce-href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Gagnon%20L" href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Gagnon%20L" target="_blank" rel="noopener">Lyne Gagnon</a>, <a data-mce-href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Grouix%20B" href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Grouix%20B" target="_blank" rel="noopener">Brigitte Grouix</a>,<a data-mce-href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Laurin%20P" href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Laurin%20P" target="_blank" rel="noopener">Pierre Laurin</a>,<a data-mce-href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Dupuis%20J" href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&amp;term=Dupuis%20J" target="_blank" rel="noopener"> Jocelyn Dupuis</a>. Cardiovascular Research, Volume 116, Issue 1, 1 January 2020, Pages 171–182, <a data-mce-href="https://doi.org/10.1093/cvr/cvz034" href="https://doi.org/10.1093/cvr/cvz034" target="_blank" rel="noopener">https://doi.org/10.1093/cvr/cvz034</a> Published: 07 February 2019 Article historyReceived: 20 September 2018 Revision received: 15 January 2019 Accepted: 06 February 2019 Published: 07 February 2019 <h2>Abstract</h2> Aims Heart failure with reduced ejection fraction (HFrEF) causes lung remodelling with myofibroblasts proliferation and fibrosis leading to a restrictive lung syndrome with pulmonary hypertension (PH) and right ventricular (RV) dysfunction. PBI-4050 is a first-in-class anti-fibrotic, anti-inflammatory, and anti-proliferative compound. The present study evaluated the therapeutic impact of PBI-4050 on PH in an HFrEF model.Methods and results HFrEF was induced after myocardial infarction (MI) in rats. Two weeks later, sham-operated and MI groups received PBI-4050 (200 mg/kg/day by gavage) or saline for 3 weeks. Animals were analysed according to infarct size as large (≥30% left ventricle) or medium MI (&lt;30%). Large MI caused PH and RV hypertrophy (RVH) with a restrictive lung syndrome. PBI-4050 did not adversely affect left ventricular (LV) function but markedly reduced PH and RVH and improved RV dysfunction. PBI-4050 reduced lung remodelling and improved respiratory compliance with decreased lung fibrosis, alveolar wall cellular proliferation and α-smooth muscle actin expression. The increased expression of endothelin-1 (ET-1), transforming growth factor beta (TGF-β), interleukin-6 (IL-6) and of tissue inhibitor of metalloprotease-1 in the lungs from HFrEF were reduced with PBI-4050 therapy. Activation of isolated human lung fibroblasts (HLFs) to a myofibroblastic pro-fibrogenic phenotype was markedly reduced by PBI-4050. The fatty acid receptor GPR84 was increased in HFrEF lungs and in activated HLFs, and reduced by PBI-4050. GPR84 agonists activated fibrogenesis in HLFs and finally, PBI-4050 reduced ERK1/2 phosphorylation.Conclusions PBI-4050 reduces PH and RVH in HFrEF by decreasing lung fibrosis and remodelling. This novel agent decreases the associated restrictive lung syndrome and recovers RV function. A contributing mechanism involves reducing the activation of lung fibroblasts by IL-6, TGF-β, and ET-1 by antagonism of GPR84 and reduced ERK1/2 phosphorylation. PBI-4050 is a novel promising therapy for targeting lung remodelling in group II PH.<a data-mce-href="https://academic.oup.com/cardiovascres/article-abstract/116/1/171/5308607?redirectedFrom=fulltext" href="https://academic.oup.com/cardiovascres/article-abstract/116/1/171/5308607?redirectedFrom=fulltext" target="_blank" rel="noopener">Full Article</a>

PBI-4050 reduces pulmonary hypertension, lung fibrosis, and right ventricular dysfunction in heart failure

