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[PMID]:29235790
[Au] Autor:Grytsay VI
[Ti] Título:A mathematical model of the metabolic process of atherosclerosis.
[So] Source:Ukr Biochem J;88(4):75-84, 2016 Jul-Aug.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:A mathematical model of the metabolic process of atherosclerosis is constructed. The functioning of the polyenzymatic prostacyclin-thromboxane system of blood and the influence of a level of "bad cholesterol", namely low density lipoproteins (LDL), on it are studied. With the help of the numerical experiment, we analyze the influence of the concentration of molecules of fat on hemostasis of blood in blood vessels. The kinetic curves for components of the system, phase-periodic bifurcation diagrams, attractors for various modes, and Poincaré cross-section and image of a strange attractor are constructed. The complete spectra of Lyapunov's exponents, divergencies, KS-entropies, predictability horizons, and Lyapunov dimensions of the fractality of strange attractors are calculated. Conclusions about the structural-functional connections, which determine the dependence of hemostasis of a circulatory system on the level of cholesterol in blood are drawn.
[Mh] Termos MeSH primário: Aterosclerose/diagnóstico
Lipoproteínas LDL/sangue
Modelos Estatísticos
Prostaglandinas I/sangue
Tromboxanos/sangue
[Mh] Termos MeSH secundário: Aterosclerose/sangue
Aterosclerose/patologia
Vasos Sanguíneos/metabolismo
Vasos Sanguíneos/patologia
Simulação por Computador
Hemostasia/fisiologia
Homeostase/fisiologia
Seres Humanos
Cinética
Dinâmica não Linear
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipoproteins, LDL); 0 (Prostaglandins I); 0 (Thromboxanes)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.04.075


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[PMID]:28887131
[Au] Autor:Misawa H; Ohashi W; Tomita K; Hattori K; Shimada Y; Hattori Y
[Ad] Endereço:Department of Molecular and Medical Pharmacology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan; Department of Japanese Oriental Medicine, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan.
[Ti] Título:Prostacyclin mimetics afford protection against lipopolysaccharide/d-galactosamine-induced acute liver injury in mice.
[So] Source:Toxicol Appl Pharmacol;334:55-65, 2017 Nov 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prostacyclin (PGI ) serves as a protective, anti-inflammatory mediator and PGI mimetics may be useful as a hepatoprotective agent. We examined whether two PGI mimetics, ONO-1301 and beraprost, are beneficial in acute liver injury and attempted to delineate the possible mechanism underlying the hepatoprotective effect. Acute liver injury was induced by lipopolysaccharide/d-galactosamine (LPS/GalN) in mice. Mice were given an intraperitoneal injection of PGI mimetics 1h before LPS/GalN challenge. Both ONO-1301 and beraprost significantly declined the LPS/GalN-induced increase in serum aminotransferase activity. ONO-1301 and, to a lesser extent, beraprost inhibited hepatic gene expression levels of pro-inflammatory cytokines, which were sharply elevated by LPS/GalN. The hepatoprotective effects of ONO-1301, to a lesser extent, of beraprost were also supported by liver histopathological examinations. The PGI receptor antagonist CAY10441 abrogated their hepatoprotective effects. The mechanisms behind the benefit of PGI mimetics in reducing LPS/GalN-induced liver injury involved, in part, their suppressive effects on increased generation of reactive oxygen species (ROS), since their ability to prevent LPS/GalN-induced hepatic apoptosis was mimicked by the antioxidant N-acetyl-l-cysteine. They significantly diminished LPS/GalN-induced activation of signal transducers and activators of transcription 3 (STAT3) in liver tissues, an effect which was highly associated with their hepatoprotective effects. We indicate that IP receptor activation with PGI mimetics can rescue the damage in the liver induced by LPS/GalN by undermining activation of STAT3 and leading to a lower production of ROS. Our findings point to PGI mimetics, especially ONO-1301, as a potential novel therapeutic modality for the treatment of acute liver injury.
