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1.
Sci Rep ; 9(1): 7822, 2019 05 24.
Article in English | MEDLINE | ID: mdl-31127136

ABSTRACT

Glucose is an important preferential substrate for energy metabolism during acute coronary syndrome (ACS) attack, although insulin resistance (IR) increases during ACS. Increasing evidence indicates that natriuretic peptides (NP) regulate glucose homeostasis. We investigated possible compensatory actions of NP in collaboration with other neurohumoral factors that facilitate glucose utilization during ACS. The study population consisted of 1072 consecutive cases with ischemic heart disease who underwent cardiac catheterization (ACS, n = 216; non-ACS, n = 856). Among ACS subjects, biochemical data after acute-phase treatment were available in 91 cases, defined as ACS-remission phase (ACS-rem). Path models based on covariance structure analyses were proposed to clarify the direct contribution of B-type NP (BNP) and noradrenaline to glucose and HOMA-IR levels while eliminating confounding biases. In non-ACS and ACS-rem subjects, although noradrenaline slightly increased glucose and/or HOMA-IR levels (P < 0.03), BNP did not significantly affect them. In contrast, in ACS subjects, high noradrenaline was a significant cause of increases in glucose and HOMA-IR levels (P < 0.001), whereas high BNP was a significant cause of decreases in both parameters (P < 0.005). These findings indicate that BNP and noradrenaline coordinately activate glucose metabolism during ACS, with noradrenaline increasing glucose levels, as an energy substrate, while BNP improves IR and promotes glucose utilization.


Subject(s)
Acute Coronary Syndrome/metabolism , Blood Glucose/metabolism , Insulin Resistance/physiology , Natriuretic Peptide, Brain/metabolism , Norepinephrine/metabolism , Acute Coronary Syndrome/blood , Acute Coronary Syndrome/therapy , Aged , Angiotensin II Type 1 Receptor Blockers/therapeutic use , Cardiac Catheterization , Female , Humans , Insulin/metabolism , Male , Middle Aged , Natriuretic Peptide, Brain/agonists , Natriuretic Peptide, Brain/blood , Norepinephrine/blood , Retrospective Studies
3.
Emergencias (St. Vicenç dels Horts) ; 26(2): 94-100, abr. 2014. ilus, tab
Article in Spanish | IBECS | ID: ibc-120729

ABSTRACT

Objetivo: Evaluar la relación entre la concentración plasmática del fragmento aminoterminal del pro-péptido natriurético cerebral (NT-ProBNP) en el momento del diagnóstico de neumonía adquiridad en la comunidad (NAC) en urgencias y su gravedad determinada como mortalidad a los 30 días. Método: Estudio observacional prospectivo tipo cohortes en el que se determina NTProBNP (medido en ng/l) como factor exposición, se realiza seguimiento durante 30 días y se analiza la frecuencia de mortalidad. Incluimos a los pacientes con diagnóstico clínico-radiográfico de NAC atendidos consecutivamente en el servicio de urgencias desde el 1 de febrero al 30 de abril de 2012. Resultados: Se valoraron 110 pacientes, y 96 fueron incluidos en el estudio (87%), 44% mujeres. La edad media fue 66 (DE 22) años. Los valores medios en sangre de NT-Pro BNP extraídos fueron de 3.747 ng/l (DE 10.732) y mediana 506 ng/l (RIC2.490). Fallecieron 13 pacientes en los primeros 30 días (14%). Los valores de NTproBNP medios en los pacientes fallecidos fueron 17.805 ng/l (DE 24.952) comparados con 1.545 ng/l (DE 2.467) en los pacientes supervivientes (p = 0,003). Conclusiones: Los valores de NT-ProBNP en el momento del diagnóstico de NAC en elSU son un buen predictor de mortalidad precoz a los 30 días (AU)