<a data-mce-href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Fran_ois-Harel-Aff1-Aff2" href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Fran_ois-Harel-Aff1-Aff2" target="_blank" rel="noopener">François Harel</a>, <a data-mce-href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Quang_T_-Nguyen-Aff1" href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Quang_T_-Nguyen-Aff1" target="_blank" rel="noopener">Quang T. Nguyen</a>, <a data-mce-href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Mohamed_J_-Nsaibia-Aff1" href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Mohamed_J_-Nsaibia-Aff1" target="_blank" rel="noopener">Mohamed J. Nsaibia</a>, <a data-mce-href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Vincent-Finnerty-Aff1" href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Vincent-Finnerty-Aff1" target="_blank" rel="noopener">Vincent Finnerty</a>, <a data-mce-href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Arielle-Morgan-Aff1" href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Arielle-Morgan-Aff1" target="_blank" rel="noopener">Arielle Morgan</a>, <a data-mce-href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Martin-Sirois-Aff1-Aff3" href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Martin-Sirois-Aff1-Aff3" target="_blank" rel="noopener">Martin Sirois</a>, <a data-mce-href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Louis-Villeneuve-Aff1" href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Louis-Villeneuve-Aff1" target="_blank" rel="noopener">Louis Villeneuve</a>, <a data-mce-href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Angelino-Calderone-Aff1-Aff3" href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Angelino-Calderone-Aff1-Aff3" target="_blank" rel="noopener">Angelino Calderone</a>, <a data-mce-href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Alexandre-Bergeron-Aff1" href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Alexandre-Bergeron-Aff1" target="_blank" rel="noopener">Alexandre Bergeron</a>, <a data-mce-href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Emmanuelle-Brochiero-Aff4-Aff5" href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Emmanuelle-Brochiero-Aff4-Aff5" target="_blank" rel="noopener">Emmanuelle Brochiero</a>, <a data-mce-href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Jean_Claude-Tardif-Aff1-Aff4" href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Jean_Claude-Tardif-Aff1-Aff4" target="_blank" rel="noopener">Jean-Claude Tardif</a>, <a data-mce-href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-YanFen-Shi-Aff1" href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-YanFen-Shi-Aff1" target="_blank" rel="noopener">YanFen Shi</a> &amp;&nbsp;<a href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Jocelyn-Dupuis-Aff1-Aff4" target="_blank" rel="noopener" data-mce-href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#auth-Jocelyn-Dupuis-Aff1-Aff4">Jocelyn Dupuis</a> <a data-mce-href="https://respiratory-research.biomedcentral.com/" href="https://respiratory-research.biomedcentral.com/" target="_blank" rel="noopener">Respiratory Research</a> volume 22, Article number: 240 (2021) <a data-mce-href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#citeas" href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3#citeas" target="_blank" rel="noopener">Cite this article</a> 2327 Accesses | 2 Citations | 2 Altmetric | <a data-mce-href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3/metrics" href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3/metrics" target="_blank" rel="noopener">Metricsdetails</a><h2>Abstract</h2> Background Pulmonary hypertension (PH) complicating idiopathic pulmonary fibrosis (IPF) is associated to worse outcome. There is a great need for a non-invasive diagnostic modality to detect and evaluate the severity of pulmonary vascular disease (PVD). 99mTc-PulmoBind is a novel imaging agent that binds to the adrenomedullin (AM) receptor on the pulmonary microvascular endothelium. SPECT imaging employing the endothelial cell tracer 99mTc-PulmoBind was used to assess PVD associated with lung fibrosis.Methods Rats with selective right lung bleomycin-induced fibrosis were compared to control rats. SPECT imaging was performed after three weeks with 99mTc-PulmoBind and 99mTc-macroaggregates of albumin (MAA). PH and right ventricular (RV) function were assessed by echocardiography. Lung perfusion was evaluated by fluorescent microangiography. Lung AM receptor expression was measured by qPCR and by immunohistology. Relevance to human IPF was explored by measuring AM receptor expression in lung biopsies from IPF patients and healthy controls.Results The bleomycin group developed preferential right lung fibrosis with remodeling and reduced perfusion as assessed with fluorescent microangiography. These rats developed PH with RV hypertrophy and dysfunction. 99mTc-PulmoBind uptake was selectively reduced by 50% in the right lung and associated with reduced AM receptor expression, PH and RV hypertrophy. AM receptor was co-expressed with the endothelial cell protein CD31 in alveolar capillaries, and markedly reduced after bleomycin. Quantitative dynamic analysis of 99mTc-PulmoBind uptake in comparison to 99mTc-MAA revealed that the latter distributed only according to flow, with about 60% increased left lung uptake while left lung uptake of 99mTc-PulmoBind was not affected. Lung from human IPF patients showed important reduction in AM receptor expression closely associated with CD31.Conclusions SPECT imaging with 99mTc-PulmoBind detects PVD and its severity in bleomycin-induced lung fibrosis. Reduced AM receptor expression in human IPF supports further clinical development of this imaging approach. <a data-mce-href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3" href="https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-021-01836-3" target="_blank" rel="noopener" data-mce-selected="inline-boundary">Full Article</a>