[Mh] Termos MeSH primário: Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle
Epoprostenol/análogos & derivados
Galactosamina/toxicidade
Lipopolissacarídeos/toxicidade
Piridinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Compostos de Benzil/farmacologia
Proteína de Ligação a CREB/genética
Proteína de Ligação a CREB/metabolismo
Epoprostenol/farmacologia
Galactosamina/administração & dosagem
Regulação da Expressão Gênica
Imidazóis/farmacologia
Lipopolissacarídeos/administração & dosagem
Camundongos
Quinases de Proteína Quinase Ativadas por Mitógeno/genética
Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo
Prostaglandinas I/química
Prostaglandinas I/farmacologia
Espécies Reativas de Oxigênio
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((2-(4-(4-isopropoxybenzyl)-phenylamino) imidazoline)); 0 (Benzyl Compounds); 0 (Imidazoles); 0 (Lipopolysaccharides); 0 (Prostaglandins I); 0 (Pyridines); 0 (Reactive Oxygen Species); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); 176391-41-6 (ONO 1301); 35E3NJJ4O6 (beraprost); 7535-00-4 (Galactosamine); DCR9Z582X0 (Epoprostenol); EC 2.3.1.48 (CREB-Binding Protein); EC 2.3.1.48 (Crebbp protein, mouse); EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170910
[St] Status:MEDLINE


  3 / 161 MEDLINE  
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[PMID]:28478717
[Au] Autor:Baker WL; Darsaklis K; Singhvi A; Salerno EL
[Ad] Endereço:1 University of Connecticut, Storrs, CT, USA.
[Ti] Título:Selexipag, an Oral Prostacyclin-Receptor Agonist for Pulmonary Arterial Hypertension.
[So] Source:Ann Pharmacother;51(6):488-495, 2017 Jun.
[Is] ISSN:1542-6270
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To evaluate the data supporting the approval of selexipag and discuss its potential place in therapy for managing pulmonary arterial hypertension (PAH). DATA SOURCES: A systematic review of the literature for all relevant articles was performed through January 16, 2017, using MEDLINE and SCOPUS. A manual search of references from reports of clinical trials, review articles, and recent conference abstracts was performed to identify additional relevant studies. STUDY SELECTION AND DATA EXTRACTION: Eligible citations included in vitro or in vivo evaluations of selexipag, with no restrictions on patient population or indication. Data related to the patient populations and outcomes of interest were extracted from each citation. DATA SYNTHESIS: Single phase II and phase III trials have been published evaluating selexipag in patients with PAH. In 43 patients, the phase II trial showed that selexipag significantly reduced pulmonary vascular resistance by 30% versus placebo ( P = 0.0045) and improved 6-minute walk distance by 24 m ( P < 0.05). The larger phase III trial enrolled 1156 patients with PAH, showing that selexipag lowered the incidence of death or PAH-related complications by 40% versus placebo ( P < 0.001). Selexipag also improved 6-minute walk distance and lowered hospitalization risk. Common adverse events included headache, diarrhea, nausea, and jaw pain. CONCLUSIONS: The specific role of selexipag for managing PAH patients is unclear because of its modest efficacy, lack of mortality reduction, and cost similar to intravenous prostacyclins. Additional clinical trials exploring combination therapy as well as its role in other types of pulmonary hypertension are needed.
[Mh] Termos MeSH primário: Acetamidas/uso terapêutico
Hipertensão Pulmonar/tratamento farmacológico
Pirazinas/uso terapêutico
[Mh] Termos MeSH secundário: Custos e Análise de Custo
Hospitalização
Seres Humanos
Prostaglandinas I/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Acetamides); 0 (Prostaglandins I); 0 (Pyrazines); 5EXC0E384L (selexipag)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170904
[Lr] Data última revisão:
170904
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE
[do] DOI:10.1177/1060028017697424


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[PMID]:27941129
[Au] Autor:Kowal-Bielecka O; Fransen J; Avouac J; Becker M; Kulak A; Allanore Y; Distler O; Clements P; Cutolo M; Czirjak L; Damjanov N; Del Galdo F; Denton CP; Distler JHW; Foeldvari I; Figelstone K; Frerix M; Furst DE; Guiducci S; Hunzelmann N; Khanna D; Matucci-Cerinic M; Herrick AL; van den Hoogen F; van Laar JM; Riemekasten G; Silver R; Smith V; Sulli A; Tarner I; Tyndall A; Welling J; Wigley F; Valentini G; Walker UA; Zulian F; Müller-Ladner U; EUSTAR Coauthors
[Ad] Endereço:Department of Rheumatology and Internal Medicine, Medical University of Bialystok, Bialystok, Poland.
[Ti] Título:Update of EULAR recommendations for the treatment of systemic sclerosis.
[So] Source:Ann Rheum Dis;76(8):1327-1339, 2017 Aug.
