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[PMID]:28453734
[Au] Autor:Hausenloy DJ; Garcia-Dorado D; Bøtker HE; Davidson SM; Downey J; Engel FB; Jennings R; Lecour S; Leor J; Madonna R; Ovize M; Perrino C; Prunier F; Schulz R; Sluijter JPG; Van Laake LW; Vinten-Johansen J; Yellon DM; Ytrehus K; Heusch G; Ferdinandy P
[Ad] Endereço:The Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London WC1E 6HX, UK; The National Institute of Health Research University College London Hospitals Biomedical Research Centre, 149 Tottenham Court Road London, W1T 7DN, UK; Cardiovascular and Metabolic Disorders Program
[Ti] Título:Novel targets and future strategies for acute cardioprotection: Position Paper of the European Society of Cardiology Working Group on Cellular Biology of the Heart.
[So] Source:Cardiovasc Res;113(6):564-585, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Ischaemic heart disease and the heart failure that often results, remain the leading causes of death and disability in Europe and worldwide. As such, in order to prevent heart failure and improve clinical outcomes in patients presenting with an acute ST-segment elevation myocardial infarction and patients undergoing coronary artery bypass graft surgery, novel therapies are required to protect the heart against the detrimental effects of acute ischaemia/reperfusion injury (IRI). During the last three decades, a wide variety of ischaemic conditioning strategies and pharmacological treatments have been tested in the clinic-however, their translation from experimental to clinical studies for improving patient outcomes has been both challenging and disappointing. Therefore, in this Position Paper of the European Society of Cardiology Working Group on Cellular Biology of the Heart, we critically analyse the current state of ischaemic conditioning in both the experimental and clinical settings, provide recommendations for improving its translation into the clinical setting, and highlight novel therapeutic targets and new treatment strategies for reducing acute myocardial IRI.
[Mh] Termos MeSH primário: Cardiologia/métodos
Fármacos Cardiovasculares/uso terapêutico
Ponte de Artéria Coronária/efeitos adversos
Insuficiência Cardíaca/prevenção & controle
Precondicionamento Isquêmico/métodos
Traumatismo por Reperfusão Miocárdica/prevenção & controle
Intervenção Coronária Percutânea/efeitos adversos
Infarto do Miocárdio com Supradesnível do Segmento ST/terapia
Pesquisa Médica Translacional/métodos
[Mh] Termos MeSH secundário: Animais
Cardiologia/normas
Fármacos Cardiovasculares/efeitos adversos
Ponte de Artéria Coronária/normas
Modelos Animais de Doenças
Insuficiência Cardíaca/etiologia
Insuficiência Cardíaca/patologia
Insuficiência Cardíaca/fisiopatologia
Seres Humanos
Pós-Condicionamento Isquêmico/métodos
Precondicionamento Isquêmico/efeitos adversos
Precondicionamento Isquêmico/normas
Precondicionamento Isquêmico Miocárdico/métodos
Traumatismo por Reperfusão Miocárdica/etiologia
Traumatismo por Reperfusão Miocárdica/patologia
Traumatismo por Reperfusão Miocárdica/fisiopatologia
Intervenção Coronária Percutânea/normas
Fatores de Proteção
Fatores de Risco
Infarto do Miocárdio com Supradesnível do Segmento ST/complicações
Infarto do Miocárdio com Supradesnível do Segmento ST/patologia
Infarto do Miocárdio com Supradesnível do Segmento ST/fisiopatologia
Pesquisa Médica Translacional/normas
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; PRACTICE GUIDELINE; REVIEW
[Nm] Nome de substância:
0 (Cardiovascular Agents)
[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:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx049


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[PMID]:28750029
[Au] Autor:Long Z; Duan G; Li H; Yi T; Wu X; Chen F; Wu Z; Gao Y
[Ad] Endereço:Department of Anesthesiology, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
[Ti] Título:Ubiquinol-cytochrome c reductase core protein 1 may be involved in delayed cardioprotection from preconditioning induced by diazoxide.
