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[PMID]:29216295
[Au] Autor:Park J; Masaki T; Mezaki Y; Yokoyama H; Nakamura M; Maehashi H; Fujimi TJ; Gouraud SS; Nagatsuma K; Nakagomi M; Kimura N; Matsuura T
[Ad] Endereço:Department of Laboratory Medicine, The Jikei University School of Medicine, Minato-ku, Tokyo, Japan.
[Ti] Título:Alpha-1 antichymotrypsin is involved in astrocyte injury in concert with arginine-vasopressin during the development of acute hepatic encephalopathy.
[So] Source:PLoS One;12(12):e0189346, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: We developed a bio-artificial liver (BAL) using a radial-flow bioreactor and rescued mini-pig models with lethal acute liver failure (ALF). The point of the rescue is the recovery from hepatic encephalopathy (HE). HE on ALF has sometimes resulted in brain death following brain edema with astrocyte swelling. Several factors, including ammonia and glutamine, have been reported to induce astrocyte swelling and injury. However, many clinicians believe that there are any other factors involved in the development of HE. Therefore, the aim of this study was to identify novel HE-inducible factors, particularly those inducing astrocyte dysfunction. METHODS: Mini-pig plasma samples were collected at three time points: before the administration of toxins (α-amanitin and LPS), when HE occurred after the administration of toxins, and after treatment with extracorporeal circulation (EC) by the BAL. To identify the causative factors of HE, each plasma sample was subjected to a comparative proteome analysis with two-dimensional gel electrophoresis and mass spectrometry. To assess the direct effects of candidate factors on the astrocyte function and injury, in vitro experiments with human astrocytes were performed. RESULTS: Using a proteome analysis, we identified alpha-1 antichymotrypsin (ACT), which was increased in plasma samples from mini-pigs with HE and decreased in those after treatment with EC by BAL. In in vitro experiments with human astrocytes, ACT showed growth-inhibitory and cytotoxic effects on astrocytes. In addition, the expression of water channel protein aquaporin-4, which is induced in injured astrocytes, was increased following ACT treatment. Interestingly, these effects of ACT were additively enhanced by adding arginine-vasopressin (AVP) and were canceled by adding an AVP receptor antagonist. CONCLUSIONS: These results suggest that ACT is involved in astrocyte injury and dysfunction in concert with AVP during the development of acute HE.
[Mh] Termos MeSH primário: Arginina Vasopressina/metabolismo
Astrócitos/metabolismo
Encefalopatia Hepática/metabolismo
alfa 1-Antiquimotripsina/farmacologia
[Mh] Termos MeSH secundário: Doença Aguda
Cloreto de Amônio/farmacologia
Animais
Astrócitos/efeitos dos fármacos
Linhagem Celular
Encefalopatia Hepática/patologia
Seres Humanos
Fígado Artificial
Masculino
Suínos
Porco Miniatura
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (alpha 1-Antichymotrypsin); 01Q9PC255D (Ammonium Chloride); 113-79-1 (Arginine Vasopressin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189346


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[PMID]:29065123
[Au] Autor:Sims CA; Yuxia G; Singh K; Werlin EC; Reilly PM; Baur JA
[Ad] Endereço:The Trauma Center at the University of Pennsylvania, Department of Surgery, Perelman School of Medicine, Philadelphia, PA, United States of America.
[Ti] Título:Supplemental arginine vasopressin during the resuscitation of severe hemorrhagic shock preserves renal mitochondrial function.
