RESUMEN
INTRODUCTION: Overpopulation and industrial growth result in an increase in air pollution, mainly due to suspended particulate matter and the formation of ozone. Repeated exposure to low doses of ozone, such as on a day with high air pollution levels, results in a state of chronic oxidative stress, causing the loss of dendritic spines, alterations in cerebral plasticity and in learning and memory mechanisms, and neuronal death and a loss of brain repair capacity. This has a direct impact on human health, increasing the incidence of chronic and degenerative diseases. DEVELOPMENT: We performed a search of the PubMed, Scopus, and Google Scholar databases for original articles and reviews published between 2000 and 2018 and addressing the main consequences of ozone exposure on synaptic plasticity, information processing in cognitive processes, and the alterations that may lead to the development of neurodegenerative diseases. CONCLUSIONS: This review describes one of the pathophysiological mechanisms of the effect of repeated exposure to low doses of ozone, which causes loss of synaptic plasticity by producing a state of chronic oxidative stress. This brain function is key to both information processing and the generation of structural changes in neuronal populations. We also address the effect of chronic ozone exposure on brain tissue and the close relationship between ozone pollution and the appearance and progression of neurodegenerative diseases.
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Contaminación del Aire , Enfermedades Neurodegenerativas , Ozono , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Humanos , Enfermedades Neurodegenerativas/inducido químicamente , Plasticidad Neuronal , Estrés Oxidativo , Ozono/efectos adversosRESUMEN
Objetivo: Evaluar la idoneidad de la prueba de respiración espontánea para predecir el fracaso de la extubación de pacientes neurológicos y determinar los factores predictivos de fracaso. Diseño: Casos y controles. De enero de 2001 a diciembre de 2010. Ámbito: Unidad de Cuidados Intensivos. Pacientes: Enfermos neurológicos agudos sometidos a ventilación mecánica y posterior extubación. Se excluyeron: pacientes con cirugías neurológicas programadas, con patología neuromuscular, lesión medular, traqueotomía, politraumatismos con predominio de afectación del resto de los sistemas sobre el neurológico, aquellos que murieron en la Unidad de Cuidados Intensivos o que fueron trasladados. Variables de interés: Tasa de fracaso, infección intrahospitalaria, necesidad de traqueotomía, duración de la ventilación mecánica, estancia en la Unidad de Cuidados Intensivos y en el hospital, mortalidad en esta Unidad, en el hospital y a los 90 días, y factores asociados al fracaso. Resultados: De 479 pacientes, 208 fueron sometidos a prueba de respiración espontánea y posterior extubación. Cincuenta y cuatro (26%) fracasaron, la tasa de complicaciones, la estancia, la duración de la ventilación mecánica y la mortalidad fueron mayores que en el grupo de éxito. Los pacientes con accidente cerebrovascular [OR 4,256 (IC95% 1,442-12,561), p = 0,009] y necesidad de aspiraciones frecuentes [OR 5,699 (IC95% 1,863-17,432), p = 0,002] son más propensos al fracaso [ROC 0,73 (IC95% 0,628-0,840)]. Conclusiones: Los pacientes neurológicos presentan una elevada tasa de fracaso de la extubación con numerosas complicaciones asociadas y muerte. La prueba de respiración espontánea no predijo el éxito de la extubación. Los pacientes con accidente cerebrovascular y necesidad de aspiraciones frecuentes de secreciones se verían abocados a un mayor fracaso de extubación.(AU)
Objective: To assess the adequacy of the spontaneous breathing test to predict extubation failure in neurological patients undergoing mechanical ventilation and to determine factors associated with extubation failure. Design: Case-control study. Between January 2001 and December 2010. Setting: Intensive Care Unit. Patients: Acute neurological patients who underwent mechanical ventilation and were subsequently extubated. Patients with scheduled neurosurgery intervention, neuromuscular disease, spinal cord injury, tracheotomy, multiple trauma with less neurological damage than in other systems, those who died in the Intensive Care Unit or in hospital or those transferred to other hospital, were excluded. Variables of interest: Extubation failure rate, nosocomial infection, need for tracheostomy, duration of mechanical ventilation, ICU and hospital stay, mortality in the ICU or hospital, and at day 90, as well as failure-related factors. Results: Two-hundred and eight patients underwent spontaneous breathing trial, and were subsequently extubated. Fifty-four (26%) patients failed. Patients who failed extubation had a higher complication rate, received mechanical ventilation for more days, their hospitalization was longer, and the mortality rate was higher than in the success group. Patients with stroke [OR 4.256 (95%CI, 1.442-12.561), p=0.009] and those who required a greater number of aspirations during weaning [OR 5.699 (95%CI, 1.863-17.432), p=0.002] were susceptible to extubation failure [ROC curve 0.73 (0.628-0.840)]. Conclusion: Extubation failure in neurological patients is common and frequently associated with severe complications. The spontaneous breathing trial does not predict a successful extubation. Patients with stroke and those who need frequent aspiration of secretions would be doomed to further failure of extubation(AU)
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Humanos , Destete , Enfermedades del Sistema Nervioso , Extubación TraquealRESUMEN
The aim of this study was to analyze the effects of chronic oxidative stress on mitochondrial function and its relationship to progressive neurodegeneration in the hippocampus of rats chronically exposed to ozone. Animals were exposed to 0.25 ppm ozone for 7, 15, 30, or 60 days. Each group was tested for (1) protein oxidation and, manganese superoxide dismutase (Mn-SOD), glutathione peroxidase (GPx) and succinate dehydrogenase (SDH) activity using spectrophotometric techniques, (2) oxygen consumption, (3) cytochrome c, inducible nitric oxide synthase (iNOS), peroxisome proliferator-activated receptor γ Co-activator 1α (PGC-1α), B-cell lymphoma (Bcl-2), and Bax expression using Western blotting, (4) histology using hematoxylin and eosin staining, and (5) mitochondrial structure using electron microscopy. Our results showed increased levels of carbonyl protein and Mn-SOD activity after 30 days of ozone exposure and decreased GPx activity. The SDH activity decreased from 7 to 60 days of exposure. The oxygen consumption decreased at 60 days. Western blotting showed an increase in cytochrome c at 60 days of ozone exposure and an increase in iNOS up to 60 days of ozone exposure. The expression of PGC-1α was decreased after 15, 30, and 60 days compared to the earlier time Bcl-2 was increased at 60 days compared to earlier time points, and Bax was increased after 30 and 60 days of exposure compared to earlier time points. We observed cellular damage, and mitochondrial swelling with a loss of mitochondrial cristae after 60 days of exposure. These changes suggest that low doses of ozone caused mitochondrial abnormalities that may lead to cell damage.
