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[PMID]:29465586
[Au] Autor:Wang Y; Li X; Li Z; Zhang Y; Wang D
[Ad] Endereço:The Second Clinical College of Guangzhou University of Chinese Medicine, Guangzhou.
[Ti] Título:YiQiFuMai injection for chronic heart failure: Protocol for a systematic review and meta-analysis.
[So] Source:Medicine (Baltimore);97(8):e9957, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Chronic heart AQ4 failure (CHF) is the final stage of various heart diseases. YiQiFuMai injection (YQFMI) has been widely applied in the treatment of CHF. However, to our knowledge, there has been no systematic review or meta-analysis of randomized controlled trails (RCTs) regarding the effectiveness of this treatment. Here, we provide a protocol to evaluate the efficacy and safety of YQFMI for CHF. METHODS: To evaluate the clinical efficacy of YQFMI in treating CHF, 2 researcher members will independently search the RCTs in the following 8 Chinese and English databases, in which the data collection will be from the time when the respective databases were established to January 2018. The databases will include MEDLINE, EMBASE, Cochrane CENTRAL, CINAHL, the Chinese Biomedical Literature Database, the China National Knowledge Infrastructure, VIP Information and Wanfang Data. The therapeutic effects according to the mortality and the New York Heart Association (NYHA) function classification will be accepted as the primary outcomes. We will use RevMan V.5.3 software as well to compute the data synthesis carefully when a meta-analysis is allowed. RESULTS: This study will provide a high-quality synthesis of current evidence of YQFMI for CHF from several aspects including mortality, NYHA function classification. CONCLUSION: The conclusion of our systematic review will provide evidence to judge whether YQFMI is an effective intervention for CHF.PROSPERO registration number: PROSPERO CRD42017079696.
[Mh] Termos MeSH primário: Cardiotônicos/administração & dosagem
Medicamentos de Ervas Chinesas/administração & dosagem
Insuficiência Cardíaca/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Doença Crônica
Protocolos Clínicos
Feminino
Seres Humanos
Injeções
Masculino
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Cardiotonic Agents); 0 (Drugs, Chinese Herbal); 0 (yi-qi-fu-mai)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180222
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009957


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[PMID]:29376560
[Au] Autor:Schumann J; Henrich EC; Strobl H; Prondzinsky R; Weiche S; Thiele H; Werdan K; Frantz S; Unverzagt S
[Ad] Endereço:Department of Anaesthesiology and Surgical Intensive Care, Martin-Luther-University Halle-Wittenberg, Halle/Saale, Germany.
[Ti] Título:Inotropic agents and vasodilator strategies for the treatment of cardiogenic shock or low cardiac output syndrome.
[So] Source:Cochrane Database Syst Rev;1:CD009669, 2018 01 29.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cardiogenic shock (CS) and low cardiac output syndrome (LCOS) as complications of acute myocardial infarction (AMI), heart failure (HF) or cardiac surgery are life-threatening conditions. While there is a broad body of evidence for the treatment of people with acute coronary syndrome under stable haemodynamic conditions, the treatment strategies for people who become haemodynamically unstable or develop CS remain less clear. We have therefore summarised here the evidence on the treatment of people with CS or LCOS with different inotropic agents and vasodilative drugs. This is the first update of a Cochrane review originally published in 2014. OBJECTIVES: To assess efficacy and safety of cardiac care with positive inotropic agents and vasodilator strategies in people with CS or LCOS due to AMI, HF or cardiac surgery. SEARCH METHODS: We searched CENTRAL, MEDLINE, Embase and CPCI-S Web of Science in June 2017. We also searched four registers of ongoing trials and scanned reference lists and contacted experts in the field to obtain further information. No language restrictions were applied. SELECTION CRITERIA: Randomised controlled trials in people with myocardial infarction, heart failure or cardiac surgery complicated by cardiogenic shock or LCOS. DATA COLLECTION AND ANALYSIS: We used standard methodological procedures expected by Cochrane. MAIN RESULTS: We identified 13 eligible studies with 2001 participants (mean or median age range 58 to 73 years) and two ongoing studies. We categorised studies into eight