[So] Source:PLoS One;12(10):e0186339, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Arginine vasopressin (AVP), a hormone secreted by the posterior pituitary, plays a vital role in maintaining vasomotor tone during acute blood loss. We hypothesized that decompensated hemorrhagic shock is associated with decreased AVP stores and supplementation during resuscitation would improve both blood pressure and renal function. Using a decompensated hemorrhagic shock model, male Long-Evans rats were bled to mean arterial blood pressure (MAP) of 40mmHg and maintained until the MAP could not be sustained without fluid. Once 40% of the shed volume was returned in lactated Ringer's (Severe Shock), animals were resuscitated over 60 minutes with 4x the shed volume in lactated Ringer's (LR) or the same fluids with AVP (0.5 units/kg+ 0.03 units/kg/min). Animals (n = 6-9/group) were sacrificed before hemorrhage (Sham), at Severe Shock, following resuscitation (60R, 60R with AVP) or 18 hours post-resuscitation (18hr, 18hr with AVP). Blood samples were taken to measure AVP levels and renal function. Pituitaries were harvested and assayed for AVP. Kidney samples were taken to assess mitochondrial function, histology, and oxidative damage. Baseline pituitary AVP stores (30,364 ± 5311 pg/mg) decreased with severe shock and were significantly depressed post-resuscitation (13,910 ± 3016 pg/ml. p<0.05) and at 18hr (15,592 ±1169 pg/ml, p<0.05). Resuscitation with LR+AVP led to higher serum AVP levels at 60R (31±8 vs 79±12; p<0.01) with an improved MAP both at 60R (125±3 vs 77±7mmHg; p<0.01) and 18hr (82±6 vs 69±5mmHg;p<0.05). AVP supplementation preserved complex I respiratory capacity at 60R and both complex I and II function at 18hr (p<0.05). AVP was also associated with decreased reactive oxygen species at 60R (856±67 vs 622±48F RFU) and significantly decreased oxidative damage as measured by mitochondrial lipid peroxidation (0.9±0.1 vs 1.7±0.1 fold change, p<0.01) and nitrosylation (0.9±0.1 vs 1.4±0.2 fold change, p<0.05). With AVP, renal damage was mitigated at 60R and histologic architecture was conserved at 18 hours. In conclusion, pituitary and serum AVP levels decrease during severe hemorrhage and may contribute to the development of decompensated hemorrhagic shock. Supplementing exogenous AVP during resuscitation improves blood pressure, preserves renal mitochondrial function, and mitigates acute kidney injury.
[Mh] Termos MeSH primário: Arginina Vasopressina/uso terapêutico
Rim/fisiopatologia
Mitocôndrias/fisiologia
Choque Hemorrágico/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Masculino
Ratos
Ratos Long-Evans
Choque Hemorrágico/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
113-79-1 (Arginine Vasopressin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186339


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[PMID]:28733450
[Au] Autor:Charkoudian N; Usselman CW; Skow RJ; Staab JS; Julian CG; Stickland MK; Chari RS; Khurana R; Davidge ST; Davenport MH; Steinback CD
[Ad] Endereço:United States Army Research Institute of Environmental Medicine, Natick, Massachusetts.
[Ti] Título:Muscle sympathetic nerve activity and volume-regulating factors in healthy pregnant and nonpregnant women.
[So] Source:Am J Physiol Heart Circ Physiol;313(4):H782-H787, 2017 Oct 01.
[Is] ISSN:1522-1539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Healthy, normotensive human pregnancies are associated with striking increases in both plasma volume and vascular sympathetic nerve activity (SNA). In nonpregnant humans, volume-regulatory factors including plasma osmolality, vasopressin, and the renin-angiotensin-aldosterone system have important modulatory effects on control of sympathetic outflow. We hypothesized that pregnancy would be associated with changes in the relationships between SNA (measured as muscle SNA) and volume-regulating factors, including plasma osmolality, plasma renin activity, and arginine vasopressin (AVP). We studied 46 healthy, normotensive young women (23 pregnant and 23 nonpregnant). We measured SNA, arterial pressure, plasma osmolality, plasma renin activity, AVP, and other volume-regulatory factors in resting, semirecumbent posture. Pregnant women had significantly higher resting SNA (38 ± 12 vs. 23 ± 6 bursts/min in nonpregnant women), lower osmolality, and higher plasma renin activity and aldosterone (all < 0.05). Group mean values for AVP were not different between groups [4.64 ± 2.57 (nonpregnant) vs. 5.17 ± 2.03 (pregnant), > 0.05]. However, regression analysis detected a significant relationship between individual values for SNA and AVP in pregnant ( = 0.71, < 0.05) but not nonpregnant women ( = 0.04). No relationships were found for other variables. These data suggest that the link between AVP release and resting SNA becomes stronger in pregnancy, which may contribute importantly to blood pressure regulation in healthy women during pregnancy. Sympathetic nerve activity and blood volume are both elevated during pregnancy, but blood pressure is usually normal. Here, we identified a relationship between vasopressin and sympathetic nerve activity in pregnant but not nonpregnant women. This may provide mechanistic insights into blood pressure regulation in normal pregnancy and in pregnancy-related hypertension.