[So] Source:PLoS One;12(7):e0181903, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study aimed to use long-term diazoxide treatment to establish a loss-of-cardioprotection model and then perform proteomics analysis to explore which proteins of mitochondrial inner membrane (MIM) are potentially involved in delayed cardioprotection. Rats received 1 to 8 weeks of diazoxide treatments (20 mg•kg-1•d-1) to establish a loss-of-cardioprotection model in different groups. Detection of serum cTnI levels and cell apoptosis assays in heart tissue were performed. Then, rats MIM after 0, 4 and 6 weeks of diazoxide treatment was isolated and proteomics analysis was performed. An invitro model of H9C2 cells was performed to explore the effects of targeted protein on delayed cardioprotection. The effect of delayed cardioprotection by diazoxide preconditioning disappeared when diazoxide treatments were given for six weeks or longer. Ubiquinol-cytochrome c reductase core protein 1 (UQCRC1) was identified in the proteomics analysis. UQCRC1 expression was upregulated by diazoxide treatment in H9C2 cells, and UQCRC1 down-regulation could increase the lactate dehydrogenase release and apoptosis rate after injury induced by oxygen glucose deprivation. These results showed that UQCRC1 might contribute to the loss-of-cardioprotection model induced by long-term diazoxide treatment and play a role in delayed cardioprotection.
[Mh] Termos MeSH primário: Cardiotônicos/farmacologia
Diazóxido/farmacologia
Complexo III da Cadeia de Transporte de Elétrons/metabolismo
Precondicionamento Isquêmico Miocárdico
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Linhagem Celular
Regulação para Baixo/efeitos dos fármacos
Glucose/deficiência
Marcação In Situ das Extremidades Cortadas
Masculino
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Membranas Mitocondriais/efeitos dos fármacos
Membranas Mitocondriais/metabolismo
Miocárdio/patologia
Oxigênio
Proteômica
Ratos
Troponina I/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cardiotonic Agents); 0 (Troponin I); EC 1.10.2.2 (Electron Transport Complex III); EC 1.10.2.2 (Uqcrc1 protein, rat); IY9XDZ35W2 (Glucose); O5CB12L4FN (Diazoxide); S88TT14065 (Oxygen)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181903


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[PMID]:28600454
[Au] Autor:Smith CO; Nehrke K; Brookes PS
[Ad] Endereço:Department of Biochemistry, University of Rochester Medical Center, Rochester, NY, U.S.A.
[Ti] Título:The Slo(w) path to identifying the mitochondrial channels responsible for ischemic protection.
[So] Source:Biochem J;474(12):2067-2094, 2017 Jun 09.
[Is] ISSN:1470-8728
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mitochondria play an important role in tissue ischemia and reperfusion (IR) injury, with energetic failure and the opening of the mitochondrial permeability transition pore being the major causes of IR-induced cell death. Thus, mitochondria are an appropriate focus for strategies to protect against IR injury. Two widely studied paradigms of IR protection, particularly in the field of cardiac IR, are ischemic preconditioning (IPC) and volatile anesthetic preconditioning (APC). While the molecular mechanisms recruited by these protective paradigms are not fully elucidated, a commonality is the involvement of mitochondrial K channel opening. In the case of IPC, research has focused on a mitochondrial ATP-sensitive K channel (mitoK ), but, despite recent progress, the molecular identity of this channel remains a subject of contention. In the case of APC, early research suggested the existence of a mitochondrial large-conductance K (BK, big conductance of potassium) channel encoded by the gene, although more recent work has shown that the channel that underlies APC is in fact encoded by In this review, we discuss both the pharmacologic and genetic evidence for the existence and identity of mitochondrial K channels, and the role of these channels both in IR protection and in regulating normal mitochondrial function.