[Is] ISSN:1468-2060
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The aim was to update the 2009 European League against Rheumatism (EULAR) recommendations for the treatment of systemic sclerosis (SSc), with attention to new therapeutic questions. Update of the previous treatment recommendations was performed according to EULAR standard operating procedures. The task force consisted of 32 SSc clinical experts from Europe and the USA, 2 patients nominated by the pan-European patient association for SSc (Federation of European Scleroderma Associations (FESCA)), a clinical epidemiologist and 2 research fellows. All centres from the EULAR Scleroderma Trials and Research group were invited to submit and select clinical questions concerning SSc treatment using a Delphi approach. Accordingly, 46 clinical questions addressing 26 different interventions were selected for systematic literature review. The new recommendations were based on the available evidence and developed in a consensus meeting with clinical experts and patients. The procedure resulted in 16 recommendations being developed (instead of 14 in 2009) that address treatment of several SSc-related organ complications: Raynaud's phenomenon (RP), digital ulcers (DUs), pulmonary arterial hypertension (PAH), skin and lung disease, scleroderma renal crisis and gastrointestinal involvement. Compared with the 2009 recommendations, the 2016 recommendations include phosphodiesterase type 5 (PDE-5) inhibitors for the treatment of SSc-related RP and DUs, riociguat, new aspects for endothelin receptor antagonists, prostacyclin analogues and PDE-5 inhibitors for SSc-related PAH. New recommendations regarding the use of fluoxetine for SSc-related RP and haematopoietic stem cell transplantation for selected patients with rapidly progressive SSc were also added. In addition, several comments regarding other treatments addressed in clinical questions and suggestions for the SSc research agenda were formulated. These updated data-derived and consensus-derived recommendations will help rheumatologists to manage patients with SSc in an evidence-based way. These recommendations also give directions for future clinical research in SSc.
[Mh] Termos MeSH primário: Gastroenteropatias/terapia
Hipertensão Pulmonar/terapia
Nefropatias/terapia
Doença de Raynaud/terapia
Escleroderma Sistêmico/terapia
Úlcera/terapia
[Mh] Termos MeSH secundário: Inibidores da Enzima Conversora de Angiotensina/uso terapêutico
Técnica Delfos
Antagonistas dos Receptores de Endotelina/uso terapêutico
Europa (Continente)
Dedos
Fluoxetina/uso terapêutico
Gastroenteropatias/etiologia
Glucocorticoides/uso terapêutico
Transplante de Células-Tronco Hematopoéticas
Seres Humanos
Hipertensão Pulmonar/etiologia
Nefropatias/etiologia
Pneumopatias/etiologia
Pneumopatias/terapia
Inibidores da Fosfodiesterase 5/uso terapêutico
Prostaglandinas I/uso terapêutico
Pirazóis/uso terapêutico
Pirimidinas/uso terapêutico
Doença de Raynaud/etiologia
Reumatologia
Escleroderma Sistêmico/complicações
Inibidores da Captação de Serotonina/uso terapêutico
Úlcera/etiologia
[Pt] Tipo de publicação:CONSENSUS DEVELOPMENT CONFERENCE; JOURNAL ARTICLE; PRACTICE GUIDELINE
[Nm] Nome de substância:
0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Endothelin Receptor Antagonists); 0 (Glucocorticoids); 0 (Phosphodiesterase 5 Inhibitors); 0 (Prostaglandins I); 0 (Pyrazoles); 0 (Pyrimidines); 0 (Serotonin Uptake Inhibitors); 01K63SUP8D (Fluoxetine); RU3FE2Y4XI (riociguat)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161213
[St] Status:MEDLINE
[do] DOI:10.1136/annrheumdis-2016-209909


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[PMID]:28151502
[Au] Autor:Marra AM; D'Alto M; Stanziola AA; Cittadini A; Bossone E
[Ad] Endereço:IRCCS Fondazione SDN, Napoli.
[Ti] Título:[Clinical trials in pulmonary arterial hypertension: a glimpse of history].
[Ti] Título:I trial clinici nell'ipertensione arteriosa polmonare: uno sguardo alla storia..
[So] Source:G Ital Cardiol (Rome);17(12):973-983, 2016 Dec.
[Is] ISSN:1827-6806
[Cp] País de publicação:Italy
[La] Idioma:ita
[Ab] Resumo:Clinical trials have remarkably changed the natural history of pulmonary arterial hypertension (PAH). Despite the relevant progresses achieved in terms of prognosis, PAH is still burned by high mortality rates, disability and low levels of quality of life. The aim of this review is to look over the history of clinical trials in PAH, starting from the little studies with prostacyclin analogues to the recent large randomized placebo-controlled trials. Moreover, the future perspectives of PAH management are addressed.