[Mh] Termos MeSH primário: Volume Sanguíneo/fisiologia
Músculo Esquelético/inervação
Músculo Esquelético/fisiologia
Gravidez/fisiologia
Sistema Nervoso Simpático/fisiologia
[Mh] Termos MeSH secundário: Adulto
Aldosterona/sangue
Arginina Vasopressina/sangue
Pressão Sanguínea/fisiologia
Feminino
Voluntários Saudáveis
Seres Humanos
Concentração Osmolar
Postura/fisiologia
Renina/sangue
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
113-79-1 (Arginine Vasopressin); 4964P6T9RB (Aldosterone); EC 3.4.23.15 (Renin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170723
[St] Status:MEDLINE
[do] DOI:10.1152/ajpheart.00312.2017


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[PMID]:28716309
[Au] Autor:Sims CA; Guan Y; Bergey M; Jaffe R; Holmes-Maguire L; Martin N; Reilly P
[Ad] Endereço:The Trauma Center at Penn, Penn Presbyterian Medical Center, University of Pennsylvania, Philadelphia, PA, USA; Penn Acute Research Collaboration, Penn Presbyterian Medical Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Electronic address: carrie.sims@uphs.up
[Ti] Título:Arginine vasopressin, copeptin, and the development of relative AVP deficiency in hemorrhagic shock.
[So] Source:Am J Surg;214(4):589-595, 2017 Oct.
[Is] ISSN:1879-1883
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Arginine vasopressin (AVP) is critical for maintaining vasomotor tone and low levels have been associated with the development of irreversible shock. We investigated the clinical relationship between AVP, copeptin (the C-terminal fragment of the AVP precursor), and the development of relative AVP deficiency following hemorrhagic shock. METHODS: A prospective, observational study of 21 hypotensive (SBP<90 mmHg X 2) or presumptively bleeding trauma patients was conducted. Demographics, mechanism of injury, vital signs, laboratory values, transfusions, crystalloid volume, and blood samples were collected on arrival and serially for 48 h. AVP and copeptin were measured post hoc. RESULTS: AVP and copeptin levels were markedly elevated on admission, but decreased rapidly over time (p < 0.001). AVP and copeptin levels were positively correlated on admission (r = 0.769, p < 0.001), in the ICU (r = 0.768, p < 0.001), and at 48 h (r = 0.537, p = 0.02). Initial AVP and copeptin levels predicted the need for ≥10 unit blood product transfusion (AUC = 81% and 87%, respectively). The development of a relative AVP deficiency occurred frequently and was associated with an increased need for blood product transfusion. CONCLUSION: Copeptin correlates well with AVP and initial values predict the need for massive transfusion in trauma patients. Copeptin demonstrates promise as a clinical biomarker in hemorrhagic shock.
[Mh] Termos MeSH primário: Arginina Vasopressina/sangue
Arginina Vasopressina/deficiência
Glicopeptídeos/sangue
Choque Hemorrágico/sangue
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/sangue
Transfusão de Componentes Sanguíneos
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Imunoensaio/métodos
Escala de Gravidade do Ferimento
Masculino
Valor Preditivo dos Testes
Estudos Prospectivos
Ressuscitação/métodos
Choque Hemorrágico/terapia
Ferimentos e Lesões/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Biomarkers); 0 (Glycopeptides); 0 (copeptins); 113-79-1 (Arginine Vasopressin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE


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[PMID]:28714397
[Au] Autor:Golembiewska E; Machowska A; Stenvinkel P; Lindholm B
[Ad] Endereço:Department of Nephrology, Transplantology and Internal Medicine, Pomeranian Medical University, Al. Powstancow Wielkopolskich 72, 70-111 Szczecin. Poland.