comparisons, all against cardiac care and additional other active drugs or placebo. These comparisons investigated the efficacy of levosimendan versus dobutamine, enoximone or placebo, epinephrine versus norepinephrine-dobutamine, amrinone versus dobutamine, dopexamine versus dopamine, enoximone versus dopamine and nitric oxide versus placebo.All trials were published in peer-reviewed journals, and analysis was done by the intention-to-treat (ITT) principle. Twelve of 13 trials were small with few included participants. Acknowledgement of funding by the pharmaceutical industry or missing conflict of interest statements emerged in five of 13 trials. In general, confidence in the results of analysed studies was reduced due to serious study limitations, very serious imprecision or indirectness. Domains of concern, which show a high risk of more than 50%, include performance bias (blinding of participants and personnel) and bias affecting the quality of evidence on adverse events.Levosimendan may reduce short-term mortality compared to a therapy with dobutamine (RR 0.60, 95% CI 0.37 to 0.95; 6 studies; 1776 participants; low-quality evidence; NNT: 16 (patients with moderate risk), NNT: 5 (patients with CS)). This initial short-term survival benefit with levosimendan vs. dobutamine is not confirmed on long-term follow up. There is uncertainty (due to lack of statistical power) as to the effect of levosimendan compared to therapy with placebo (RR 0.48, 95% CI 0.12 to 1.94; 2 studies; 55 participants, very low-quality evidence) or enoximone (RR 0.50, 95% CI 0.22 to 1.14; 1 study; 32 participants, very low-quality evidence).All comparisons comparing other positive inotropic, inodilative or vasodilative drugs presented uncertainty on their effect on short-term mortality with very low-quality evidence and based on only one RCT. These single studies compared epinephrine with norepinephrine-dobutamine (RR 1.25, 95% CI 0.41 to 3.77; 30 participants), amrinone with dobutamine (RR 0.33, 95% CI 0.04 to 2.85; 30 participants), dopexamine with dopamine (no in-hospital deaths from 70 participants), enoximone with dobutamine (two deaths from 40 participants) and nitric oxide with placebo (one death from three participants). AUTHORS' CONCLUSIONS: Apart from low quality of evidence data suggesting a short-term mortality benefit of levosimendan compared with dobutamine, at present there are no robust and convincing data to support a distinct inotropic or vasodilator drug-based therapy as a superior solution to reduce mortality in haemodynamically unstable people with cardiogenic shock or LCOS.Considering the limited evidence derived from the present data due to a generally high risk of bias and imprecision, it should be emphasised that there remains a great need for large, well-designed randomised trials on this topic to close the gap between daily practice in critical care medicine and the available evidence. It seems to be useful to apply the concept of 'early goal-directed therapy' in cardiogenic shock and LCOS with early haemodynamic stabilisation within predefined timelines. Future clinical trials should therefore investigate whether such a therapeutic concept would influence survival rates much more than looking for the 'best' drug for haemodynamic support.
[Mh] Termos MeSH primário: Baixo Débito Cardíaco/tratamento farmacológico
Cardiotônicos/uso terapêutico
Infarto do Miocárdio/complicações
Choque Cardiogênico/tratamento farmacológico
Vasodilatadores/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
Baixo Débito Cardíaco/etiologia
Baixo Débito Cardíaco/mortalidade
Causas de Morte
Dobutamina/uso terapêutico
Enoximona/uso terapêutico
Seres Humanos
Hidrazonas/uso terapêutico
Meia-Idade
Infarto do Miocárdio/mortalidade
Óxido Nítrico/uso terapêutico
Piridazinas/uso terapêutico
Ensaios Clínicos Controlados Aleatórios como Assunto
Choque Cardiogênico/etiologia
Choque Cardiogênico/mortalidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Cardiotonic Agents); 0 (Hydrazones); 0 (Pyridazines); 0 (Vasodilator Agents); 31C4KY9ESH (Nitric Oxide); 349552KRHK (simendan); 3S12J47372 (Dobutamine); C7Z4ITI7L7 (Enoximone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180130
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD009669.pub3


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[PMID]:28610437
[Au] Autor:Song Y; Zhou J; Wang X; Xie X; Zhao Y; Ni F; Huang W; Wang Z; Xiao W
[Ad] Endereço:a Jiangsu Kanion Pharmaceutical Co., Ltd. , Lianyungang , People's Republic of China.