[Mh] Termos MeSH primário: Desenho de Drogas
Hipertensão Pulmonar/tratamento farmacológico
Qualidade de Vida
[Mh] Termos MeSH secundário: Ensaios Clínicos como Assunto
Seres Humanos
Hipertensão Pulmonar/mortalidade
Hipertensão Pulmonar/fisiopatologia
Prognóstico
Prostaglandinas I/uso terapêutico
Ensaios Clínicos Controlados Aleatórios como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Prostaglandins I)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170601
[Lr] Data última revisão:
170601
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170203
[St] Status:MEDLINE
[do] DOI:10.1714/2612.26890


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[PMID]:27903664
[Au] Autor:Farber HW; Gin-Sing W
[Ad] Endereço:The Pulmonary Center, Boston University School of Medicine, Boston, MA, USA hfarber@bu.edu.
[Ti] Título:Practical considerations for therapies targeting the prostacyclin pathway.
[So] Source:Eur Respir Rev;25(142):418-430, 2016 Dec.
[Is] ISSN:1600-0617
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Therapies that target the prostacyclin pathway play a key role in the treatment of both early- and late-stage pulmonary arterial hypertension, and provide significant clinical benefits for patients. A number of agents have been approved, which are administered via intravenous, subcutaneous, inhaled or oral routes. The use of these therapies is associated with practical challenges, relating to the need for up-titration and their routes of administration. We discuss here a number of measures that can be taken to support patients and healthcare professionals in order to address the complexities of using these therapies and to encourage compliance. Providing patients with timely information and education, together with practical advice on managing their medication and associated equipment, assists patients with day-to-day management of therapy. Referral to patient associations and support groups can be of further benefit. With an effective management plan and an experienced multidisciplinary team, the use of therapies that target the prostacyclin pathway can be optimised.
[Mh] Termos MeSH primário: Anti-Hipertensivos/uso terapêutico
Pressão Arterial/efeitos dos fármacos
Hipertensão Pulmonar/tratamento farmacológico
Prostaglandinas I/metabolismo
Artéria Pulmonar/efeitos dos fármacos
[Mh] Termos MeSH secundário: Anti-Hipertensivos/administração & dosagem
Anti-Hipertensivos/efeitos adversos
Quimioterapia Combinada
Seres Humanos
Hipertensão Pulmonar/diagnóstico
Hipertensão Pulmonar/metabolismo
Hipertensão Pulmonar/fisiopatologia
Terapia de Alvo Molecular
Artéria Pulmonar/fisiopatologia
Transdução de Sinais/efeitos dos fármacos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Prostaglandins I)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170412
[Lr] Data última revisão:
170412
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161202
[St] Status:MEDLINE
[do] DOI:10.1183/16000617.0083-2016


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[PMID]:27601478
[Au] Autor:Austin SA; Katusic ZS
[Ad] Endereço:From the Departments of Anesthesiology and Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic College of Medicine, Rochester, MN.
[Ti] Título:Loss of Endothelial Nitric Oxide Synthase Promotes p25 Generation and Tau Phosphorylation in a Murine Model of Alzheimer's Disease.
[So] Source:Circ Res;119(10):1128-1134, 2016 Oct 28.
[Is] ISSN:1524-4571
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Alzheimer's disease has an unknown pathogenesis; however, cardiovascular risk factors are associated with a higher incidence of Alzheimer's disease. A defining feature of endothelial dysfunction induced by cardiovascular risk factors is reduced bioavailable endothelial nitric oxide (NO). We previously demonstrated that endothelial NO acts as an important signaling molecule in neuronal tissue. OBJECTIVE: We sought to determine the relationship between the loss of endothelial NO synthase (eNOS) and tau phosphorylation in neuronal tissue. METHODS AND RESULTS: We used eNOS knockout ( ) mice as well as an Alzheimer's disease mouse model, amyloid precursor protein (APP)/PSEN1dE9 (PS1) that lacked eNOS (APP/PS1/eNOS ) to examine expression of tau kinases and tau phosphorylation. Brain tissue from eNOS mice had statistically higher ratios of p25/p35, indicative of increased cyclin-dependent kinase 5 activity as compared with wild-type (n=8, P<0.05). However, tau phosphorylation was unchanged in eNOS mice (P>0.05). Next, we determined the role of NO in tau pathology in APP/PS1/eNOS . These mice had significantly higher levels of p25, a higher p25/p35 ratio (n=12-14; P<0.05), and significantly higher cyclin-dependent kinase 5 activity (n=4; P<0.001). Importantly, APP/PS1/eNOS mice also had significantly increased tau phosphorylation (n=4-6; P<0.05). No other changes in amyloid pathology, antioxidant pathways, or neuroinflammation were observed in APP/PS1/eNOS mice as compared with APP/PS1 mice. CONCLUSIONS: Our data suggests that loss of endothelial NO plays an important role in the generation of p25 and resulting tau phosphorylation in neuronal tissue. These findings provide important new insights into the molecular mechanisms linking endothelial dysfunction with the pathogenesis of Alzheimer's disease.