SPECT imaging of pulmonary vascular disease in bleomycin-induced lung fibrosis using a vascular endothelium tracer

Human heart, 3d rendering, medically accurate illustration of the human heart anatomy  with venous system

<a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Jiang+BH&amp;cauthor_id=20537565" href="https://pubmed.ncbi.nlm.nih.gov/?term=Jiang+BH&amp;cauthor_id=20537565" target="_blank" rel="noopener">Bao Hua Jiang</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Nguyen+QT&amp;cauthor_id=20537565" href="https://pubmed.ncbi.nlm.nih.gov/?term=Nguyen+QT&amp;cauthor_id=20537565" target="_blank" rel="noopener">Quang Trinh Nguyen</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Tardif+JC&amp;cauthor_id=20537565" href="https://pubmed.ncbi.nlm.nih.gov/?term=Tardif+JC&amp;cauthor_id=20537565" target="_blank" rel="noopener">Jean-Claude Tardif</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Shi+Y&amp;cauthor_id=20537565" href="https://pubmed.ncbi.nlm.nih.gov/?term=Shi+Y&amp;cauthor_id=20537565" target="_blank" rel="noopener">Yanfen Shi</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Dupuis+J&amp;cauthor_id=20537565" href="https://pubmed.ncbi.nlm.nih.gov/?term=Dupuis+J&amp;cauthor_id=20537565" target="_blank" rel="noopener">Jocelyn Dupuis</a>Affiliations ExpandPMID: 20537565 DOI: <a data-mce-href="https://doi.org/10.1016/j.carpath.2010.04.005" href="https://doi.org/10.1016/j.carpath.2010.04.005" target="_blank" rel="noopener">10.1016</a>/<a data-mce-href="https://doi.org/10.1016/j.carpath.2010.04.005" href="https://doi.org/10.1016/j.carpath.2010.04.005" target="_blank" rel="noopener">j.carpath.2010.04.005</a> Abstract Background: Early prediction of infarct size and of the subsequent development of congestive heart failure (CHF) and pulmonary hypertension (PH) would be useful in therapeutic trials using the rat myocardial infarction (MI) model.Methods: A total of 194 rats were subjected to MI or sham surgery, and plasma cardiac troponin T (cTnT) was measured 24 h after surgery in rats. Echocardiography was performed after 2 and 5 weeks. Hemodynamic and morphometric parameters were evaluated 5 weeks after MI.Results: cTnT had strong positive correlations with left ventricular (LV) wall motion abnormalities at 2 and 5 weeks (R=.85 and .89; P&lt;.0001), and with histological infarct size (R=.87, P&lt;.0001). cTnT ≥5.1 μg/l predicted LV wall motion abnormalities ≥ 30% with a sensitivity of 90.9% and specificity of 84.0%. Rats with cTnT≥5.1 μg/l developed PH [right ventricular (RV) systolic pressure 37 ± 3 vs. 23 ± 0.6 mmHg], RV hypertrophy (RV/LV+septum weight 42 ± 4% vs. 24 ± 0.5%), and lung structural remodeling (all P&lt;.01).Conclusion: Early single cTnT measurement correlates with infarct size in rats, and a cutoff value of 5.1 μg/l provides good sensitivity and specificity to predict CHF with secondary PH. cTnT could be used for treatment allocations in therapeutic trials of secondary pulmonary hypertension using this model.