[Ti] Título:A new ferulic acid ester from Rhodiola wallichiana var. cholaensis (Crassulaceae).
[So] Source:Nat Prod Res;32(1):77-84, 2018 Jan.
[Is] ISSN:1478-6427
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A new ferulic acid ester, 6-feruloyloxyhexanoic acid (1), was isolated along with 10 known ones (2-11), from the concentrated water extract of Rhodiola wallichiana var. cholaensis. Their chemical structures were elucidated on the basis of extensive spectroscopic methods including Two-dimensional nuclear magnetic resonance (2D NMR) experiments. Compound 3 was isolated from this plant for the first time. The protective effects against H O -induced myocardial cell injury in cultured H9c2 cells were also evaluated. Compounds 1, 5 and 7-11 provided significant protective effects on H O -induced H9c2 cells injury at the concentration of 25 µg/mL. And the protective effects of compound 1 was also investigated by the oxygen-glucose deprivation/reperfusion (OGD/R) tests.
[Mh] Termos MeSH primário: Caproatos/farmacologia
Cardiotônicos/farmacologia
Ácidos Cumáricos/farmacologia
Rhodiola/química
[Mh] Termos MeSH secundário: Animais
Antioxidantes/química
Antioxidantes/farmacologia
Caproatos/administração & dosagem
Caproatos/química
Cardiotônicos/administração & dosagem
Cardiotônicos/química
Células Cultivadas
Ácidos Cumáricos/administração & dosagem
Ácidos Cumáricos/química
Relação Dose-Resposta a Droga
Ésteres/administração & dosagem
Ésteres/química
Ésteres/farmacologia
Peróxido de Hidrogênio/toxicidade
Espectroscopia de Ressonância Magnética
Estrutura Molecular
Miócitos Cardíacos/citologia
Miócitos Cardíacos/efeitos dos fármacos
Extratos Vegetais/química
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Caproates); 0 (Cardiotonic Agents); 0 (Coumaric Acids); 0 (Esters); 0 (Plant Extracts); BBX060AN9V (Hydrogen Peroxide)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170615
[St] Status:MEDLINE
[do] DOI:10.1080/14786419.2017.1335724


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[PMID]:29373815
[Au] Autor:Deshpande GP; Imamdin A; Lecour S; Opie LH
[Ad] Endereço:Hatter Institute for cardiovascular Research in Africa, Department of Medicine, University of Cape Town, South Africa. Electronic address: gdeshpande@sun.ac.za.
[Ti] Título:Sphingosine-1-phosphate (S1P) activates STAT3 to protect against de novo acute heart failure (AHF).
[So] Source:Life Sci;196:127-132, 2018 Mar 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Acute heart failure (AHF) is a burden disease, with high mortality and re-hospitalisations. Using an ex-vivo model of AHF, we have previously reported that sphingosine-1-phosphate (S1P) confers cardioprotection. However, the mechanisms remain to be elucidated. In the present study, we aimed to examine the role of the cardioprotective signal transducer and activator of transcription 3 (STAT3) in S1P mediated improved functional recovery in AHF. MATERIAL AND METHODS: Isolated hearts from male Long-Evans rats were subjected to hypotensive AHF for 35 min followed by a recovery phase of 30 min (n ≥ 4/group). S1P (10 nM) was given during either the hypotensive or the recovery phase with/without an inhibitor of STAT3, AG490. Functional parameters were recorded throughout the experiment. KEY FINDINGS: Following an AHF insult, S1P, given during the recovery phase, improved the heart rate (HR) compared to the control (175.2 ±â€¯30.7 vs. 71.6 ±â€¯27.4 beats per minute (BPM); p < 0.05), with no changes in the left ventricular developed pressure. This effect was associated with an increase in phosphorylated STAT3 levels in the nucleus. Addition of AG490 with S1P abolished the cardioprotective effect of S1P (42.3 ±â€¯17.1 vs. 148.8 ±â€¯26.4 BPM for S1P; p < 0.05). SIGNIFICANCE: Our data suggest that S1P protects in an ex-vivo rat heart model of AHF by activation of STAT3 and provide further evidence for the usage of S1P as a potential therapy in patients suffering from AHF.