[Ti] Título:Prognostic Value of Copeptin in Chronic Kidney Disease: From General Population to End-Stage Renal Disease.
[So] Source:Curr Protein Pept Sci;18(12):1232-1243, 2017.
[Is] ISSN:1875-5550
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Arginine vasopressin (AVP), also known as antidiuretic hormone (ADH), is released in response to osmotic and non-osmotic stimuli and plays a key role in many physiologic and pathologic processes. The main function of AVP is the control of fluid homeostasis by inducing water conservation by the kidney, but it also stimulates arteriolar vasoconstriction and the release of adrenocorticotropic hormone (ACTH). These actions are mediated by different AVP receptors located on various target cells. Produced in hypothalamus from a larger precursor, pre-proAVP, AVP is produced in equimolar amounts to copeptin, a glycopeptide with yet unknown biologic function. Copeptin remains stable in plasma and its circulating concentrations correlate directly with those of AVP. Because AVP is unstable in isolated plasma or serum and its half-life is short, copeptin has become an easily measured surrogate marker reflecting vasopressin concentration. Recently, associations between high circulating copeptin and decline in glomerular filtration rate as well as greater risk of new-onset chronic kidney disease (CKD) have been reported. In addition, copeptin has been shown to be associated with increased risk of complications such as myocardial infarction, heart failure, diabetes mellitus and metabolic syndrome. In this brief review, studies on the prognostic value of copeptin measurement in the general population and in CKD are presented and discussed.
[Mh] Termos MeSH primário: Arginina Vasopressina/genética
Glicopeptídeos/genética
Hipotálamo/metabolismo
Falência Renal Crônica/diagnóstico
[Mh] Termos MeSH secundário: Hormônio Adrenocorticotrópico/sangue
Hormônio Adrenocorticotrópico/genética
Arginina Vasopressina/sangue
Biomarcadores/sangue
Progressão da Doença
Feminino
Regulação da Expressão Gênica
Taxa de Filtração Glomerular
Glicopeptídeos/sangue
Seres Humanos
Falência Renal Crônica/sangue
Falência Renal Crônica/genética
Falência Renal Crônica/patologia
Masculino
Prognóstico
Receptores de Vasopressinas/sangue
Receptores de Vasopressinas/genética
Fatores Sexuais
Transdução de Sinais
Vasopressinas/sangue
Vasopressinas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (Glycopeptides); 0 (Receptors, Vasopressin); 0 (copeptins); 0 (proAVP hormone); 11000-17-2 (Vasopressins); 113-79-1 (Arginine Vasopressin); 9002-60-2 (Adrenocorticotropic Hormone)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE
[do] DOI:10.2174/1389203718666170717095301


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[PMID]:28683273
[Au] Autor:Snyder-Mackler N; Tung J
[Ad] Endereço:Department of Evolutionary Anthropology, Duke University, Durham, NC 27708, USA; Duke Center for the Study of Aging and Human Development, Duke University, Durham, NC 27708, USA.
[Ti] Título:Vasopressin and the Neurogenetics of Parental Care.
[So] Source:Neuron;95(1):9-11, 2017 Jul 05.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Making robust connections between genetic variation, neurophysiology, and social behavior remains a challenge. A study by Bendesky et al. (2017) tackles this challenge by dissecting the genetic architecture of parental care in deer mice to discover an important contribution of vasopressin signaling to the evolution of nest building.
[Mh] Termos MeSH primário: Arginina Vasopressina/genética
Vasopressinas
[Mh] Termos MeSH secundário: Animais
Camundongos
Neurociências
Peromyscus
Comportamento Social
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
11000-17-2 (Vasopressins); 113-79-1 (Arginine Vasopressin)
[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:170707
[St] Status:MEDLINE


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[PMID]:28579251
[Au] Autor:Mucio-Ramírez S; Sánchez-Islas E; Sánchez-Jaramillo E; Currás-Collazo M; Juárez-González VR; Álvarez-González MY; Orser LE; Hou B; Pellicer F; Kodavanti PRS; León-Olea M
[Ad] Endereço:Departamento de Neuromorfología Funcional, Dirección de Investigaciones en Neurociencias, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, Calz. México Xochimilco No. 101, Col. San Lorenzo Huipulco, México D.F. C.P. 14370, México. Electronic address: mucios@imp.edu.mx.
