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Pesquisa : D06.472.699.584.500 [Categoria DeCS]
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Id: biblio-1057263
Autor: Mendes, Adriano Assis; Roncal, Carlos Guilhermo Piscoya; Oliveira, Flávio Roberto Azevedo de; Albuquerque, Eugênio Soares de; Góes, Gustavo Henrique Belarmino; Piscoya, Isabelle Cecília de Vasconcellos; Sobral Filho, Dário Celestino.
Título: Demographic and clinical characteristics of pulmonary arterial hypertension caused by schistosomiasis are indistinguishable from other etiologies
Fonte: Rev. Soc. Bras. Med. Trop;53:e20190418, 2020. tab, graf.
Idioma: en.
Resumo: Abstract INTRODUCTION: Pulmonary arterial hypertension (PAH) is a serious pulmonary circulation disease caused by several etiologies, including schistosomiasis. The present study retrospectively evaluated the clinical and hemodynamic characteristics of patients with schistosomal PAH (PAH-Sch) compared to those of non-Sch PAH patients (non-Sch PAH). METHODS: Patients treated at the Pronto-Socorro Cardiológico de Pernambuco and diagnosed by right cardiac catheterization were divided into PAH-Sch and non-Sch PAH groups. Their socio-demographic and clinical characteristics, N-terminal-pro B-type natriuretic peptide (NT-proBNP), and echocardiography and hemodynamic parameters were retrospectively reviewed. RESULTS: Among the included 98 patients (mean age, 45 ± 14 years; 68 women [69.4%]), we found 56 PAH-Sch and 42 non-Sch PAH. The age distribution was heterogeneous in the PAH-Sch group, with patients predominantly ranging from 50-59 (p <0.004). Dyspnea was the most common symptom, reported by 92 patients (93.8%), and commonly present for over two years prior to diagnosis. Clinical symptoms were similar in both groups, with no differences in functional class, pulmonary artery systolic pressure (p = 0.102), 6-minute walk test score (p = 0.234), NT-proBNP serum levels (p = 0.081), or hemodynamic parameters. CONCLUSIONS: Patients with PAH-Sch present clinical, laboratory, and hemodynamic profiles similar to those with PAH resulting from other etiologies of poor prognosis. PAH is an important manifestation of schistosomiasis in endemic regions that is often diagnosed late.
Descritores: Precursores de Proteínas/sangue
Esquistossomose/complicações
Fator Natriurético Atrial/sangue
Hipertensão Arterial Pulmonar/etiologia
-Fatores Socioeconômicos
Ecocardiografia
Biomarcadores/sangue
Estudos Retrospectivos
Hipertensão Arterial Pulmonar/sangue
Pessoa de Meia-Idade
Limites: Humanos
Masculino
Feminino
Adulto
Idoso
Tipo de Publ: Estudo Comparativo
Responsável: BR1.1 - BIREME


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Id: biblio-1165171
Autor: Ogawa Tsuneo; de Bold Adolfo J.
Título: El corazón endocrino y el proceso inflamatorio / [The endocrine heart and inflammation].
Fonte: Medicina (B.Aires);73(6):562-6, Dec. 2013.
Idioma: es.
Resumo: The endocrine heart produces the polypeptide hormones Atrial Natriuretic Factor (ANF or ANP) and Brain Natriuretic Peptide (BNP). Through the peripheral actions of these hormones the heart contributes to the regulation of the cardiac preload and afterload. More recently, new functions for these hormones have been described including the modulation of the immune response. Plasma levels of BNP but not those of ANF, increase following an acute rejection episode of a cardiac allotransplant but return to levels pre-rejection with successful treatment. This observation constitutes the first observation leading to characterizing the interactions of BNP with the immune response. Several other pathologies with an inflammatory component are now known to be associated with an increase in the production of BNP. Such an increase is due to an increase in the transcriptional activity of the BNP gene induced by cytokines and related substances. In vitro investigations have shown that an increase in BNP directly modulates immunological activity. Inflammation and hemodynamic changes co-exist in several cardiovascular diseases and therefore it may be beneficial to measure circulating levels of both ANF and BNP as biomarkers of changes in intravascular volume and of changes in intravascular volume plus inflammation, respectively. Changes in plasma ANF, that are relatively larger than those of BNP, might be an indication of hemodynamic deterioration while important changes in circulating BNP could indicate a worsening of the inflammatory process.
Descritores: Fator Natriurético Atrial/metabolismo
Inflamação/metabolismo
Miócitos Cardíacos/metabolismo
Peptídeo Natriurético Encefálico/metabolismo
-Animais
Fator Natriurético Atrial/imunologia
Hemodinâmica/imunologia
Humanos
Miocardite/imunologia
Miocardite/metabolismo
Peptídeo Natriurético Encefálico/genética
Peptídeo Natriurético Encefálico/imunologia
Pesquisa Biomédica
Sepse/imunologia
Sepse/metabolismo
Tipo de Publ: Resumo em Inglês
Artigo de Revista
Revisão
Responsável: AR5.1 - Centro de Gestión del Conocimiento y las Comunicaciónes