[Mh] Termos MeSH primário: Alostase
Mitocôndrias Cardíacas/metabolismo
Modelos Biológicos
Isquemia Miocárdica/metabolismo
Traumatismo por Reperfusão Miocárdica/metabolismo
Canais de Potássio/metabolismo
[Mh] Termos MeSH secundário: Animais
Cardiotônicos/farmacologia
Seres Humanos
Ativação do Canal Iônico/efeitos dos fármacos
Precondicionamento Isquêmico Miocárdico
Canais KATP/agonistas
Canais KATP/antagonistas & inibidores
Canais KATP/genética
Canais KATP/metabolismo
Subunidades alfa do Canal de Potássio Ativado por Cálcio de Condutância Alta/agonistas
Subunidades alfa do Canal de Potássio Ativado por Cálcio de Condutância Alta/antagonistas & inibidores
Subunidades alfa do Canal de Potássio Ativado por Cálcio de Condutância Alta/genética
Subunidades alfa do Canal de Potássio Ativado por Cálcio de Condutância Alta/metabolismo
Moduladores de Transporte de Membrana/farmacologia
Mitocôndrias Cardíacas/efeitos dos fármacos
Isquemia Miocárdica/terapia
Traumatismo por Reperfusão Miocárdica/prevenção & controle
Bloqueadores dos Canais de Potássio/farmacologia
Canais de Potássio/agonistas
Canais de Potássio/química
Canais de Potássio/genética
Isoformas de Proteínas/agonistas
Isoformas de Proteínas/antagonistas & inibidores
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Terminologia como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cardiotonic Agents); 0 (KATP Channels); 0 (KCNMA1 protein, human); 0 (KCNT2 protein, human); 0 (Large-Conductance Calcium-Activated Potassium Channel alpha Subunits); 0 (Membrane Transport Modulators); 0 (Potassium Channel Blockers); 0 (Potassium Channels); 0 (Protein Isoforms)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170611
[St] Status:MEDLINE
[do] DOI:10.1042/BCJ20160623


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[PMID]:28596216
[Au] Autor:Fernández-Jiménez R; Galán-Arriola C; Sánchez-González J; Agüero J; López-Martín GJ; Gomez-Talavera S; Garcia-Prieto J; Benn A; Molina-Iracheta A; Barreiro-Pérez M; Martin-García A; García-Lunar I; Pizarro G; Sanz J; Sánchez PL; Fuster V; Ibanez B
[Ad] Endereço:From the Department of Clinical Research, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain (R.F.-J., C.G.-A., J.A., G.J.L.-M., S.G.-T., J.G.-P., A.B., A.M.-I., I.G.-L., G.P., J.S., V.L., B.I.); Centro de Investigación Biomédica en Red de enfermedades CardioVascula
[Ti] Título:Effect of Ischemia Duration and Protective Interventions on the Temporal Dynamics of Tissue Composition After Myocardial Infarction.
[So] Source:Circ Res;121(4):439-450, 2017 Aug 04.
[Is] ISSN:1524-4571
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: The impact of cardioprotective strategies and ischemia duration on postischemia/reperfusion (I/R) myocardial tissue composition (edema, myocardium at risk, infarct size, salvage, intramyocardial hemorrhage, and microvascular obstruction) is not well understood. OBJECTIVE: To study the effect of ischemia duration and protective interventions on the temporal dynamics of myocardial tissue composition in a translational animal model of I/R by the use of state-of-the-art imaging technology. METHODS AND RESULTS: Four 5-pig groups underwent different I/R protocols: 40-minute I/R (prolonged ischemia, controls), 20-minute I/R (short-duration ischemia), prolonged ischemia preceded by preconditioning, or prolonged ischemia followed by postconditioning. Serial cardiac magnetic resonance (CMR)-based tissue characterization was done in all pigs at baseline and at 120 minutes, day 1, day 4, and day 7 after I/R. Reference myocardium at risk was assessed by multidetector computed tomography during the index coronary occlusion. After the final CMR, hearts were excised and processed for water content quantification and histology. Five additional healthy pigs were euthanized after baseline CMR as reference. Edema formation followed a bimodal pattern in all 40-minute I/R pigs, regardless of cardioprotective strategy and the degree of intramyocardial hemorrhage or microvascular obstruction. The hyperacute edematous wave was ameliorated only in pigs showing cardioprotection (ie, those undergoing short-duration ischemia or preconditioning). In all groups, CMR-measured edema was barely detectable at 24 hours postreperfusion. The deferred healing-related edematous wave was blunted or absent in pigs undergoing preconditioning or short-duration ischemia, respectively. CMR-measured infarct size declined progressively after reperfusion in all groups. CMR-measured myocardial salvage, and the extent of intramyocardial hemorrhage and microvascular obstruction varied dramatically according to CMR timing, ischemia duration, and cardioprotective strategy. CONCLUSIONS: Cardioprotective therapies, duration of index ischemia, and the interplay between these greatly influence temporal dynamics and extent of tissue composition changes after I/R. Consequently, imaging techniques and protocols for assessing edema, myocardium at risk, infarct size, salvage, intramyocardial hemorrhage, and microvascular obstruction should be standardized accordingly.