[Mh] Termos MeSH primário: Cardiotônicos/farmacologia
Insuficiência Cardíaca/prevenção & controle
Lisofosfolipídeos/farmacologia
Fator de Transcrição STAT3/metabolismo
Esfingosina/análogos & derivados
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Pressão Sanguínea/efeitos dos fármacos
Frequência Cardíaca/efeitos dos fármacos
Técnicas In Vitro
Masculino
Fosforilação/efeitos dos fármacos
Ratos
Ratos Long-Evans
Fator de Transcrição STAT3/antagonistas & inibidores
Fator de Transcrição STAT3/efeitos dos fármacos
Esfingosina/farmacologia
Tirfostinas/farmacologia
Disfunção Ventricular Esquerda/induzido quimicamente
Disfunção Ventricular Esquerda/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cardiotonic Agents); 0 (Lysophospholipids); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, rat); 0 (Tyrphostins); 0 (alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide); 26993-30-6 (sphingosine 1-phosphate); NGZ37HRE42 (Sphingosine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180127
[St] Status:MEDLINE


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[PMID]:29254304
[Au] Autor:Li JK; Wang C; Gong HD; Li HZ
[Ad] Endereço:Department of Neurosurgery, Affiliated HongQi Hospital of Mu Dan Jiang Medical University, Mudanjiang City, China.
[Ti] Título:Coagulation in hindbrain membrane meningioma patients treated with different injections using acute hypervolemic hemodilution.
[So] Source:J Biol Regul Homeost Agents;31(4):991-996, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to analyze the changes in coagulation in meningioma patients treated with different injections using the method of acute hypervolemic hemodilution (AHH). One hundred fifty hindbrain membrane meningioma patients were randomly divided into 5 groups, 30 per group. The first group were injected 40ml/time with Danhong after anesthesia induction; the second group were injected with 40ml~60ml/time Kangai and combined with interventional chemotherapy and embolization procedure; the third group of AHH were injected with polygeline 15ml/kg; the fourth group were injected with hydroxyethyl starch (130/0.4) sodium chloride in doses of 15ml/kg; the control group underwent basic treatment for lowering blood pressure and lowering blood fat. The changes of coagulation index were recorded before and after surgery and before and after the injection of different medications. Compared to the control group, for the first group of AHH, after being treated for 10 days and 30 days, the concentrations of bone specific alkaline phosphatase (BALP), bone Gla protein (BGP) and pro-collagen carboxy-terminal propeptide (PICP) were higher than that of the control group, the levels of endotoxin (ET) and C-reactive protein (CRP) were decreased compared to the control group (p less than 0.05); for the second group of AHH, after being treated for 10 days, the index of prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), fibrinogen (Fg) were not significantly changed, but the related level of vascular endothelial growth factor (VEGF) significantly decreased (p less than 0.05). Comparing the coagulation function index after surgery in the third and fourth groups, there were no significant changes in mean arterial pressure (MAP) level, heart rate (HR) value presented a low decrease, central venous pressure (CVP) level increased and the level of interleukin IL-6 showed a steady state after increasing. Analyzing the levels of interleukin IL-8 and tumor necrosis factor-α (TNF-α) after surgery, it was seen that in the third group they increased and in the fourth group they decreased (p less than 0.05). Danhong injection improved the coagulation function and microcirculation of patients, Kangai injection and interventional chemotherapy and embolization restrained the appearance of tumor angiogenesis, AHH operation with polygeline injection and hydroxyethyl starch (130/0.4) sodium chloride kept blood flow in normal parameters.