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Id: biblio-1026452
Autor: Parisi, Horacio Carlos.
Título: La Hormona Natriurética y la Insuficiencia Renal / Natriuretic Hormone and Kidney Failure
Fonte: Rev. Asoc. Med. Bahía Blanca;2(1):2-6, Mar. 1991.
Idioma: es.
Descritores: Fator Natriurético Atrial
Insuficiência Renal
Limites: Humanos
Tipo de Publ: Revisão
Responsável: AR393.1 - Centro de Información y Documentación Dr H. Urquiola


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ARAUJO, SEBASTIAO
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Id: lil-787736
Autor: Gasparotto, Ana Paula Devite Cardoso; Falcão, Antonio Luis Eiras; Kosour, Carolina; Araújo, Sebastião; Cintra, Eliane Araújo; Oliveira, Rosmari Aparecida Rosa Almeida de; Martins, Luiz Claudio; Dragosavac, Desanka.
Título: Fator natriurético atrial: ele é o responsável pela hiponatremia e natriurese em neurocirurgia? / Atrial natriuretic factor: is it responsible for hyponatremia and natriuresis in neurosurgery?
Fonte: Rev. bras. ter. intensiva;28(2):154-160tab, graf.
Idioma: pt.
Projeto: Fundação de Amparo à Pesquisa do Estado de São Paulo.
Resumo: RESUMO Objetivo: Avaliar a presença de hiponatremia e natriurese, bem como suas associações com o fator natriurético atrial em pacientes de neurocirurgia. Métodos: Foram incluídos 30 pacientes submetidos à ressecção de tumor intracraniano e à clipagem de aneurisma cerebral. Os níveis plasmáticos e urinários de fator natriurético atrial foram medidos durante os períodos pré e pós-operatório. Resultados: Hiponatremia esteve presente em 63,33% dos pacientes, particularmente no primeiro dia pós-operatório. Observou-se natriurese em 93,33% dos pacientes, principalmente no segundo dia pós-operatório. Os níveis plasmáticos de fator natriurético atrial estavam aumentados em 92,60% dos pacientes em pelo menos um dos dias pós-operatórios, mas não houve associação estatisticamente significante entre fator natriurético atrial e sódio plasmático, e entre fator natriurético atrial e sódio urinário. Conclusão: Após neurocirurgia, na maior parte dos pacientes, estiveram presentes hiponatremia e natriurese; contudo, o fator natriurético atrial não pôde ser considerado diretamente responsável por tais alterações nos pacientes neurocirúrgicos. Provavelmente, há o envolvimento de outros fatores natriuréticos.

