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LINK . SPRINGER . COM {}

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We are analyzing https://link.springer.com/article/10.1186/s13049-020-00819-5.

Title:
The protective effects of phosphodiesterase-5 inhibitor, sildenafil on post-resuscitation cardiac dysfunction of cardiac arrest: by regulating the miR-155-5p and miR-145-5p | Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine
Description:
Background MiRNA-155 and miRNA-145 have been demonstrated to function as a key regulator in the development of the cardiovascular system. Recent experimental and clinical studies have indicated the cardioprotective role of sildenafil during ischemia/reperfusion (I/R) injury. This study was designed to investigate if administration of sildenafil will attenuate post-resuscitation myocardial dysfunction by regulating miRNA-155 and miR-145 expressions. Methods Thirty-two male pigs (weighing 30 ± 2 kg) were randomly divided into 4 groups, sildenafil group (n = 8), sildenafil +NG-nitro-l-arginine methyl ester (L-NAME) (20 mg/kg L) group (n = 8), saline (SA group, n = 8); and sham operation group (sham group, n = 8). Eight minutes of untreated VF was followed by defibrillation in anesthetized, closed-chest pigs. Hemodynamic status and blood samples were obtained at 0 min, 0.5, 1, 2, 4 and 6 h after return of spontaneous circulation (ROSC), and the hearts were removed and analyzed under electron microscopy, quantitative real-time polymerase chain reaction and ultra structural analysis were performed to evaluate myocardial injury. Results Compared with the sildenafil + L-NAME and saline groups, the sildenafil group had better outcomes in terms of hemodynamic and oxygen metabolism parameters as well as 24-h survival rate, and attenuated myocardial injury; In this study, CA pigs showed evidently increased levels of miR-155-5p and miR-145-5p, while the sildenafil treatment decreased the levels of miR-155-5p and miR-145-5p in CA pigs. In addition, the levels of eNOS was decreased in CA pigs, validating sildenafil attenuating post-resuscitation myocardial dysfunction by regulating miRNA-155 and miR-145 expressions. Conclusions Sildenafil group had better outcomes in terms of hemodynamic and oxygen metabolism parameters as well as 24-h survival rate, inhibited the increases in the miR-155-5p and miR-145-5p levels and attenuated myocardial injury in a porcine model of CA and resuscitation.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

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Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

We can't figure out the monetization strategy.

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Keywords {🔍}

sildenafil, group, myocardial, article, pubmed, postresuscitation, dysfunction, mirp, google, scholar, rosc, expression, resuscitation, min, cardiac, study, lname, animals, cas, injury, data, groups, enos, cpr, arrest, pigs, blood, oxygen, survival, pressure, table, function, wang, mirna, animal, research, sham, baseline, mins, significantly, fig, regulating, hemodynamic, rate, levels, model, heart, medical, central, analysis,

Topics {✒️}

nf-κb-dependent mir-155/enos pathway tumor necrosis factor-α microrna-155 aggravates ischemia-reperfusion injury quantitative real-time pcr post-resuscitation myocardial dysfunction 59-cyclic guanosine monophosphate cyclic guanosine monophosphate post-resuscitation cardiac dysfunction article download pdf specific pathogen-free environment post-cardiac arrest syndrome nitric oxide synthase postcardiac arrest myocardial dysfunction myocardial oxygen metabolism define myocardial ischemia/reperfusion injury myocardial ischemia reperfusion injury left ventricular function long-term treatment outcomes arterial blood gases 5 mg/kg intramuscular midazolam post-resuscitation myocardial maintain end-tidal co2 kaplan-meier survival curve real-time pcr post-resuscitation measurements global ventilation/perfusion values 30 ml/kg acetated ringer physiol renal physiol dose-dependent effects privacy choices/manage cookies rat isolated heart full access postresuscitation myocardial dysfunction postresuscitation myocardial dysfunction attenuate myocardial injury capital medical university resuscitation significantly increased postresuscitation cardiac dysfunction reperfusion injury induced post-resuscitation groups myocardial tissue injuries coronary perfusion pressure microvascular endothelial cells nitric oxide blood gas values postresuscitation myocardiac dysfunction intestinal microcirculatory dysfunction inflammatory cell recruitment 5 mg/kg 30 min prior philips medical systems