[Ti] Título:Perinatal exposure to organohalogen pollutants decreases vasopressin content and its mRNA expression in magnocellular neuroendocrine cells activated by osmotic stress in adult rats.
[So] Source:Toxicol Appl Pharmacol;329:173-189, 2017 Aug 15.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) are environmental pollutants that produce neurotoxicity and neuroendocrine disruption. They affect the vasopressinergic system but their disruptive mechanisms are not well understood. Our group reported that rats perinatally exposed to Aroclor-1254 (A1254) and DE-71 (commercial mixtures of PCBs and PBDEs) decrease somatodendritic vasopressin (AVP) release while increasing plasma AVP responses to osmotic activation, potentially emptying AVP reserves required for body-water balance. The aim of this research was to evaluate the effects of perinatal exposure to A1254 or DE-71 (30mgkg/day) on AVP transcription and protein content in the paraventricular and supraoptic hypothalamic nuclei, of male and female rats, by in situ hybridization and immunohistochemistry. cFOS mRNA expression was evaluated in order to determine neuroendocrine cells activation due to osmotic stimulation. Animal groups were: vehicle (control); exposed to either A1254 or DE-71; both, control and exposed, subjected to osmotic challenge. The results confirmed a physiological increase in AVP-immunoreactivity (AVP-IR) and gene expression in response to osmotic challenge as reported elsewhere. In contrast, the exposed groups did not show this response to osmotic activation, they showed significant reduction in AVP-IR neurons, and AVP mRNA expression as compared to the hyperosmotic controls. cFOS mRNA expression increased in A1254 dehydrated groups, suggesting that the AVP-IR decrease was not due to a lack of the response to the osmotic activation. Therefore, A1254 may interfere with the activation of AVP mRNA transcript levels and protein, causing a central dysfunction of vasopressinergic system.
[Mh] Termos MeSH primário: Arginina Vasopressina/metabolismo
/toxicidade
Poluentes Ambientais/toxicidade
Éteres Difenil Halogenados/toxicidade
Células Neuroendócrinas/efeitos dos fármacos
Pressão Osmótica
Núcleo Hipotalâmico Paraventricular/efeitos dos fármacos
Efeitos Tardios da Exposição Pré-Natal
RNA Mensageiro/metabolismo
Núcleo Supraóptico/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Arginina Vasopressina/genética
Regulação para Baixo
Feminino
Masculino
Exposição Materna/efeitos adversos
Células Neuroendócrinas/metabolismo
Células Neuroendócrinas/patologia
Núcleo Hipotalâmico Paraventricular/metabolismo
Núcleo Hipotalâmico Paraventricular/patologia
Gravidez
Proteínas Proto-Oncogênicas c-fos/genética
Proteínas Proto-Oncogênicas c-fos/metabolismo
RNA Mensageiro/genética
Ratos Sprague-Dawley
Ratos Wistar
Cloreto de Sódio/administração & dosagem
Núcleo Supraóptico/metabolismo
Núcleo Supraóptico/patologia
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Environmental Pollutants); 0 (Halogenated Diphenyl Ethers); 0 (Proto-Oncogene Proteins c-fos); 0 (RNA, Messenger); 11097-69-1 (Chlorodiphenyl (54% Chlorine)); 113-79-1 (Arginine Vasopressin); 451W47IQ8X (Sodium Chloride); 7REL09ZX35 (pentabromodiphenyl ether)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE


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[PMID]:28558702
[Au] Autor:Jang EA; Song JA; Shin JY; Yoon JJ; Yoo KY; Jeong S
[Ad] Endereço:Department of Anesthesiology and Pain Medicine, Chonnam National University Medical School, 42 Jebong-ro, Dong-gu, Gwangju, 61469, South Korea.