[Mh] Termos MeSH primário: Doença de Alzheimer/metabolismo
Óxido Nítrico Sintase Tipo III/deficiência
Fosfotransferases/biossíntese
Proteínas tau/metabolismo
[Mh] Termos MeSH secundário: Precursor de Proteína beta-Amiloide/genética
Animais
Antioxidantes/metabolismo
Química Encefálica
Quinase 5 Dependente de Ciclina/metabolismo
Modelos Animais de Doenças
Feminino
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Microglia/metabolismo
Neurônios/metabolismo
Óxido Nítrico Sintase Tipo III/fisiologia
Fosforilação
Fosfotransferases/genética
Presenilina-1/genética
Prostaglandina-Endoperóxido Sintases/metabolismo
Prostaglandinas I/metabolismo
Processamento de Proteína Pós-Traducional
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Protein Precursor); 0 (Antioxidants); 0 (Cdk5r1 protein, mouse); 0 (Mapt protein, mouse); 0 (Presenilin-1); 0 (Prostaglandins I); 0 (tau Proteins); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 1.14.13.39 (Nos3 protein, mouse); EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases); EC 2.7.- (Phosphotransferases); EC 2.7.11.1 (Cyclin-Dependent Kinase 5); EC 2.7.11.22 (Cdk5 protein, mouse)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171028
[Lr] Data última revisão:
171028
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160908
[St] Status:MEDLINE


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[PMID]:27598071
[Au] Autor:Stewart T
[Ad] Endereço:Heart and Vascular Center, University of Iowa Hospitals and Clinics, Iowa City, Iowa. Traci Stewart, MSN, RN, CHFN, is a nurse clinician specialist in the Heart and Vascular Center of the University of Iowa Hospitals and Clinics in Iowa City, Iowa.
[Ti] Título:Pulmonary Arterial Hypertension: A Focus on Infused Prostacyclins.
[So] Source:J Infus Nurs;39(5):315-26, 2016 Sep-Oct.
[Is] ISSN:1539-0667
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pulmonary arterial hypertension (PAH) is characterized by vasoconstriction and cell proliferation in the pulmonary vasculature. Guideline-driven interventions with infused prostacyclin treatment are the mainstay for patients with advanced symptoms. Infused prostacyclin therapy is complex. It is critical to manage prostacyclin therapy with precision because boluses or interruptions can be fatal. Education of patients and inpatient staff nurses is necessary to prevent negative outcomes. Nurses are an essential part of the multidisciplinary team caring for patients with PAH. The diagnostic evaluation and treatment of PAH are reviewed here, and challenges associated with the care of patients on prostacyclin therapy are discussed.
[Mh] Termos MeSH primário: Hipertensão Pulmonar/tratamento farmacológico
Bombas de Infusão
Recursos Humanos de Enfermagem no Hospital/educação
Prostaglandinas I/administração & dosagem
[Mh] Termos MeSH secundário: Seres Humanos
Hipertensão Pulmonar/diagnóstico
Hipertensão Pulmonar/enfermagem
Educação de Pacientes como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Prostaglandins I)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170627
[Lr] Data última revisão:
170627
[Sb] Subgrupo de revista:N
[Da] Data de entrada para processamento:160907
[St] Status:MEDLINE
[do] DOI:10.1097/NAN.0000000000000190


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[PMID]:27492004
[Au] Autor:Sommer N; Hecker M; Tello K; Richter M; Liebetrau C; Weigand MA; Seeger W; Ghofrani A; Gall H
[Ad] Endereço:Medizinische Klinik II, Universitätsklinikum Gießen und Marburg, Standort Gießen; Deutsches Zentrum für Lungenforschung (DZL), Klinikstr. 33, 35392, Gießen, Deutschland. Natascha.Sommer@innere.med.uni-giessen.de.