ABSTRACT Objective: To evaluate the presence of hyponatremia and natriuresis and their association with atrial natriuretic factor in neurosurgery patients. Methods: The study included 30 patients who had been submitted to intracranial tumor resection and cerebral aneurism clipping. Both plasma and urinary sodium and plasma atrial natriuretic factor were measured during the preoperative and postoperative time periods. Results: Hyponatremia was present in 63.33% of the patients, particularly on the first postoperative day. Natriuresis was present in 93.33% of the patients, particularly on the second postoperative day. Plasma atrial natriuretic factor was increased in 92.60% of the patients in at least one of the postoperative days; however, there was no statistically significant association between the atrial natriuretic factor and plasma sodium and between the atrial natriuretic factor and urinary sodium. Conclusion: Hyponatremia and natriuresis were present in most patients after neurosurgery; however, the atrial natriuretic factor cannot be considered to be directly responsible for these alterations in neurosurgery patients. Other natriuretic factors are likely to be involved.
Descritores: Fator Natriurético Atrial/sangue
Procedimentos Neurocirúrgicos/métodos
Hiponatremia/epidemiologia
Natriurese/fisiologia
-Período Pós-Operatório
Sódio/urina
Neoplasias Encefálicas/cirurgia
Aneurisma Intracraniano/cirurgia
Estudos Prospectivos
Período Pré-Operatório
Pessoa de Meia-Idade
Limites: Humanos
Masculino
Feminino
Adulto
Tipo de Publ: Estudo Observacional
Responsável: BR1.1 - BIREME


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Texto completo SciELO Chile
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Id: biblio-954227
Autor: Eid, Refaat A; Zaki, Mohamed Samir Ahmed; Alghamdi, Mansour A; Al-Shraim, Mubarak; El-kott, Attalla Farag; Al-Hashem, Fahaid H; Aldera, Hussain; Alkhateeb, Mahmoud A.
Título: Ghrelin improves the fine structure of atrial natriuretic factor (ANF) granules and intercalated disc junctions in experimentally-induced myocardial infarction in rats / La grelina mejora las estructuras finas de los gránulos de factor natriurético atrial (ANF) y las uniones intercaladas de disco en el infarto de miocardio inducido experimentalmente en ratas
Fonte: Int. j. morphol;36(3):1031-1042, Sept. 2018. tab, graf.
Idioma: en.
Projeto: King Khalid University.
Resumo: Ghrelin is a novel growth hormone-releasing peptide administered to treat myocardial infarction (MI). However, the underlying mechanism of its protective effects against MI remains unclear. A total of sixty healthy Sprague Dawley male rats were included. The first one is the sham-operated control group were the rats that underwent the same surgical used to induce MI but without tying the left anterior descending coronary artery (LAD) and received normal saline (0.5 ml) as vehicle; the second MI model group were rats with LAD ligation and received normal saline (0. 5 ml) and the third one is MI+ghrelin group were rats that were exposed to surgery to induce MI but received ghrelin (100 µ/kg, orally, 2x/day). At the end of the experiment after 21 days post-MI, rats were sacrificed and processed for ultrastructural demonstration. Our experiment showed that ghrelin inhibited cardiomyocyte apoptosis. Concomitant administration of ghrelin with MI treated rats of this study appeared to show a considerable protection of the atrial tissues. This study revealed that the sarcoplasm was occupied by normal myofibrils with clear striations and others appeared with minor disruption. Normal distribution of atrionatriuretic factor (ANF) granules and well preserved mitochondrial integrity (preserved cristae, normal size and shape), nucleus chromatin arrangement and striated pattern of clear bands (Z and H) compared to the MI group. Intact intercalated disc with clear identification of fully formed fascia adherence and desmosomes with a reconstruction of gap junction (nexus) was also noticed. Atrial myocytes after myocardial infarction is often associated with subsequent heart failure, which could lead to a fatal outcome. In a rat model of experimental myocardial infarction, peripheral ghrelin administration attenuated myocyte dysfunction, well-preserved desmosome, adherent and gap junction of the intercalated disc and normally distributed ANF granules.

