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1.
Rev. Fac. Med. (Guatemala) ; 1(23 Segunda Época): 2-7, Jul-Dic 2017.
Artigo em Espanhol | LILACS-Express | LILACS | ID: biblio-1140389

RESUMO

Introducción: El uso inadecuado de antibióticos es un problema de salud internacional que trae consecuencias devastadoras como resistencia bacteriana, aumento de morbi-mortalidad, etc. Objetivos: El objetivo del presente estudio fue evaluar y analizar los patrones de las prescripciones de los antibióticos utilizados en pacientes internados en un hospital privado de Guatemala. Metodología: Durante el primer semestre del año 2013 se realizó un estudio observacional, descriptivo de corte transversal. Fueron incluidos todos los pacientes hospitalizados en los servicios del Hospital Privado, y se excluyeron aquellos que recibían tratamiento antibiótico profiláctico, pacientes recién nacidos y de la unidad de intensivo. Resultado y Conclusión: De un total de 631 registros médicos revisados, 563 fueron incluidos en el estudio y 42.5% de los pacientes recibieron tratamiento antibiótico. Hubo en total 239 prescripciones de antibiótico, de la cual 89.5% de los prescripciones se clasificaron como uso inadecuado. Palabras clave: antibiótico, evaluación, adecuado, hospital


Introduction: The inadequate use of antibiotic is an international health problem with devastating consequences like, bacterial resistance and an increased morbidity and mortality. Objectives: The purpose of the present study was to evaluate and analyze the patterns of antibiotic use in hospitalized patients in a private hospital of Guatemala. Methodology: A cross-sectional observational and descriptive study was carried out. All patients hospitalized in a private hospital were included for analysis, and patients with antibiotics given as surgical prophylaxis, newborns and patients in intensive care units were excluded. Results and Conclusion: A total of 631 medical charts were revised, and 563 of them were included in the study for analysis. 42.5% of the patients included in the study received antibiotic therapy and a total of 239 antibiotics were prescribed, in which 89.5% were classified as an inadequate use. Keywords: antibiotic, evaluation, adequate, hospital

3.
Ann Thorac Surg ; 84(1): 126-33, 2007 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-17588398

RESUMO

BACKGROUND: Hypertrophied myocardium is more susceptible to ischemia/reperfusion injury, in part owing to impaired insulin-mediated glucose uptake. Glycogen synthase kinase-3beta (GSK-3beta) is a key regulatory enzyme in glucose metabolism that, when activated, phosphorylates/inactivates target enzymes of the insulin signaling pathway. Glycogen synthase kinase-3beta is regulated upstream by Akt-1. We sought to determine whether GSK-3beta is activated in ischemic hypertrophied myocardium owing to impaired Akt-1 function, and whether inhibition with lithium (Li) or indirubin-3'-monoxime,5-iodo- (IMI), a specific inhibitor, improves post-ischemic myocardial recovery by improving glucose metabolism. METHODS: Pressure-overload hypertrophy was achieved by aortic banding in neonatal rabbits. At 6 weeks, isolated hypertrophied hearts underwent 30 minutes of normothermic ischemia and reperfusion with or without a GSK-3beta inhibitor (0.1 mM Li; 1 microM IMI) as cardioplegic additives. Cardiac function was measured before and after ischemia. Expression, activity of Akt-1 and GSK-3beta, and lactate were determined at end-ischemia. RESULTS: Contractile function after ischemia was better preserved in hypertrophied hearts treated with GSK-3beta inhibitors. Activity of Akt-1 was significantly impaired in hypertrophied myocardium at end-ischemia. Glycogen synthase kinase-3beta enzymatic activity at end-ischemia was increased in hypertrophied hearts and was blocked by Li or IMI concomitant with significantly increased lactate production, indicating increased glycolysis. CONCLUSIONS: Regulatory inhibition of GSK-3beta by Akt-1 in hypertrophied hearts is impaired, leading to activation during ischemia. Inhibition of GSK-3beta by Li or IMI improves tolerance to ischemia/reperfusion injury in hypertrophied myocardium. The likely protective mechanism is an increase in insulin-mediated glucose uptake, resulting in greater substrate availability for glycolysis during ischemia and early reperfusion.