[Mh] Termos MeSH primário: Precondicionamento Isquêmico Miocárdico/métodos
Infarto do Miocárdio/prevenção & controle
Infarto do Miocárdio/fisiopatologia
Isquemia Miocárdica/prevenção & controle
Isquemia Miocárdica/fisiopatologia
Reperfusão Miocárdica/métodos
[Mh] Termos MeSH secundário: Animais
Masculino
Tomografia Computadorizada Multidetectores/métodos
Infarto do Miocárdio/diagnóstico por imagem
Isquemia Miocárdica/diagnóstico por imagem
Suínos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCRESAHA.117.310901


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[PMID]:28551796
[Au] Autor:Totzeck M; Hendgen-Cotta UB; Rassaf T
[Ad] Endereço:Department of Cardiology and Vascular Medicine, West German Heart and Vascular Center, University Hospital Essen, Essen, Germany.
[Ti] Título:Nitrite-Nitric Oxide Signaling and Cardioprotection.
[So] Source:Adv Exp Med Biol;982:335-346, 2017.
[Is] ISSN:0065-2598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cardioprotective strategies to prevent damage to mitochondria in acute myocardial infarction are warranted to reduce lethal myocardial ischemia/reperfusion (I/R) injury. Mitochondrial antagonists in I/R are reactive oxygen species (ROS), deteriorated calcium signaling, permeabilization of the mitochondrial outer membrane (MOM) and deranged mitochondrial structural dynamism (fusion and fission). Nitric oxide (NO) related signaling can protect hearts from I/R. Albeit the underlying signaling is incompletely resolved, recent data point to a particular involvement of protective posttranslational modification of mitochondrial elements. We and others have demonstrated that hypoxic NO signaling in cardiomyocytes is associated with a posttranslational mitochondrial complex I modification to reduce the burden of ROS. Induction of cardioprotective NO signaling may occur through several pathways. These include (i) the supplementation with mitochondria unspecific and specific NO-donors, (ii) the administration of the 'hypoxic-NO donors nitrate and nitrite' and (iii) the enhancement of endogenous NO formation, e.g. by remote ischemic preconditioning maneuvers (rIPC). In this chapter, we outline how NO signaling is activated in the cardiomyocyte, characterize the downstream signaling pathways and discuss how this could translate into a tractable therapeutic approach in patients requiring cardioprotection.
[Mh] Termos MeSH primário: Precondicionamento Isquêmico Miocárdico/métodos
Mitocôndrias Cardíacas/efeitos dos fármacos
Infarto do Miocárdio/prevenção & controle
Traumatismo por Reperfusão Miocárdica/prevenção & controle
Miócitos Cardíacos/efeitos dos fármacos
Doadores de Óxido Nítrico/uso terapêutico
Óxido Nítrico/metabolismo
Nitritos/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Citoproteção
Seres Humanos
Mitocôndrias Cardíacas/metabolismo
Mitocôndrias Cardíacas/patologia
Infarto do Miocárdio/metabolismo
Infarto do Miocárdio/patologia
Infarto do Miocárdio/fisiopatologia
Traumatismo por Reperfusão Miocárdica/metabolismo
Traumatismo por Reperfusão Miocárdica/patologia
Traumatismo por Reperfusão Miocárdica/fisiopatologia
Miócitos Cardíacos/metabolismo
Miócitos Cardíacos/patologia
Doadores de Óxido Nítrico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Nitric Oxide Donors); 0 (Nitrites); 31C4KY9ESH (Nitric Oxide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170529
[St] Status:MEDLINE
[do] DOI:10.1007/978-3-319-55330-6_18


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[PMID]:28479248
[Au] Autor:An MY; Li Y; Chen WH; Zhang Y; Wu YN; Sun K; Pan YY; Yin YQ; Lou JS
[Ad] Endereço:Department of Pharmacology, College of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, PR China.