Schema {🗺️}

WebPage:
      mainEntity:
         headline:The protective effects of phosphodiesterase-5 inhibitor, sildenafil on post-resuscitation cardiac dysfunction of cardiac arrest: by regulating the miR-155-5p and miR-145-5p
         description:MiRNA-155 and miRNA-145 have been demonstrated to function as a key regulator in the development of the cardiovascular system. Recent experimental and clinical studies have indicated the cardioprotective role of sildenafil during ischemia/reperfusion (I/R) injury. This study was designed to investigate if administration of sildenafil will attenuate post-resuscitation myocardial dysfunction by regulating miRNA-155 and miR-145 expressions. Thirty-two male pigs (weighing 30 ± 2 kg) were randomly divided into 4 groups, sildenafil group (n = 8), sildenafil +NG-nitro-l-arginine methyl ester (L-NAME) (20 mg/kg L) group (n = 8), saline (SA group, n = 8); and sham operation group (sham group, n = 8). Eight minutes of untreated VF was followed by defibrillation in anesthetized, closed-chest pigs. Hemodynamic status and blood samples were obtained at 0 min, 0.5, 1, 2, 4 and 6 h after return of spontaneous circulation (ROSC), and the hearts were removed and analyzed under electron microscopy, quantitative real-time polymerase chain reaction and ultra structural analysis were performed to evaluate myocardial injury. Compared with the sildenafil + L-NAME and saline groups, the sildenafil group had better outcomes in terms of hemodynamic and oxygen metabolism parameters as well as 24-h survival rate, and attenuated myocardial injury; In this study, CA pigs showed evidently increased levels of miR-155-5p and miR-145-5p, while the sildenafil treatment decreased the levels of miR-155-5p and miR-145-5p in CA pigs. In addition, the levels of eNOS was decreased in CA pigs, validating sildenafil attenuating post-resuscitation myocardial dysfunction by regulating miRNA-155 and miR-145 expressions. Sildenafil group had better outcomes in terms of hemodynamic and oxygen metabolism parameters as well as 24-h survival rate, inhibited the increases in the miR-155-5p and miR-145-5p levels and attenuated myocardial injury in a porcine model of CA and resuscitation.
         datePublished:2021-01-06T00:00:00Z
         dateModified:2021-01-06T00:00:00Z
         pageStart:1
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         sameAs:https://doi.org/10.1186/s13049-020-00819-5
         keywords:
            Sildenafil
            Post-resuscitation myocardial dysfunction
            miR-155-5p
            miR-145-5p
            Emergency Medicine
            Traumatic Surgery
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                        name:Heart Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China
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ScholarlyArticle:
      headline:The protective effects of phosphodiesterase-5 inhibitor, sildenafil on post-resuscitation cardiac dysfunction of cardiac arrest: by regulating the miR-155-5p and miR-145-5p
      description:MiRNA-155 and miRNA-145 have been demonstrated to function as a key regulator in the development of the cardiovascular system. Recent experimental and clinical studies have indicated the cardioprotective role of sildenafil during ischemia/reperfusion (I/R) injury. This study was designed to investigate if administration of sildenafil will attenuate post-resuscitation myocardial dysfunction by regulating miRNA-155 and miR-145 expressions. Thirty-two male pigs (weighing 30 ± 2 kg) were randomly divided into 4 groups, sildenafil group (n = 8), sildenafil +NG-nitro-l-arginine methyl ester (L-NAME) (20 mg/kg L) group (n = 8), saline (SA group, n = 8); and sham operation group (sham group, n = 8). Eight minutes of untreated VF was followed by defibrillation in anesthetized, closed-chest pigs. Hemodynamic status and blood samples were obtained at 0 min, 0.5, 1, 2, 4 and 6 h after return of spontaneous circulation (ROSC), and the hearts were removed and analyzed under electron microscopy, quantitative real-time polymerase chain reaction and ultra structural analysis were performed to evaluate myocardial injury. Compared with the sildenafil + L-NAME and saline groups, the sildenafil group had better outcomes in terms of hemodynamic and oxygen metabolism parameters as well as 24-h survival rate, and attenuated myocardial injury; In this study, CA pigs showed evidently increased levels of miR-155-5p and miR-145-5p, while the sildenafil treatment decreased the levels of miR-155-5p and miR-145-5p in CA pigs. In addition, the levels of eNOS was decreased in CA pigs, validating sildenafil attenuating post-resuscitation myocardial dysfunction by regulating miRNA-155 and miR-145 expressions. Sildenafil group had better outcomes in terms of hemodynamic and oxygen metabolism parameters as well as 24-h survival rate, inhibited the increases in the miR-155-5p and miR-145-5p levels and attenuated myocardial injury in a porcine model of CA and resuscitation.
      datePublished:2021-01-06T00:00:00Z
      dateModified:2021-01-06T00:00:00Z
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      pageEnd:10
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      sameAs:https://doi.org/10.1186/s13049-020-00819-5
      keywords:
         Sildenafil
         Post-resuscitation myocardial dysfunction
         miR-155-5p
         miR-145-5p
         Emergency Medicine
         Traumatic Surgery
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                     name:Heart Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China
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               type:PostalAddress
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            address:
               name:Heart Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China
               type:PostalAddress
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      name:Yuxing Wang
      affiliation:
            name:Capital Medical University
            address:
               name:Heart Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China
               type:PostalAddress
            type:Organization
      name:Qian Zhang
      url:http://orcid.org/0000-0003-2251-6190
      affiliation:
            name:Capital Medical University
            address:
               name:Heart Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China
               type:PostalAddress
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      name:Department of Emergency Medicine, Beijing Friendship Hospital, Capital Medical University, Beijing, China
      name:Department of Emergency Medicine, Beijing Friendship Hospital, Capital Medical University, Beijing, China
      name:Heart Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China
      name:Heart Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China
      name:Heart Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China

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