[Mh] Termos MeSH primário: Coagulação Sanguínea/efeitos dos fármacos
Cardiotônicos/uso terapêutico
Medicamentos de Ervas Chinesas/uso terapêutico
Hemodiluição/métodos
Neoplasias Meníngeas/tratamento farmacológico
Meningioma/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Fosfatase Alcalina/genética
Fosfatase Alcalina/metabolismo
Pressão Arterial/efeitos dos fármacos
Pressão Arterial/fisiologia
Biomarcadores/metabolismo
Viscosidade Sanguínea/efeitos dos fármacos
Proteína C-Reativa/genética
Proteína C-Reativa/metabolismo
Embolização Terapêutica/métodos
Endotoxinas/metabolismo
Feminino
Fibrinogênio/genética
Fibrinogênio/metabolismo
Expressão Gênica
Frequência Cardíaca/efeitos dos fármacos
Frequência Cardíaca/fisiologia
Seres Humanos
Derivados de Hidroxietil Amido/administração & dosagem
Masculino
Neoplasias Meníngeas/sangue
Neoplasias Meníngeas/patologia
Neoplasias Meníngeas/cirurgia
Meningioma/sangue
Meningioma/patologia
Meningioma/cirurgia
Meia-Idade
Osteocalcina/genética
Osteocalcina/metabolismo
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Substitutos do Plasma/administração & dosagem
Poligelina/administração & dosagem
Pró-Colágeno/genética
Pró-Colágeno/metabolismo
Rombencéfalo/efeitos dos fármacos
Rombencéfalo/metabolismo
Rombencéfalo/patologia
Rombencéfalo/cirurgia
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cardiotonic Agents); 0 (Drugs, Chinese Herbal); 0 (Endotoxins); 0 (Hydroxyethyl Starch Derivatives); 0 (Peptide Fragments); 0 (Plasma Substitutes); 0 (Procollagen); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 0 (danhong); 0 (procollagen type I carboxy terminal peptide); 104982-03-8 (Osteocalcin); 9001-32-5 (Fibrinogen); 9007-41-4 (C-Reactive Protein); 9015-56-9 (Polygeline); EC 3.1.3.1 (Alkaline Phosphatase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE


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[PMID]:29249634
[Au] Autor:Hirose M; Takano H; Hasegawa H; Tadokoro H; Hashimoto N; Takemura G; Kobayashi Y
[Ad] Endereço:Department of Cardiovascular Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.
[Ti] Título:The effects of dipeptidyl peptidase-4 on cardiac fibrosis in pressure overload-induced heart failure.
[So] Source:J Pharmacol Sci;135(4):164-173, 2017 Dec.
[Is] ISSN:1347-8648
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Dipeptidyl peptidase-4 (DPP-4) inhibitors are hypoglycemic agents. DPP-4 inhibitor has cardioprotective effects after transverse aortic constriction (TAC), but role of DPP-4 on cardiac fibrosis after TAC is not well known. Our aim was to determine the effects of DPP-4 on cardiac fibrosis in murine TAC model. Wild-type mice and DPP-4 knockout mice were subjected to TAC. Wild-type mice were then treated with vehicle or DPP-4 inhibitor. DPP-4 activities in serum and heart tissue were significantly increased at 2 weeks after TAC, but they were significantly decreased by DPP-4 inhibitor treatment. The inhibition of DPP-4 did not affect left ventricular hypertrophy, but improved cardiac function and decreased myocardial and perivascular fibrosis after TAC. The inhibition of DPP-4 decreased the collagen type III/I ratio in myocardium. These results suggest that DPP-4 inhibition ameliorates the progression of heart failure after TAC by changing the quality and quantity of cardiac fibrosis.