[Ti] Título:Effects of non-invasive remote ischemic conditioning on rehabilitation after myocardial infarction.
[So] Source:Biochem Biophys Res Commun;488(2):278-284, 2017 Jun 24.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent studies have demonstrated that remote ischemic conditioning (RIC) creates cardioprotection against ischemia/reperfusion injury and myocardial infarction (MI); however, the effects of non-invasive remote ischemic conditioning (nRIC) on prognosis and rehabilitation after MI (post-MI) remain unknown. We successfully established MI models involving healthy adult male Sprague-Dawley rats. The nRIC group repeatedly underwent 5 min of ischemia and 5 min of reperfusion in the left hind limb for three cycles every other day until weeks 4, 6, and 8 after MI. nRIC improved cardiac hemodynamic function and mitochondrial respiratory function through increasing myocardial levels of mitochondrial respiratory chain complexes I, II, III, IV, and adenosine triphosphate (ATP) and decreasing the activity of nitric oxide synthase (NOS). nRIC could inhibit cardiomyocytes apoptosis and reduce myocardium injury through raising the expression of Bcl-2 and reduced the content of creatine kinase-MB, cardiac troponin I and Bax. The results indicated that long-term nRIC could accelerate recovery and improve prognosis and rehabilitation in post-MI rats.
[Mh] Termos MeSH primário: Precondicionamento Isquêmico Miocárdico
Infarto do Miocárdio/reabilitação
Infarto do Miocárdio/terapia
[Mh] Termos MeSH secundário: Animais
Masculino
Infarto do Miocárdio/metabolismo
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE


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[PMID]:28434264
[Au] Autor:Herajärvi J; Anttila T; Dimova EY; Laukka T; Myllymäki M; Haapanen H; Olenchock BA; Tuominen H; Puistola U; Karihtala P; Kiviluoma K; Koivunen P; Anttila V; Juvonen T
[Ad] Endereço:a Research Unit of Surgery, Anesthesia and Intensive Care , University of Oulu and MRC Oulu , Oulu, Finland.
[Ti] Título:Exploring effects of remote ischemic preconditioning in a pig model of hypothermic circulatory arrest.
[So] Source:Scand Cardiovasc J;51(4):233-241, 2017 Aug.
[Is] ISSN:1651-2006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: During aortic and cardiac surgery, risks for mortality and morbidity are inevitable. Surgical setups involving deep hypothermic circulatory arrest (DHCA) are effective to achieve organ protection against ischemic injury. The aim of this study was to identify humoural factors mediating additive protective effects of remote ischemic preconditioning (RIPC) in a porcine model of DHCA. DESIGN: Twenty-two pigs were randomized into the RIPC group (n = 11) and the control group (n = 11). The RIPC group underwent four 5-minute hind limb ischemia-reperfusion cycles prior to cardiopulmonary bypass and DHCA. All animals underwent identical surgical procedures including 60 min DHCA at 18 °C. Blood samples were collected from vena cava and sagittal sinus at several time points. After the 8-hour follow-up period, the brain, heart, and kidney tissue samples were collected for tissue analyses. RESULTS: Serum levels of brain damage marker S100B recovered faster in the RIPC group, after 4 hours of the arrest, (p < .05). Systemic lactate levels were lower and cardiac index was higher in the RIPC group postoperatively. Immunohistochemical cerebellum regional scores of antioxidant response regulator Nrf2 were better in the RIPC group (mean: 1.1, IQR: 0.0-2.5) compared with the control group (mean: 0.0, IQR: 0.0-0.0), reaching borderline statistical significance (p = .064). RIPC induced detectable modulations of plasma proteome and metabolites. CONCLUSIONS: The faster recovery of S100B, lower systemic lactate levels and favourable regional antioxidant response suggest possible neuronal cellular and mitochondrial protection by RIPC, whereas better cardiac index underlines functional effects of RIPC. The exact humoural factor remains unclear.