La grelina es un nuevo péptido liberador de hormona de crecimiento administrado para tratar el infarto de miocardio (IM). Sin embargo, el mecanismo subyacente de sus efectos protectores contra el IM aún no se conocen. Se incluyeron un total de 60 ratas macho Sprague Dawley saludables. En el grupo control se incluyeron ratas que fueron sometidas a una cirugía utilizada para inducir el IM, pero sin ligar la arteria coronaria descendente anterior izquierda (ACDAI) y recibieron suero fisiológico normal (0,5 ml) como vehículo; el segundo grupo modelo de IM fueron ratas con ligadura de ACDAI y recibieron suero fisiológico normal (0,5 ml); el tercer grupo estuvo formado por ratas con IM + grelina, expuestas a la cirugía para inducir IM pero luego recibieron grelina (100 m/kg, oralmente, 2x/día). Al final del experimento, 21 días después del infarto de miocardio, los animales fueron sacrificados y procesados para el estudio ultraestructural. Nuestro experimento mostró que la grelina inhibe la apoptosis de los cardiomiocitos. La administración concomitante de grelina en ratas con IM parece indicar una protección considerable de los tejidos atriales. Además, el estudio reveló que el sarcoplasma estaba ocupado por miofibrillas normales con estriaciones claras y otras con una alteración menor. Se encontró una distribución normal de los gránulos del factor natriurético atrial (FNA) e integridad mitocondrial bien conservada (crestas conservadas, tamaño y forma normales), disposición de la cromatina del núcleo y patrón estriado de bandas claras (Z y H) en comparación con el grupo IM. También se observó un disco intercalado intacto con una clara identificación de la adherencia de la fascia completamente formada y desmosomas con una reconstrucción de la unión gap (nexo). Los miocitos atriales, después de un infarto de miocardio, a menudo se asocian con insuficiencia cardíaca posterior, que podría conducir a un desenlace fatal. En un modelo de rata de infarto de miocardio experimental, la administración de grelina periférica atenuó la disfunción de miocitos, con conservación del desmosoma, adherencia y unión de la brecha del disco intercalado y una distribución normal de los los gránulos de FNA.
Descritores: Fator Natriurético Atrial/metabolismo
Hormônios Peptídicos/metabolismo
Infarto do Miocárdio/metabolismo
-Fator Natriurético Atrial/ultraestrutura
Ratos Sprague-Dawley
Microscopia Eletrônica de Transmissão
Modelos Animais de Doenças
Grelina
Limites: Animais
Masculino
Ratos
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-979817
Autor: Ferraboli, Roberto; Ornelas, Elisabete De Marco; Fonseca, Luiz Affonso; Veiga, Glaucia Luciano da; Cardoso, Clever Gomes; Marques, Mara Rubia; Maifrino, Laura Beatriz Mesiano.
Título: Effect of mild aerobic exercise in atrial granules of mice with chronic Chagas Disease / Efeito do exercício aeróbico leve em grânulos atriais de camundongos com doença de Chagas crônica
Fonte: Int. j. cardiovasc. sci. (Impr.);31(6):585-593, nov.- dez. 2018. tab, ilus, graf.
Idioma: en.
Resumo: Background: Chagas disease presents in different clinical forms, ranging from asymptomatic to acute, with destruction of heart cells and a possibility of death. In the chronic phase, the parasites can cause serious injuries to different tissues.Objectives: Our objective was to study the effects of physical exercise (swimming) in atrial granules and components of cardiomyocytes in mice with chronic Chagas disease. Methods: In total, 20 male mice were divided into four different groups: untrained control (UC), trained control (TC), untrained infected (UI), and trained infected (TI). In the UI and TI groups, 1,000 forms of Trypanosoma cruzi (Y strain) were inoculated intraperitoneally. After 40 days of infection and proof of chronic phase, the exercise protocol began. The UC and UI groups performed exercise for 10 min/day, and the TC and TI groups followed a training protocol five times a week for 30 minutes during 8 weeks. Ultrathin sections were subjected to morphometric and stereological analyses using electron photomicrographs (x15000) obtained by transmission electron microscopy.Results: The TI group showed the lowest percentage of small granules (58%), while the UI group presented 80% of these granules. The volume density of the Golgi complex and myofibrils in the TI group were reduced compared with those in the UI group, while the parameters of atrial granules and mitochondria increased. Conclusion: Our results suggest that mild physical exercise changes the morphological and morphometric parameters of granules and organelles in the cardiac atrium of mice infected with T. cruzi, and produces moderate beneficial effects on the cardiovascular system
Descritores: Exercício Físico
Doença de Chagas
Fator Natriurético Atrial
-Trypanosoma cruzi
Análise Estatística
Análise de Variância
Peptídeo Natriurético Encefálico
Modelos Animais
Miócitos Cardíacos
Camundongos
Limites: Animais
Camundongos
Responsável: BR44.1 - Serviço de Biblioteca, Documentação Científica e Didática Prof. Dr. Luiz Venere Décourt