[Mh] Termos MeSH primário: Cardiotônicos
Dipeptidil Peptidase 4/fisiologia
Inibidores da Dipeptidil Peptidase IV/farmacologia
Inibidores da Dipeptidil Peptidase IV/uso terapêutico
Insuficiência Cardíaca/tratamento farmacológico
Insuficiência Cardíaca/etiologia
Miocárdio/patologia
[Mh] Termos MeSH secundário: Animais
Aorta
Estenose da Valva Aórtica/complicações
Colágeno Tipo I/metabolismo
Colágeno Tipo III/metabolismo
Constrição Patológica
Dipeptidil Peptidase 4/metabolismo
Modelos Animais de Doenças
Fibrose
Insuficiência Cardíaca/patologia
Hipertensão/complicações
Hipertrofia
Masculino
Camundongos Endogâmicos C57BL
Miocárdio/metabolismo
Pressão
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cardiotonic Agents); 0 (Collagen Type I); 0 (Collagen Type III); 0 (Dipeptidyl-Peptidase IV Inhibitors); EC 3.4.14.5 (Dipeptidyl Peptidase 4)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE


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[PMID]:29384879
[Au] Autor:Jung KJ; Nho JH; Cho HK; Hong S; Won SH; Chun DI; Kim B
[Ad] Endereço:Department of Orthopaedic Surgery, Soonchunhyang University Hospital Cheonan, Cheonan-si.
[Ti] Título:Amputation of multiple limbs caused by use of inotropics: Case report, a report of 4 cases.
[So] Source:Medicine (Baltimore);97(5):e9800, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: We present 4 cases of symmetrical peripheral gangrene (SPG) associated with use of inotropic agent to elevate blood pressure. SPG is a relatively rare phenomenon characterized by symmetrical distal ischemic damage that leads to gangrene of 2 or more sites in the absence of large blood vessel obstruction, where vasoconstriction rather than thrombosis is implicated as the underlying pathophysiology. We present 4 SPG cases of the multiple limbs amputation, associated with inevitable use of inotropic agents. PATIENT CONCERNS: Inotropic agents including dopamine and norepinephrine are used frequently in the treatment of hypotension, and its effectiveness in treating shock is firmly established. However, it can be caused peripheral gangrene by prolonged administration of high dose inotropics, inducing the constant contraction of the peripheral blood vessels. DIAGNOSIS: These 4 patients had different clinical histories and background factors, but each experienced sepsis. The level of amputation is determined by the line of demarcation in concert with considerations of the biomechanics of stump stability, weight bearing, and ambulation. INTERVENTIONS: After recovering of general conditions and completion of demarcation, these 4 patients underwent the amputation of multiple limbs.(bilateral amputations of upper extremities or bilateral amputations of lower extremities). OUTCOMES: In each patient, there was no additional amputation caused by extension of SPG, and the rehabilitation with appropriate orthosis was performed. Treatment of underlying disease were continued too. LESSONS: It is important to alert the possibility of amputations, according to the use of inevitable inotropics. We recommended the careful use of the inotropic agents to the physicians in treating septic shock.
[Mh] Termos MeSH primário: Amputação
Cardiotônicos/efeitos adversos
Dopamina/efeitos adversos
Extremidades/irrigação sanguínea
Extremidades/patologia
Norepinefrina/efeitos adversos
[Mh] Termos MeSH secundário: Adulto
Idoso
Extremidades/cirurgia
Feminino
Gangrena
Seres Humanos
Masculino
Meia-Idade
Vasoconstritores/efeitos adversos
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cardiotonic Agents); 0 (Vasoconstrictor Agents); VTD58H1Z2X (Dopamine); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009800


  8 / 15831 MEDLINE  
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[PMID]:29217190
[Au] Autor:Unuma K; Aki T; Nagano S; Watanabe R; Uemura K
[Ad] Endereço:Department of Forensic Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo, 113-8519, Japan.
[Ti] Título:The down-regulation of cardiac contractile proteins underlies myocardial depression during sepsis and is mitigated by carbon monoxide.