[Ti] Título:Background anaesthetic agents do not influence the impact of arginine vasopressin on haemodynamic states and cerebral oxygenation during shoulder surgery in the beach chair position: a prospective, single-blind study.
[So] Source:BMC Anesthesiol;17(1):73, 2017 May 30.
[Is] ISSN:1471-2253
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Administration of arginine vasopressin (AVP) is associated with reducing jugular venous (SjvO ) and regional cerebral (rScO ) oxygen saturation under propofol-remifentanil (P/R) anaesthesia. We determined whether background anaesthetics modulate the effect of AVP on cerebral oxygenation and haemodynamics. METHODS: We randomly allocated 60 adult patients scheduled for shoulder surgery in the beach chair position (BCP) into 4 groups, to receive either an intravenous bolus of saline (groups PR-S and SN-S) or 0.05 U/kg AVP (groups PR-AVP and SN-AVP) under P/R or sevoflurane-nitrous oxide (S/N) anaesthesia (n = 15 each). Haemodynamic variables, SjvO and rScO were measured. RESULTS: AVP significantly increased mean arterial blood pressure (MAP) and decreased rScO in either anaesthetic group. AVP also decreased SjvO in the P/R groups but not in the S/N groups. The AVP-treated groups showed higher MAP and cerebral desaturation (>20% rScO decrease from baseline), along with lower HR and rScO in the BCP than those in the saline-treated groups. In contrast, AVP did not affect SjvO values or the incidence of SjvO  < 50%. Baseline SjvO was lower and the magnitude of its reduction in the BCP was greater in the PR-AVP group than in the SN-AVP group, and the lowest SjvO values were 37 ± 6 and 57 ± 8%, respectively (P < 0.001). CONCLUSIONS: The choice of anaesthetic regimen did not affect cerebral oxygenation or haemodynamics of AVP in the BCP. However, the negative effect of AVP on cerebral oxygenation should be considered, especially under P/R anaesthesia. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT01687894 , registered on September 18, 2012.
[Mh] Termos MeSH primário: Arginina Vasopressina/administração & dosagem
Encéfalo/metabolismo
Oxigênio/metabolismo
Posicionamento do Paciente
Vasoconstritores/administração & dosagem
[Mh] Termos MeSH secundário: Idoso
Anestésicos/administração & dosagem
Pressão Sanguínea/efeitos dos fármacos
Circulação Cerebrovascular
Feminino
Frequência Cardíaca/efeitos dos fármacos
Seres Humanos
Masculino
Éteres Metílicos/administração & dosagem
Meia-Idade
Óxido Nitroso/administração & dosagem
Oximetria
Piperidinas/administração & dosagem
Propofol/administração & dosagem
Estudos Prospectivos
Articulação do Ombro/cirurgia
Método Simples-Cego
Espectroscopia de Luz Próxima ao Infravermelho
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Anesthetics); 0 (Methyl Ethers); 0 (Piperidines); 0 (Vasoconstrictor Agents); 113-79-1 (Arginine Vasopressin); 38LVP0K73A (sevoflurane); K50XQU1029 (Nitrous Oxide); P10582JYYK (remifentanil); S88TT14065 (Oxygen); YI7VU623SF (Propofol)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170601
[St] Status:MEDLINE
[do] DOI:10.1186/s12871-017-0364-9


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[PMID]:28432473
[Au] Autor:Vishram-Nielsen JK; Gustafsson F
[Ad] Endereço:Department of Cardiology, The Heart Centre, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
[Ti] Título:Vasopressin and Vasopressin Antagonists in Heart Failure.
[So] Source:Handb Exp Pharmacol;243:307-328, 2017.