[Mh] Termos MeSH primário: Parada Circulatória Induzida por Hipotermia Profunda
Membro Posterior/irrigação sanguínea
Precondicionamento Isquêmico Miocárdico/métodos
Traumatismo por Reperfusão Miocárdica/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Antioxidantes/metabolismo
Biomarcadores/sangue
Encéfalo/metabolismo
Encéfalo/patologia
Ponte Cardiopulmonar
Modelos Animais de Doenças
Feminino
Ácidos Cetoglutáricos/sangue
Ácido Cinurênico/sangue
Ácido Láctico/sangue
Mitocôndrias/metabolismo
Mitocôndrias/patologia
Traumatismo por Reperfusão Miocárdica/sangue
Traumatismo por Reperfusão Miocárdica/patologia
Miocárdio/metabolismo
Miocárdio/patologia
Fator 2 Relacionado a NF-E2/metabolismo
Neurônios/metabolismo
Neurônios/patologia
Proteômica/métodos
Fluxo Sanguíneo Regional
Subunidade beta da Proteína Ligante de Cálcio S100/sangue
Sus scrofa
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Biomarkers); 0 (Ketoglutaric Acids); 0 (NF-E2-Related Factor 2); 0 (S100 Calcium Binding Protein beta Subunit); 33X04XA5AT (Lactic Acid); H030S2S85J (Kynurenic Acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170425
[St] Status:MEDLINE
[do] DOI:10.1080/14017431.2017.1319574


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[PMID]:28380047
[Au] Autor:Casós K; Ferrer-Curriu G; Soler-Ferrer P; Pérez ML; Permanyer E; Blasco-Lucas A; Gracia-Baena JM; Castro MA; Sureda C; Barquinero J; Galiñanes M
[Ad] Endereço:Reparative Therapy of the Heart, Vall d'Hebron Research Institute (VHIR), University Hospital Vall d'Hebron, Autonomous University of Barcelona (UAB), Barcelona, Spain.
[Ti] Título:Response of the human myocardium to ischemic injury and preconditioning: The role of cardiac and comorbid conditions, medical treatment, and basal redox status.
[So] Source:PLoS One;12(4):e0174588, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The diseased human myocardium is highly susceptible to ischemia/reoxygenation (I/R)-induced injury but its response to protective interventions such as ischemic preconditioning (IPreC) is unclear. Cardiac and other pre-existing clinical conditions as well as previous or ongoing medical treatment may influence the myocardial response to I/R injury and protection. This study investigated the effect of both on myocardial susceptibility to I/R-induced injury and the protective effects of IPreC. METHODS AND RESULTS: Atrial myocardium from cardiac surgery patients (n = 300) was assigned to one of three groups: aerobic control, I/R alone, and IPreC. Lactate dehydrogenase leakage, as a marker of cell injury, and cell viability were measured. The basal redox status was determined in samples from 90 patients. The response to I/R varied widely. Myocardium from patients with aortic valve disease was the most susceptible to injury whereas myocardium from dyslipidemia patients was the least susceptible. Tissue from females was better protected than tissue from males. Myocardium from patients with mitral valve disease was the least responsive to IPreC. The basal redox status was altered in the myocardium from patients with mitral and aortic valve disease. CONCLUSIONS: The response of the myocardium to I/R and IPreC is highly variable and influenced by the underlying cardiac pathology, dyslipidemia, sex, and the basal redox status. These results should be taken into account in the design of future clinical studies on the prevention of I/R injury and protection.