[So] Source:Biochem Biophys Res Commun;495(2):1668-1674, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aim of this study is to investigate the mechanism underling cardiac dysfunction during sepsis, as well as the possible amelioration of this dysfunction by exogenous carbon monoxide (CO) administration. For this purpose, rats (six-week-old, male, Sprague-Dawley) were administered LPS (15 mg/kg body weight, i.p. 6 h) and/or CORM (30 mg/kg, i.p.). The decreased left ventricular ejection fraction (EF) observed in LPS group rats was recovered in the LSP + CORM group, confirming the protective role of CO against sepsis-induced myocardial depression. Proteomic as well as immunoblot analysis showed that the levels of myosin heavy and light chains (MHC and MLC) as well as α-cardiac actin (ACTC) were decreased in the LPS group, and these decreases were mitigated in the LSP + CORM group, suggesting that the amounts of major contractile proteins are decreased in depressed myocardium. Not only LPS-induced inflammatory cytokine (TNFα and IL-1ß) production but also the decrease in myofilament proteins was mitigated by CORM. These results confirm the protective action of exogenously administered CO against myocardial depression during sepsis, and reveal a novel mechanism underling cardiac dysfunction during sepsis.
[Mh] Termos MeSH primário: Monóxido de Carbono/metabolismo
Proteínas Musculares/metabolismo
Miocárdio/metabolismo
Sepse/metabolismo
[Mh] Termos MeSH secundário: Actinas/genética
Actinas/metabolismo
Animais
Miosinas Cardíacas/genética
Miosinas Cardíacas/metabolismo
Cardiotônicos/farmacologia
Linhagem Celular
Citocinas/genética
Modelos Animais de Doenças
Regulação para Baixo
Expressão Gênica/efeitos dos fármacos
Lipopolissacarídeos/toxicidade
Masculino
Proteínas Musculares/genética
Contração Miocárdica/efeitos dos fármacos
Contração Miocárdica/fisiologia
Miocárdio/patologia
Compostos Organometálicos/farmacologia
Ratos
Ratos Sprague-Dawley
Proteínas Ligases SKP Culina F-Box/metabolismo
Sepse/tratamento farmacológico
Sepse/patologia
Proteínas com Motivo Tripartido/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Actins); 0 (Cardiotonic Agents); 0 (Cytokines); 0 (Lipopolysaccharides); 0 (Muscle Proteins); 0 (Organometallic Compounds); 0 (Tripartite Motif Proteins); 0 (tricarbonylchloro(glycinato)ruthenium(II)); 7U1EE4V452 (Carbon Monoxide); EC 2.3.2.27 (Fbxo32 protein, rat); EC 2.3.2.27 (SKP Cullin F-Box Protein Ligases); EC 2.3.2.27 (Trim63 protein, rat); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 3.6.1.- (Cardiac Myosins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE


  9 / 15831 MEDLINE  
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[PMID]:29406244
[Au] Autor:Ashokkumar R; Jamuna S; Sakeena Sadullah MS; Niranjali Devaraj S
[Ad] Endereço:Department of Biochemistry, University of Madras, Guindy Campus, Chennai 600 025, India.
[Ti] Título:Vitexin protects isoproterenol induced post myocardial injury by modulating hipposignaling and ER stress responses.
[So] Source:Biochem Biophys Res Commun;496(2):731-737, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The molecular mechanisms involved in ER stress-induced post myocardial injury remain elusive. In this study, we have investigated the molecular mechanism of ER stress-mediated myocyte death in Isoproterenol (ISO) induced myocardial infarction and its inhibition by a potent anti oxidant and anti-apoptotic bioflavonoid, Vitexin. ISO mediated apoptosis was found to be associated with ER permeabilization and characterized by enhanced production of ROS, activation of caspase-3, modulation of Bcl2 family proteins and activation of bnip3. Moreover, post treatment with Vitexin inhibits the ISO induced translocation of CHOP to nucleus during MI. Further results have demonstrated that, activation of Mst1 through ER stress was diminished upon treatment with Vitexin. In addition to this, Vitexin treatment significantly downregulated the expression of p-Yap and p-Mst1 which were enhanced during post myocardial injury. Taken together, our data indicate that co-ordinated activation of ER stress and hipposignaling by ISO was ameliorated by the potent cardioprotective effects of Vitexin.