[Is] ISSN:0171-2004
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Despite the introduction of multiple new pharmacological agents over the past three decades in the field of heart failure (HF), overall prognosis remains poor. Hyponatremia is prevalent in HF patients and has been suggested as a contributor to poor response to standard therapy. Elevated levels of arginine vasopressin (AVP), a peptide hormone produced in the hypothalamus, play a role in development of hyponatremia, and AVP and its surrogate, copeptin, are related to changes in osmolality, hemodynamics, neuro-hormones as well as in overall outcome in HF patients. Of current pharmacological interest are the selective and non-selective vasopressin receptor antagonists (VRAs), which inhibit vasoconstriction and cardiac remodeling mediated by the V receptors in smooth blood vessels, and water retention (increased urine osmolality and decreased water excretion) by increasing aquaporin-2 water channels mediated by the V receptors in the renal collecting tubules. The optimal use of VRAs is yet to be determined, especially in patients with congestive HF. Although long-term effects on improvement in mortality have not been shown in the Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study with Tolvaptan (EVEREST) trial, the only long-term outcome trial to date, many short-term studies indicate beneficial aquaretic- and hemodynamic-effects of the VRAs. In contrast to loop diuretics, these new agents tend to increase urine flow and the excretion of electrolyte-free water (so-called aquaresis) in patients with HF, without substantial changes in sodium or potassium excretion. This chapter reviews the role of AVP and copeptin in HF, and the treatment potential of VRAs in HF.
[Mh] Termos MeSH primário: Antagonistas de Receptores de Hormônios Antidiuréticos/uso terapêutico
Insuficiência Cardíaca/tratamento farmacológico
[Mh] Termos MeSH secundário: Arginina Vasopressina/metabolismo
Benzazepinas/uso terapêutico
Glicopeptídeos/metabolismo
Insuficiência Cardíaca/metabolismo
Hemodinâmica
Seres Humanos
Hiponatremia/metabolismo
Receptores de Vasopressinas/metabolismo
Vasopressinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antidiuretic Hormone Receptor Antagonists); 0 (Benzazepines); 0 (Glycopeptides); 0 (Receptors, Vasopressin); 0 (copeptins); 11000-17-2 (Vasopressins); 113-79-1 (Arginine Vasopressin); 21G72T1950 (tolvaptan)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170423
[St] Status:MEDLINE
[do] DOI:10.1007/164_2017_28


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[PMID]:28413003
[Au] Autor:Toustrup LB; Zhou Y; Kvistgaard H; Gregersen N; Rittig S; Aagaard L; Corydon TJ; Luo Y; Christensen JH
[Ad] Endereço:Department of Paediatrics, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, 8200 Aarhus N, Denmark.
[Ti] Título:Induced pluripotent stem cells derived from a patient with autosomal dominant familial neurohypophyseal diabetes insipidus caused by a variant in the AVP gene.
[So] Source:Stem Cell Res;19:37-42, 2017 Mar.
[Is] ISSN:1876-7753
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI) is caused by variants in the arginine vasopressin (AVP) gene. Here we report the generation of induced pluripotent stem cells (iPSCs) from a 42-year-old man carrying an adFNDI causing variant in exon 1 of the AVP gene using lentivirus-mediated nuclear reprogramming. The iPSCs carried the expected variant in the AVP gene. Furthermore, the iPSCs expressed pluripotency markers; displayed in vitro differentiation potential to the three germ layers and had a normal karyotype consistent with the original fibroblasts. This iPSC line is useful in future studies focusing on the pathogenesis of adFNDI.
[Mh] Termos MeSH primário: Diabetes Insípido Neurogênico/patologia
Células-Tronco Pluripotentes Induzidas/citologia
[Mh] Termos MeSH secundário: Adulto
Arginina Vasopressina/genética
Arginina Vasopressina/metabolismo
Sequência de Bases
Diferenciação Celular
Linhagem Celular
Reprogramação Celular
Diabetes Insípido Neurogênico/metabolismo
Corpos Embrioides/citologia
Vetores Genéticos/genética
Vetores Genéticos/metabolismo
Seres Humanos
Células-Tronco Pluripotentes Induzidas/metabolismo
Cariótipo
Lentivirus/genética
Masculino
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Transcription Factors); 113-79-1 (Arginine Vasopressin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170504
[Lr] Data última revisão:
170504
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE



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