[Mh] Termos MeSH primário: Cardiopatias/complicações
Precondicionamento Isquêmico Miocárdico
Isquemia Miocárdica/complicações
Traumatismo por Reperfusão Miocárdica/complicações
[Mh] Termos MeSH secundário: Idoso
Catalase/metabolismo
Feminino
Doenças das Valvas Cardíacas/complicações
Seres Humanos
Precondicionamento Isquêmico Miocárdico/efeitos adversos
Masculino
Isquemia Miocárdica/metabolismo
Isquemia Miocárdica/terapia
Traumatismo por Reperfusão Miocárdica/metabolismo
Traumatismo por Reperfusão Miocárdica/terapia
Óxido Nítrico/metabolismo
Oxirredução
Fatores de Risco
Fatores Sexuais
Superóxido Dismutase/metabolismo
Superóxidos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
11062-77-4 (Superoxides); 31C4KY9ESH (Nitric Oxide); EC 1.11.1.6 (Catalase); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170830
[Lr] Data última revisão:
170830
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0174588


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[PMID]:28376800
[Au] Autor:Nakadate Y; Sato H; Oguchi T; Sato T; Kawakami A; Ishiyama T; Matsukawa T; Schricker T
[Ad] Endereço:Department of Anesthesia, McGill University Health Centre Glen Site, Royal Victoria Hospital, 1001 Blvd, Decarie, Montreal, QC H4A 3J1, Canada. yosuke.nakadate@mail.mcgill.ca.
[Ti] Título:Glycemia and the cardioprotective effects of insulin pre-conditioning in the isolated rat heart.
[So] Source:Cardiovasc Diabetol;16(1):43, 2017 Apr 04.
[Is] ISSN:1475-2840
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: While acute hyperglycemia has been shown to mitigate the beneficial effects of ischemic preconditioning, its effect on insulin-induced preconditioning remains unclear. METHODS: The study was designed to test the hypothesis that acute hyperglycemia diminishes the cardioprotective effects following a 20-min pre-ischemic pre-conditioning with insulin in the isolated rat heart using the Langendorff system. Forty hearts were assigned to receive modified Krebs-Henseleit (KH) buffer containing 0.5 U/L insulin and 100 mg/dL glucose (InsG100, n = 10), KH buffer with 100 mg/dL glucose (G100, n = 10), KH buffer supplemented with 0.5 U/L insulin and 600 mg/dL glucose (InsG600, n = 10), or with 600 mg/dL glucose (G600, n = 10). To match the osmotic pressure of the InsG600 group, 27.5 mmol/L of mannitol was added to KH solution in the InsG100 and G100 group. The four groups were perfused with each solution for 20 min prior to 15 min of no-flow ischemia, and during 20 min of reperfusion. Only during the ischemic period the heart was paced at 222 beats/min. Measurements of heart rate, coronary flow and maximum of LV derivative of pressure development (dP/dt max) were recorded. Myocardial phospho-protein kinase B (p-Akt) and tumor necrosis factor-α (TNF-α) levels were assayed by enzyme-linked immunosorbent assay and sandwich ELISA, respectively following reperfusion. RESULTS: After reperfusion, LV dP/dt max and heart rate in the InsG100 group was significantly higher than that in the other three groups. The myocardial p-Akt level in the InsG100 group was significantly elevated when compared to the InsG600 group at the end of reperfusion. The p-Akt levels in the InsG600 and InsG100 group were significantly higher than in the corresponding non-insulin groups. CONCLUSIONS: Acute hyperglycemia diminishes the cardioprotective effects of insulin preconditioning in the isolated rat heart, possibly mediated through the suppression of myocardial Akt phosphorylation.