[Mh] Termos MeSH primário: Antioxidantes/uso terapêutico
Apigenina/uso terapêutico
Cardiotônicos/uso terapêutico
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Infarto do Miocárdio/tratamento farmacológico
Miócitos Cardíacos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Caspase 3/metabolismo
Isoproterenol
Masculino
Infarto do Miocárdio/induzido quimicamente
Infarto do Miocárdio/patologia
Miócitos Cardíacos/patologia
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Ratos Wistar
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antioxidants); 0 (Cardiotonic Agents); 0 (Proto-Oncogene Proteins c-bcl-2); 7V515PI7F6 (Apigenin); 9VP70K75OK (vitexin); EC 3.4.22.- (Caspase 3); L628TT009W (Isoproterenol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


  10 / 15831 MEDLINE  
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[PMID]:29241711
[Au] Autor:Wang ZY; Liu YY; Liu GH; Lu HB; Mao CY
[Ad] Endereço:Department of Cardiology, China-Japan Union Hospital, Jilin University, Changchun, PR China.
[Ti] Título:l-Carnitine and heart disease.
[So] Source:Life Sci;194:88-97, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Cardiovascular disease (CVD) is a key cause of deaths worldwide, comprising 15-17% of healthcare expenditure in developed countries. Current records estimate an annual global average of 30 million cardiac dysfunction cases, with a predicted escalation by two-three folds for the next 20-30years. Although ß-blockers and angiotensin-converting-enzymes are commonly prescribed to control CVD risk, hepatotoxicity and hematological changes are frequent adverse events associated with these drugs. Search for alternatives identified endogenous cofactor l-carnitine, which is capable of promoting mitochondrial ß-oxidation towards a balanced cardiac energy metabolism. l-Carnitine facilitates transport of long-chain fatty acids into the mitochondrial matrix, triggering cardioprotective effects through reduced oxidative stress, inflammation and necrosis of cardiac myocytes. Additionally, l-carnitine regulates calcium influx, endothelial integrity, intracellular enzyme release and membrane phospholipid content for sustained cellular homeostasis. Carnitine depletion, characterized by reduced expression of "organic cation transporter-2" gene, is a metabolic and autosomal recessive disorder that also frequently associates with CVD. Hence, exogenous carnitine administration through dietary and intravenous routes serves as a suitable protective strategy against ventricular dysfunction, ischemia-reperfusion injury, cardiac arrhythmia and toxic myocardial injury that prominently mark CVD. Additionally, carnitine reduces hypertension, hyperlipidemia, diabetic ketoacidosis, hyperglycemia, insulin-dependent diabetes mellitus, insulin resistance, obesity, etc. that enhance cardiovascular pathology. These favorable effects of l-carnitine have been evident in infants, juvenile, young, adult and aged patients of sudden and chronic heart failure as well. This review describes the mechanism of action, metabolism and pharmacokinetics of l-carnitine. It specifically emphasizes upon the beneficial role of l-carnitine in cardiomyopathy.
[Mh] Termos MeSH primário: Cardiotônicos/uso terapêutico
Carnitina/uso terapêutico
Cardiopatias/tratamento farmacológico
Coração/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Arritmias Cardíacas/tratamento farmacológico
Arritmias Cardíacas/metabolismo
Arritmias Cardíacas/patologia
Cardiotônicos/metabolismo
Carnitina/metabolismo
Cardiopatias/metabolismo
Cardiopatias/patologia
Seres Humanos
Traumatismo por Reperfusão Miocárdica/tratamento farmacológico
Traumatismo por Reperfusão Miocárdica/metabolismo
Traumatismo por Reperfusão Miocárdica/patologia
Miocárdio/metabolismo
Miocárdio/patologia
Disfunção Ventricular/tratamento farmacológico
Disfunção Ventricular/metabolismo
Disfunção Ventricular/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cardiotonic Agents); S7UI8SM58A (Carnitine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE



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