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Texto completo SciELO Brasil
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Id: biblio-839308
Autor: Li, Q; Yu, Q; Na, R; Liu, B.
Título: Etanercept protects rat cardiomyocytes against hypertrophy by regulating inflammatory cytokines secretion and cell apoptosis
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;50(6):e5868, 2017. tab, graf.
Idioma: en.
Resumo: We aimed to investigate the effect of etanercept, a tumor necrosis factor-α (TNF-α) inhibitor, on rat cardiomyocyte hypertrophy and its underlying mechanism. Primary neonatal rat cardiomyocytes were isolated from Sprague-Dawley rats. The model of rat cardiomyocyte hypertrophy was induced by endothelin, and then treated with different concentrations of etanercept (1, 10, and 50 μM). After treatment, cell counts, viability and cell apoptosis were evaluated. The mRNA levels of myocardial hypertrophy marker genes, including atrial natriuretic factor (ANF), matrix metalloproteinase (MMP)-9 and MMP-13, were detected by qRT-PCR, and the expressions of apoptosis-related proteins (Bcl-2 and Bax) were measured by western blotting. The protein levels of transforming growth factor-β1 (TGF-β1), interleukin (IL)-1β, IL-6, leukemia inhibitory factor (LIF) and cardiotrophin-1 (CT-1) were determined using enzyme linked immunosorbent assay (ELISA) kits. In the present study, TNF-α level in cardiomyocytes with hypertrophy was significantly enhanced (P<0.05). Compared to the model group, cell number and viability were significantly increased and ratio of apoptotic cells was reduced by etanercept (P<0.05, P<0.01, or P<0.001). In addition, etanercept remarkably reduced the mRNA levels of ANF, MMP-9 and MMP-13, inhibited the expression of Bax, and increased the expression of Bcl-2 compared to the model group (P<0.05). ELISA results further showed that etanercept lowered the levels of IL-1β, IL-6, LIF and CT-1 but not TGF-β1 compared to the model group (P<0.05). Etanercept may protect rat cardiomyocytes from hypertrophy by inhibiting inflammatory cytokines secretion and cell apoptosis.
Descritores: Anti-Inflamatórios não Esteroides/farmacologia
Cardiomegalia/metabolismo
Etanercepte/farmacologia
Miócitos Cardíacos/efeitos dos fármacos
Substâncias Protetoras/farmacologia
-Animais Recém-Nascidos
Apoptose/efeitos dos fármacos
Fator Natriurético Atrial/metabolismo
Cardiomegalia/induzido quimicamente
Proliferação de Células/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Citocinas/efeitos dos fármacos
Modelos Animais de Doenças
Inflamação/metabolismo
Metaloproteinase 13 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Miócitos Cardíacos/metabolismo
Ratos Sprague-Dawley
Fator de Necrose Tumoral alfa/metabolismo
Limites: Animais
Responsável: BR1.1 - BIREME