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Hipocampo/metabolismo , Hipocampo/patología , Mitocondrias/metabolismo , Mitocondrias/patología , Estrés Oxidativo/fisiología , Animales , Western Blotting , Inmunohistoquímica , Oxidantes Fotoquímicos/toxicidad , Ozono/toxicidad , Ratas , Ratas WistarRESUMEN
Para el desarrollo de esta investigación se realiza un estudio con el objetivo de elaborar un conjunto de acciones de capacitación que permita elevar el nivel de conocimientos sobre el VIH/sida en estudiantes del perfil de Servicios Farmacéuticos de la Filial de Ciencias Médicas de Guantánamo. Teóricamente se aporta el conjunto de acciones dirigidas a estos estudiantes, las cuales son aceptadas desde su estructura, posibilidades metodológicas y factibilidad de aplicación en cualquier población (AU)
A study is done in order to develop a set of training activities that will raise the level of knowledge about HIV / AIDS among students of the profile of the Pharmaceutical Services at Medical Sciences in Guantanamo. Theoretically is provided a set of actions aimed at these students, which are accepted from its structure, methodological possibilities and feasibility of implementation in any population
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Conocimientos, Actitudes y Práctica en Salud , VIH , Estudiantes de FarmaciaRESUMEN
We studied the effect of an acute infusion of quinolinic acid (QUIN) on in vivo hydroxyl radical (.OH) formation in the striatum of awake rats. Using the microdialysis technique, the generation of.OH was assessed through electrochemical detection of the salicylate hydroxylation product 2,3-dihydroxybenzoic acid (2,3-DHBA). The .OH extracellular levels increased up to 30 times over basal levels after QUIN infusion (240 nmol/microl), returning to the baseline 2 h later. This response was attenuated, but not abolished, by pretreatment with the NMDA receptor antagonist MK-801 (10 mg/kg, i.p.) 60 min before QUIN infusion. The mitochondrial toxin 3-nitropropionic acid (3-NPA, 500 nmol/microl) had stronger effects than QUIN on .OH generation, as well as on other markers of oxidative stress explored as potential consequences of .OH increased levels. These results support the hypothesis that early .OH generation contributes to the pattern of toxicity elicited by QUIN. The partial protection by MK-801 suggests that QUIN neurotoxicity is not completely explained through NMDA receptor overactivation, but it may also involve intrinsic QUIN oxidative properties.
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Cuerpo Estriado/efectos de los fármacos , Cuerpo Estriado/metabolismo , Radical Hidroxilo/metabolismo , Ácido Quinolínico/administración & dosificación , Animales , Cromatografía Líquida de Alta Presión , Maleato de Dizocilpina/farmacología , Antagonistas de Aminoácidos Excitadores/farmacología , Glutatión/metabolismo , Glutatión Peroxidasa/metabolismo , Hidroxibenzoatos/análisis , Hidroxibenzoatos/metabolismo , Peroxidación de Lípido/efectos de los fármacos , Masculino , Microdiálisis , Microinyecciones , Fármacos Neuroprotectores/farmacología , Nitrocompuestos , Estrés Oxidativo , Perfusión , Propionatos/administración & dosificación , Ratas , Ratas Wistar , Ácido Salicílico/administración & dosificación , Ácido Salicílico/metabolismo , VigiliaRESUMEN
The response of endogenous antioxidants to the N-methyl-D-aspartate (NMDA) receptor agonist and excitotoxin, quinolinic acid (QUIN), was investigated in rat corpus striatum. Animals treated with QUIN (240 nmol/microl), were sacrificed at 120 min after a single intrastriatal injection to examine the alterations in the levels of both reduced (GSH) and oxidized (GSSG) glutathione, and the activities of the antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (Gpx). Changes in the rate of lipid peroxidation (LP) were also measured after exposure to different doses of QUIN (60, 120, 240 and 480 nmol/microl) as an index of oxidative stress. When compared to control, lipid peroxidation was increased at QUIN doses of 240 and 480 nmol/microl. Striatal levels of GSH and GSSG were decreased and increased, respectively, after QUIN injection; whereas GPx activity was unchanged. Cytosolic copper/zinc SOD (CuZn-SOD) activity decreased after treatment, while mitochondrial manganese SOD (Mn-SOD) was unchanged. The alterations observed on these antioxidant systems suggest that QUIN toxicity is mediated by specific mechanisms leading to oxidative stress.