Objective: To assess the association between plasma concentration of the N-terminal fragment of the precursor to brain type natriuretic peptide (NT-proBNP) and severity of community-acquired pneumonia (CAP) (30-day mortality) at the moment of emergency department diagnosis. Methods: Prospective observational cohort study of NT-proBNP plasma concentration as the potential indicator of risk of 30-day mortality. Emergency department patients with a clinical-radiographic diagnosis of CAP were enrolled consecutively from February 1 to April 30, 2012. Results: A total of 110 patients were recruited; 96 (87%) were included. Women comprised 44% of the cohort. The mean (SD) age was 66 (22) years. The mean NT-proBNP concentration was 3747 (10 732) ng/L; the median concentration was 506 ng/L (interquartile range, 2490 ng/L). Thirteen patients (14%) died within 30 days. The mean NT-proBNP concentration was 17 804.85 (24 952) ng/L in patients who died and 1545 (2467) ng/L in survivors (P=.003). Conclusions: NT-proBNP concentration at the time of CAP diagnosis in the emergency department provides a good predictor of early (30-day) mortality (AU)


Subject(s)
Humans , Pneumonia/diagnosis , Community-Acquired Infections/diagnosis , Biomarkers/analysis , Emergency Medical Services/methods , Emergency Treatment/methods , Natriuretic Peptide, Brain/agonists
4.
J Cell Mol Med ; 17(6): 743-53, 2013 Jun.
Article in English | MEDLINE | ID: mdl-23617620

ABSTRACT

Atrial fibrillation (AF) often occurs in the presence of an underlying disease. These underlying diseases cause atrial remodelling, which make the atria more susceptible to AF. Stretch is an important mediator in the remodelling process. The aim of this study was to develop an atrial cell culture model mimicking remodelling due to atrial pressure overload. Neonatal rat atrial cardiomyocytes (NRAM) were cultured and subjected to cyclical stretch on elastic membranes. Stretching with 1 Hz and 15% elongation for 30 min. resulted in increased expression of immediate early genes and phosphorylation of Erk and p38. A 24-hr stretch period resulted in hypertrophy-related changes including increased cell diameter, reinduction of the foetal gene program and cell death. No evidence of apoptosis was observed. Expression of atrial natriuretic peptide, brain natriuretic peptide and growth differentiation factor-15 was increased, and calcineurin signalling was activated. Expression of several potassium channels was decreased, suggesting electrical remodelling. Atrial stretch-induced change in skeletal α-actin expression was inhibited by pravastatin, but not by eplerenone or losartan. Stretch of NRAM results in elevation of stress markers, changes related to hypertrophy and dedifferentiation, electrical remodelling and cell death. This model can contribute to investigating the mechanisms involved in the remodelling process caused by stretch and to the testing of pharmaceutical agents.


Subject(s)
Atrial Remodeling , Heart Atria/pathology , Myocytes, Cardiac/pathology , Actins/genetics , Actins/metabolism , Animals , Animals, Newborn , Anticholesteremic Agents/pharmacology , Atrial Fibrillation/genetics , Atrial Fibrillation/metabolism , Atrial Fibrillation/pathology , Atrial Natriuretic Factor/agonists , Atrial Natriuretic Factor/genetics , Atrial Natriuretic Factor/metabolism , Calcineurin/genetics , Calcineurin/metabolism , Cell Death , Extracellular Signal-Regulated MAP Kinases/genetics , Extracellular Signal-Regulated MAP Kinases/metabolism , Gene Expression Regulation, Developmental , Growth Differentiation Factor 15/agonists , Growth Differentiation Factor 15/genetics , Growth Differentiation Factor 15/metabolism , Heart Atria/drug effects , Heart Atria/metabolism , Myocytes, Cardiac/drug effects , Myocytes, Cardiac/metabolism , Natriuretic Peptide, Brain/agonists , Natriuretic Peptide, Brain/genetics , Natriuretic Peptide, Brain/metabolism , Potassium Channels/genetics , Potassium Channels/metabolism , Pravastatin/pharmacology , Pressure , Rats , Rats, Sprague-Dawley , Signal Transduction/drug effects , Stress, Mechanical , p38 Mitogen-Activated Protein Kinases/genetics , p38 Mitogen-Activated Protein Kinases/metabolism
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