[Ti] Título:[Pulmonary hypertension : What is new in therapy?].
[Ti] Título:Pulmonale Hypertonie : Was ist neu in der Therapie?.
[So] Source:Anaesthesist;65(8):635-52, 2016 Aug.
[Is] ISSN:1432-055X
[Cp] País de publicação:Germany
[La] Idioma:ger
[Ab] Resumo:Pulmonary hypertension (PH) comprises a group of pulmonary vascular diseases that are characterized by progressive exertional dyspnea and right heart insufficiency ultimately resulting in right heart decompensation. The classification is into five clinical subgroups that form the absolutely essential basis for decisions on the indications for different pharmacological and non-pharmacological forms of treatment. The guidelines were updated in 2015 and in addition to the hitherto existing pharmacological treatment options of phosphodiesterase type 5 inhibitors, endothelin receptor antagonists and prostacyclins, the soluble guanylate cyclase stimulator riociguat has now been incorporated for treatment of certain forms of PH. This article provides an overview of the new treatment recommendations in the current guidelines, e. g. for PH patients who are in intensive care units due to surgical interventions or progressive right heart insufficiency.
[Mh] Termos MeSH primário: Hipertensão Pulmonar/terapia
[Mh] Termos MeSH secundário: Inibidores Enzimáticos/uso terapêutico
Seres Humanos
Hipertensão Pulmonar/tratamento farmacológico
Inibidores da Fosfodiesterase 5/uso terapêutico
Prostaglandinas I/uso terapêutico
Receptores de Endotelina/efeitos dos fármacos
Guanilil Ciclase Solúvel/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Phosphodiesterase 5 Inhibitors); 0 (Prostaglandins I); 0 (Receptors, Endothelin); EC 4.6.1.2 (Soluble Guanylyl Cyclase)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170916
[Lr] Data última revisão:
170916
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160806
[St] Status:MEDLINE
[do] DOI:10.1007/s00101-016-0207-y


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[PMID]:27259806
[Au] Autor:Schreiber C; Edlinger C; Eder S; Ausserwinkler M; Wernly B; Pretsch I; Jung C; Hoppe UC; Lichtenauer M
[Ad] Endereço:Clinic for Cardiac Surgery, Paracelsus Medical University of Salzburg, Austria; Clinic for Internal Medicine II, Department of Cardiology, Medical University Vienna, Austria. Electronic address: catharina.schreiber@gmx.net.
[Ti] Título:Global research trends in the medical therapy of pulmonary arterial hypertension 2000-2014.
[So] Source:Pulm Pharmacol Ther;39:21-7, 2016 Aug.
[Is] ISSN:1522-9629
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Pulmonary arterial hypertension is a progressive disease of the pulmonary vasculature that affects more than 200.000 patients worldwide. Without medical treatment it leads to right heart failure and death. Extensive fundamental and clinical research has been performed throughout the globe to modify the disease and improve survival. METHODS: We performed a bibliometric study on medical treatment for pulmonary arterial hypertension to identify study characteristics, impact factors and the countries of origin of basic and clinical studies that were published between 2000 and 2014. For visualization of the obtained data density equalizing maps were prepared. RESULTS: A total of 681 studies were eligible, of these 56% were clinical studies that have included a total of 30960 patients. Most studies were performed on endothelin receptor antagonists, followed by prostacyclins and phosphodiesterase type 5 inhibitors. Impact factors did not differ between clinical and basic science studies. The United States for clinical studies, and China for basic science studies were identified as main contributors to the global scientific output. CONCLUSIONS: This first bibliometric study in the field of pulmonary arterial hypertension shows that a significant amount of scientific research was performed within the last 14 years mainly in North America, Asia and Europe. As current trends in this field of research we identified combination therapies and Asian countries being a new hatchery for emerging experimental and clinical studies.
[Mh] Termos MeSH primário: Antagonistas dos Receptores de Endotelina/uso terapêutico
Hipertensão Pulmonar/tratamento farmacológico
Inibidores da Fosfodiesterase 5/uso terapêutico
Prostaglandinas I/uso terapêutico
[Mh] Termos MeSH secundário: Bibliometria
Ensaios Clínicos como Assunto/estatística & dados numéricos
Saúde Global
Seres Humanos
Hipertensão Pulmonar/epidemiologia
Hipertensão Pulmonar/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin Receptor Antagonists); 0 (Phosphodiesterase 5 Inhibitors); 0 (Prostaglandins I)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160605
[St] Status:MEDLINE



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