Single measurement of troponin T for early prediction of infarct size, congestive heart failure, and pulmonary hypertension in an animal model of myocardial infarction

Doctor radiology looking chest or lung x-ray image to diagnose pneumonia or inflamed lungs. medical checkup concept.

<a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Jiang+BH&amp;cauthor_id=12166581" href="https://pubmed.ncbi.nlm.nih.gov/?term=Jiang+BH&amp;cauthor_id=12166581" target="_blank" rel="noopener">B H Jiang</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Maruyama+J&amp;cauthor_id=12166581" href="https://pubmed.ncbi.nlm.nih.gov/?term=Maruyama+J&amp;cauthor_id=12166581" target="_blank" rel="noopener">J Maruyama</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Yokochi+A&amp;cauthor_id=12166581" href="https://pubmed.ncbi.nlm.nih.gov/?term=Yokochi+A&amp;cauthor_id=12166581" target="_blank" rel="noopener">A Yokochi</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Amano+H&amp;cauthor_id=12166581" href="https://pubmed.ncbi.nlm.nih.gov/?term=Amano+H&amp;cauthor_id=12166581" target="_blank" rel="noopener">H Amano</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Mitani+Y&amp;cauthor_id=12166581" href="https://pubmed.ncbi.nlm.nih.gov/?term=Mitani+Y&amp;cauthor_id=12166581" target="_blank" rel="noopener">Y Mitani</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Maruyama+K&amp;cauthor_id=12166581" href="https://pubmed.ncbi.nlm.nih.gov/?term=Maruyama+K&amp;cauthor_id=12166581" target="_blank" rel="noopener">K Maruyama</a>Affiliations ExpandPMID: 12166581 DOI: <a data-mce-href="https://doi.org/10.1183/09031936.02.00249302" href="https://doi.org/10.1183/09031936.02.00249302" target="_blank" rel="noopener">10.1183</a>/<a data-mce-href="https://doi.org/10.1183/09031936.02.00249302" href="https://doi.org/10.1183/09031936.02.00249302" target="_blank" rel="noopener">09031936.02.00249302</a> Free articleAbstract The purpose of the present study was to determine the relationship between hypertensive pulmonary vascular remodelling and the changes in mean pulmonary artery pressure (mPAP) during low-dose nitric oxide (NO) inhalation. Rats were exposed to chronic hypobaric hypoxia (air at 50.5 kPa (380 mmHg), 10% oxygen, for 5-29 days) to induce chronic pulmonary hypertension (PH) with pulmonary vascular structural changes. After the chronic hypoxic exposure, the rats had an indwelling pulmonary artery catheter inserted and changes in mPAP with NO were correlated to morphometrical analysis of pulmonary vascular changes. All concentrations of inhaled NO (0.1-2.0 parts per million) reduced mPAP with a similar per cent reduction from baseline mPAP in PH rats, while no changes were observed in control rats. During NO inhalation in PH rats, the absolute value of the decrease in mPAP, but not per cent reduction in mPAP, significantly correlated with baseline mPAP, the percentage of muscularised arteries at the alveolar wall level and at the alveolar duct level, and the per cent medial wall thickness of muscularised arteries. In the chronic hypoxic pulmonary hypertension model, the severity of pulmonary vascular remodelling did not alter the reactivity of the pulmonary arteries to nitric oxide and might, in part, determine the magnitude of nitric-oxide induced absolute reduction in mean pulmonary artery pressure. <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/disclaimer/" href="https://pubmed.ncbi.nlm.nih.gov/disclaimer/" target="_blank" rel="noopener">PubMed Disclaimer</a><a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/12166581/" href="https://pubmed.ncbi.nlm.nih.gov/12166581/" target="_blank" rel="noopener">Link</a>

Correlation of inhaled nitric-oxide induced reduction of pulmonary artery pressure and vascular changes

Pulmonologist doctor, lungs specialist. Aesthetic handdrawn highlighted illustration of human lings. Neutral grey background, studio photo and collage.