Assuntos
Quinase 3 da Glicogênio Sintase/antagonistas & inibidores , Hipertrofia Ventricular Esquerda/tratamento farmacológico , Indóis/uso terapêutico , Compostos de Lítio/uso terapêutico , Isquemia Miocárdica/enzimologia , Traumatismo por Reperfusão Miocárdica/prevenção & controle , Oximas/uso terapêutico , Inibidores de Proteínas Quinases/uso terapêutico , Animais , Peso Corporal , Quinase 3 da Glicogênio Sintase/metabolismo , Glicogênio Sintase Quinase 3 beta , Glicólise , Hipertrofia Ventricular Esquerda/fisiopatologia , Ácido Láctico/biossíntese , Contração Miocárdica , Fosforilação , Proteínas Proto-Oncogênicas c-akt/metabolismo , Coelhos
4.
Circulation ; 114(1 Suppl): I290-5, 2006 Jul 04.
Artigo em Inglês | MEDLINE | ID: mdl-16820588

RESUMO

BACKGROUND: Cardiac hypertrophy is an adaptive response to increased workload that, if unrelieved, leads to heart failure. It has been reported that cardiomyocyte apoptosis contributes to failure, and that vascular endothelial growth factor (VEGF) treatment of hypertrophied myocardium increases capillary density and improves myocardial perfusion. In this study we hypothesized that VEGF treatment reduces cardiomyocyte apoptosis and thereby preserves myocardial contractile function. METHODS AND RESULTS: Newborn rabbits underwent aortic banding. At 4 and 6 weeks of age, hypertrophied animals were treated with intrapericardial administration of recombinant VEGF protein. Three groups of animals were investigated: age-matched controls (C), untreated hypertrophied (H), and VEGF-treated hypertrophied hearts (T). Cardiomyocyte apoptosis was determined by TUNEL staining and PARP cleavage (immunoblotting of nuclear extracts) and cardiac function by transthoracic echocardiography. Death attributable to severe heart failure occurred in 14 of 43 untreated and 2 of 29 VEGF-treated animals (P<0.01). TUNEL-positive cardiomyocyte nuclei (n/1000 nuclei) were significantly increased in untreated hearts at 5 weeks (H: 10+/-1.8 versus T: 3+/-0.7) and at 7 weeks (H: 13+/-3.6 versus T: 5+/-1.5; P<0.05). Increased apoptosis in untreated hypertrophy was also confirmed by the presence of PARP cleavage (H: 74+/-7 versus T: 41+/-4 arbitrary densitometry units; P<0.05). VEGF treatment preserved left ventricular mass, prevented dilation (T: 1.01+/-0.06 versus H: 0.77+/-0.07; P<0.05), and preserved contractility indices compared with untreated hearts. CONCLUSIONS: Lack of adaptive capillary growth impairs myocardial perfusion and substrate delivery in hypertrophying myocardium. VEGF treatment reduces myocardial apoptosis and prolongs survival in a model of severe progressive left ventricular hypertrophy. Promoting capillary growth with VEGF reduces apoptosis, preserves myocardial contractile function, and delays the onset of failure in pressure-loaded infant myocardium.


Assuntos
Apoptose/efeitos dos fármacos , Cardiomiopatia Hipertrófica/tratamento farmacológico , Hipertrofia Ventricular Esquerda/tratamento farmacológico , Contração Miocárdica/efeitos dos fármacos , Fator A de Crescimento do Endotélio Vascular/uso terapêutico , Animais , Animais Recém-Nascidos , Aorta Torácica , Capilares/efeitos dos fármacos , Cardiomiopatia Hipertrófica/etiologia , Cardiomiopatia Hipertrófica/patologia , Cardiomiopatia Hipertrófica/fisiopatologia , Progressão da Doença , Avaliação Pré-Clínica de Medicamentos , Hipertrofia Ventricular Esquerda/etiologia , Hipertrofia Ventricular Esquerda/patologia , Hipertrofia Ventricular Esquerda/fisiopatologia , Marcação In Situ das Extremidades Cortadas , Ligadura , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/patologia , Neovascularização Fisiológica/efeitos dos fármacos , Poli(ADP-Ribose) Polimerases/metabolismo , Coelhos , Proteínas Recombinantes/uso terapêutico , Fator A de Crescimento do Endotélio Vascular/genética
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