[Mh] Termos MeSH primário: Glicemia/metabolismo
Índice Glicêmico/efeitos dos fármacos
Frequência Cardíaca/efeitos dos fármacos
Hiperglicemia/sangue
Insulina/farmacologia
Precondicionamento Isquêmico Miocárdico/métodos
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
Índice Glicêmico/fisiologia
Coração
Frequência Cardíaca/fisiologia
Hiperglicemia/induzido quimicamente
Insulina/toxicidade
Masculino
Contração Miocárdica/efeitos dos fármacos
Contração Miocárdica/fisiologia
Traumatismo por Reperfusão Miocárdica/sangue
Traumatismo por Reperfusão Miocárdica/prevenção & controle
Técnicas de Cultura de Órgãos
Distribuição Aleatória
Ratos
Ratos Wistar
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE
[do] DOI:10.1186/s12933-017-0527-5


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[PMID]:28364777
[Au] Autor:Baranyai T; Giricz Z; Varga ZV; Koncsos G; Lukovic D; Makkos A; Sárközy M; Pávó N; Jakab A; Czimbalmos C; Vágó H; Ruzsa Z; Tóth L; Garamvölgyi R; Merkely B; Schulz R; Gyöngyösi M; Ferdinandy P
[Ad] Endereço:Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary.
[Ti] Título:In vivo MRI and ex vivo histological assessment of the cardioprotection induced by ischemic preconditioning, postconditioning and remote conditioning in a closed-chest porcine model of reperfused acute myocardial infarction: importance of microvasculature.
[So] Source:J Transl Med;15(1):67, 2017 Apr 01.
[Is] ISSN:1479-5876
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cardioprotective value of ischemic post- (IPostC), remote (RIC) conditioning in acute myocardial infarction (AMI) is unclear in clinical trials. To evaluate cardioprotection, most translational animal studies and clinical trials utilize necrotic tissue referred to the area at risk (AAR) by magnetic resonance imaging (MRI). However, determination of AAR by MRI' may not be accurate, since MRI-indices of microvascular damage, i.e., myocardial edema and microvascular obstruction (MVO), may be affected by cardioprotection independently from myocardial necrosis. Therefore, we assessed the effect of IPostC, RIC conditioning and ischemic preconditioning (IPreC; positive control) on myocardial necrosis, edema and MVO in a clinically relevant, closed-chest pig model of AMI. METHODS AND RESULTS: Acute myocardial infarction was induced by a 90-min balloon occlusion of the left anterior descending coronary artery (LAD) in domestic juvenile female pigs. IPostC (6 × 30 s ischemia/reperfusion after 90-min occlusion) and RIC (4 × 5 min hind limb ischemia/reperfusion during 90-min LAD occlusion) did not reduce myocardial necrosis as assessed by late gadolinium enhancement 3 days after reperfusion and by ex vivo triphenyltetrazolium chloride staining 3 h after reperfusion, however, the positive control, IPreC (3 × 5 min ischemia/reperfusion before 90-min LAD occlusion) did. IPostC and RIC attenuated myocardial edema as measured by cardiac T2-weighted MRI 3 days after reperfusion, however, AAR measured by Evans blue staining was not different among groups, which confirms that myocardial edema is not a measure of AAR, IPostC and IPreC but not RIC decreased MVO. CONCLUSION: We conclude that IPostC and RIC interventions may protect the coronary microvasculature even without reducing myocardial necrosis.
[Mh] Termos MeSH primário: Cardiotônicos/metabolismo
Pós-Condicionamento Isquêmico
Precondicionamento Isquêmico Miocárdico
Imagem por Ressonância Magnética/métodos
Microvasos/patologia
Traumatismo por Reperfusão Miocárdica/diagnóstico
[Mh] Termos MeSH secundário: Animais
Edema/patologia
Eletrocardiografia
Feminino
Testes de Função Cardíaca
Hemodinâmica
Traumatismo por Reperfusão Miocárdica/diagnóstico por imagem
Traumatismo por Reperfusão Miocárdica/patologia
Traumatismo por Reperfusão Miocárdica/fisiopatologia
Necrose
Coloração e Rotulagem
Sus scrofa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cardiotonic Agents)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170403
[St] Status:MEDLINE
[do] DOI:10.1186/s12967-017-1166-z



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