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Id: lil-759921
Autor: Palheta Júnior, Raimundo Campos.
Título: Caracterização das vias neuro-humorais no retarde do esvaziamento gástrico de líquidos advindo da distensão mecânica atrial direta em ratos acordados [manuscrito] / Characterization of neurohumoral pathways in the delay gastric emptying of liquids arising from direct mechanical atrial distension in awake rats [manuscript].
Fonte: Fortaleza; s.n; 2010.
Idioma: pt.
Tese: Apresentada a Universidade Federal do Ceará para obtenção do grau de Doutor.
Resumo: A distensão mecânica do átrio direito (DA) aumenta a motilidade gástrica em ratos anestesiados (Palheta et al., 2010). Resolvemos avaliar o efeito da DA sobre o esvaziamento gástrico (EG) de líquido em ratos acordados e as eventuais vias neuro-humorais relacionadas ao fenômeno. Utilizamos ratos albinos machos (n = 361, 250 - 280 g) que receberam um balão de silicone posicionado no átrio direito. Decorridos 24 h, monitoramos a pressão venosa central (PVC), frequência cardíaca (FC) e a pressão arterial média (PAM) e após os 20-min iniciais os animais foram aleatoriamente pré-tratados com: Salina (S, 0,1 ml/100g, i.v.), Atropina (A, 0,5 mg/kg, i.v.), Guanetidina (GT, 10 mg/kg, i.p.), Hexametônio (H, 10mg/kg, i.v.), L-NAME (3mg/kg,i.v.), L-Arg (100 mg/kg, i.v.) + L-NAME (3mg/kg,i.v.), Azul de metileno (MB,3mg/kg, i.v.), Glibenclamida (GB, 1mg/kg, i.p.) ou Glibenclamida + Diazóxido (3mg/kg, i.v.) [GB + D], Dexametasona (DEX, 1mg/kg, i.p.), Anantin (ANT, 5μg, i.v.) ou Atosibana (AT, 40μg/kg/h, i.v.). Além disto, em grupos separados realizamos 72h antes da DA a vagotomia (V), ou esplancnotomia + gangliectomia celíaca (SC) ou denervação cardíaca aferente com capsaicina (ACD). Em outro conjunto de animais realizamos aurilectomia direita uma semana antes da DA (AX). Em seguida ao tratamento farmacológico realizamos protocolo de falsa DA (controle) ou DA com 50 μL do balão intra-atrial durante...
Descritores: Fator Natriurético Atrial
Volume Sanguíneo
Limites: Animais
Masculino
Ratos
Responsável: BR6.1 - BCS - Biblioteca de Ciências da Saúde


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Texto completo SciELO Chile
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Id: lil-742564
Autor: Bertoló, María Soledad; Ruiz, Marcelo; Contreras, Caterina.
Título: Pioderma gangrenoso: excelente respuesta a tratamiento tópico / Pyoderma gangrenosum: excellent response to topical therapy
Fonte: Rev. méd. Chile;143(1):130-131, ene. 2015. ilus.
Idioma: es.
Descritores: Fator Natriurético Atrial/metabolismo
Cálcio/farmacologia
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/enzimologia
Poli(ADP-Ribose) Polimerases/metabolismo
-Animais Recém-Nascidos
Angiotensina II/farmacologia
Fator Natriurético Atrial/genética
Cálcio/metabolismo
Ativação Enzimática/efeitos dos fármacos
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
/metabolismo
GATAABBREVIATIONS AS TOPIC TRANSCRIPTION FACTOR/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Espaço Intracelular/efeitos dos fármacos
Espaço Intracelular/metabolismo
Contração Miocárdica/efeitos dos fármacos
Fosforilação/efeitos dos fármacos
Regiões Promotoras Genéticas/genética
Ligação Proteica/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-fos/genética
Proteínas Proto-Oncogênicas c-fos/metabolismo
Ratos Sprague-Dawley
Ribose/metabolismo
Limites: Animais
Ratos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


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Id: lil-734384
Autor: de Bold, Adolfo J..
Título: Péptidos natriuréticos en enfermedades extracardíacas
Fonte: Medicina (B.Aires);74(3):266-266, jun. 2014.
Idioma: es.
Descritores: Fator Natriurético Atrial/metabolismo
Inflamação/metabolismo
Miócitos Cardíacos
Peptídeo Natriurético Encefálico/metabolismo
Limites: Animais
Humanos
Tipo de Publ: Comentário
Carta
Responsável: AR1.2 - Instituto de Investigaciónes Epidemiológicas



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