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.
Background-Hypertrophied myocardium is more susceptible to ischemia/reperfusion injury, in part owing to impaired insulin-mediated glucose uptake. Glycogen synthase kinase-3β (GSK-3β) is a key regulatory enzyme in glucose metabolism that, when activated, phosphorylates/inactivates target enzymes of the insulin signaling pathway. Glycogen synthase kinase-3β is regulated upstream by Akt-1. We sought to determine whether GSK-3β 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.
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.
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