<a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Jiang+BH&amp;cauthor_id=20670847" href="https://pubmed.ncbi.nlm.nih.gov/?term=Jiang+BH&amp;cauthor_id=20670847" target="_blank" rel="noopener">Bao Hua Jiang</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Tardif+JC&amp;cauthor_id=20670847" href="https://pubmed.ncbi.nlm.nih.gov/?term=Tardif+JC&amp;cauthor_id=20670847" target="_blank" rel="noopener">Jean-Claude Tardif</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Sauvageau+S&amp;cauthor_id=20670847" href="https://pubmed.ncbi.nlm.nih.gov/?term=Sauvageau+S&amp;cauthor_id=20670847" target="_blank" rel="noopener">Stephanie Sauvageau</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Ducharme+A&amp;cauthor_id=20670847" href="https://pubmed.ncbi.nlm.nih.gov/?term=Ducharme+A&amp;cauthor_id=20670847" target="_blank" rel="noopener">Anique Ducharme</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Shi+Y&amp;cauthor_id=20670847" href="https://pubmed.ncbi.nlm.nih.gov/?term=Shi+Y&amp;cauthor_id=20670847">Yanfen Shi</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Martin+JG&amp;cauthor_id=20670847" href="https://pubmed.ncbi.nlm.nih.gov/?term=Martin+JG&amp;cauthor_id=20670847">James G Martin</a>, <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/?term=Dupuis+J&amp;cauthor_id=20670847" href="https://pubmed.ncbi.nlm.nih.gov/?term=Dupuis+J&amp;cauthor_id=20670847" target="_blank" rel="noopener">Jocelyn Dupuis</a>Affiliations ExpandPMID: 20670847 DOI: <a data-mce-href="https://doi.org/10.1016/j.cardfail.2010.03.003" href="https://doi.org/10.1016/j.cardfail.2010.03.003" target="_blank" rel="noopener">10.1016</a>/<a data-mce-href="https://doi.org/10.1016/j.cardfail.2010.03.003" href="https://doi.org/10.1016/j.cardfail.2010.03.003">j.cardfail.2010.03.003</a> Abstract Background: Studies have suggested some benefit of 3-hydroxy-3-methyl-glutaryl-CoA reductase inhibitors in congestive heart failure (CHF), although the mechanisms remain uncertain. We hypothesized that statins could improve pulmonary hypertension and right ventricular function in ischemic CHF by reducing lung remodeling.Methods and results: Two weeks after myocardial infarct, rats received atorvastatin (n = 23) or no treatment (n = 23) for 3 weeks and were compared with a sham group (n = 16). Infarct size was similar by echocardiography and pathologic evaluations. Atorvastatin greatly reduced pulmonary hypertension and right ventricular hypertrophy: right ventricular systolic pressure 42 +/- 5 vs. 28 +/- 2 mm Hg (P &lt; .01). Atorvastatin did not reduce left ventricular fibrosis and had minimal effects on left ventricular function. Right ventricular myocardial performance index was markedly improved by therapy (P &lt; .01). CHF caused a restrictive lung syndrome with a downward shift of the respiratory pressure-volume loop, increased dry lung weight, and interstitial fibrosis that were greatly improved by atorvastatin. Reduced lung nitric oxide synthase expression was normalized by treatment. Atorvastatin also reduced isolated lung myofibroblasts proliferation after transforming growth factor-beta stimulation (-36 +/- 6%, P &lt; 0.01).Conclusions: 3-hydroxy-3-methyl-glutaryl-CoA reductase inhibition reduces lung remodeling and dysfunction associated with heart failure with prevention of right ventricular hypertrophy and pulmonary hypertension. <a data-mce-href="https://pubmed.ncbi.nlm.nih.gov/20670847/" href="https://pubmed.ncbi.nlm.nih.gov/20670847/" target="_blank" rel="noopener" data-mce-selected="inline-boundary">Link</a>

Beneficial effects of atorvastatin on lung structural remodeling and function in ischemic heart failure

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