This controlled, prospective, nonrandomized clinical investigation has as its chief strength the fact that it was done in humans with active disease and apparently on fairly modest therapeutic regimens. The aim was to present the results of oxidative-stress biomarkers in humans suffering from pulmonary artery hypertension (PAH). Inflammation and oxidative stress are essential in PAH with increased lipid peroxidation and reduced antioxidant defenses. Twenty-four adult patients of both sexes, with a mean age of 21 years, were subdivided into 2 groups: a control group of 12 healthy, nonsmoking volunteers and a PAH group (PAHG) of 12 volunteers with PAH receiving outpatient treatment. Oxidative stress was evaluated by plasma activity of reduced glutathione (GSH); lipid peroxidation was expressed by malondialdehyde (MDA) and lipid hydroperoxide (ferrous oxidation of xylenol orange [FOX] assay); vitamin E was measured by high-performance liquid chromatography and tumor necrosis factor-α (TNF-α) by enzymelinked immunosorbent assay. Statistical analyses showed significant differences for (1) the TNF-α measure, with highest values in PAHG patients; (2) the plasma GSH, with lowest values in PAHG patients; (3) vitamin E, with the lowest concentrations in PAHG patients; (4) MDA measure, with highest values in PAHG patients; and (5) the lipid hydroperoxide FOX measure, with highest values in PAHG patients. In conclusion, inflammation and oxidative stress are present in patients with PAH, as confirmed by increased lipid peroxidation, reduced GSH, and low concentrations of vitamin E.

Hepatic ischemia followed by reperfusion (IR) results in mild to severe remote organ injury. Oxidative stress and nitric oxide (NO) seem to be involved in the IR injury. Our aim was to investigate the effects of liver I/R on hepatic function and lipid peroxidation, leukocyte infiltration and NO synthase (NOS) immunostaining in the lung and the kidney. We randomized 24 male Wistar rats into 3 groups: 1) control; 2) 60 minutes of partial (70%) liver I and 2 hours of global liver R; and 3) 60 minutes of partial (70%) liver I and 6 hours of global liver R. Groups 2 and 3 showed significant increases in plasma alanine and aspartate aminotransferase levels and in tissue malondialdehyde and myeloperoxidase contents. In the kidney, positive endothelial NOS (eNOS) staining was significantly decreased in group 3 compared with group 1. However, staining for inducible NOS (iNOS) and neuronal NOS (nNOS) did not differ among the groups. In the lung, the staining for eNOS and iNOS did not show significant differences among the groups; no positive nNOS staining was observed in any group. These results suggested that partial liver I followed by global liver R induced liver, kidney, and lung injuries characterized by neutrophil sequestration and increased oxidative stress. In addition, we supposed that the reduced NO formation via eNOS may be implicated in the moderate impairment of renal function, observed by others at 24 hours after liver I/R.

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Vascular endothelial cells are exposed to a variety of in vivo mechanical forces, specifically, shear stress for the blood flow, tensile stress from the compliance of the vessel wall and the hydrostatic pressure from containment of blood within inside the vasculature. Many authors studied hemodynamic, functional and morphological human saphenous veins alterations caused by these different forces with conflictant results. This review text was motivated with the specific aim of analyze literature data and some experimental data carried out in our laboratory. The adopted review subjects were: 1) Endothelial responses and gene regulation to shear stress; 2) Effects of the hydrostatic pressure in the endothelial cell morphology, gene expression of the endothelial cellular surface and proliferation of endothelial cells; 3) Effects of the traction on the human saphenous vein endothelium.

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There is currently no consensus on the treatment sequence in chronic obstructive pulmonary disease (COPD), although it is recognized that early diagnosis is of paramount importance to start treatment in the early stages of the disease. Although it is fairly consensual that initial treatment should be with an inhaled short-acting beta agonist, a short-acting muscarinic antagonist, a long-acting beta-agonist or a long-acting muscarinic antagonist. As the disease progresses, several therapeutic options are available, and which to choose at each disease stage remains controversial. When and in which patients to use dual bronchodilation? When to use inhaled corticosteroids? And triple therapy? Are the existing non-inhaled therapies, such as mucolytic agents, antibiotics, phosphodiesterase-4 inhibitors, methylxanthines and immunostimulating agents, useful? If so, which patients would benefit? Should co-morbidities be taken into account when choosing COPD therapy for a patient? This paper reviews current guidelines and available evidence and proposes a therapeutic scheme for COPD patients. We also propose a treatment algorithm in the hope that it will help physicians to decide the best approach for their patients. The authors conclude that, at present, a full consensus on optimal treatment sequence in COPD cannot be found, mainly due to disease heterogeneity and lack of biomarkers to guide treatment. For the time being, and although some therapeutic approaches are consensual, treatment of COPD should be patient-oriented.

Purpose: Standardization of a simple and low cost technique of exhaled breath condensate (EBC) collection to measure nitrite. Methods: Two devices were mounted in polystyrene boxes filled either with crushed ice/salt crystals or dry ice/crushed ice. Blood samples were stored at -70º C for posterior nitrite dosages by chemiluminescence and the Griess reaction. Results: a) The use of crushed ice/dry ice or salt revealed sufficient EBC room air collection, but was not efficient for patients under ventilation support; b) the method using crushed ice/salt collected greater EBC volumes, but the nitrite concentrations were not proportional to the volume collected; c) The EBC nitrite values were higher in the surgical group using both methods; d) In the surgical group the nasal clip use diminished the EBC nitrite concentrations in both methods. Conclusions: The exhaled breath condensate (EBC) methodology collection was efficient on room air breathing. Either cooling methods provided successful EBC collections showing that it is possible to diminish costs, and, amongst the two used methods, the one using crushed ice/salt crystals revealed better efficiency compared to the dry ice method. Key words: Extracorporeal Circulation. Thoracic Surgery. Nitrites. RESUMOObjetivo: Padronizar técnica simples e barata de coleta do condensado do ar exalado pulmonar (CEP) para medir nitrito. Métodos: Dois dispositivos foram montados em caixas de isopor e preenchidos com gelo picado/sal grosso ou gelo picado/gelo seco. Amostras de sangue foram armazenadas a -70º C para dosagem de nitrito por quimiluminescência e pela reação de Griess. Resultados: a) a utilização de gelo picado/gelo seco ou sal foi eficiente para a coleta em respiração espontânea, mas ineficiente durante ventilação mecânica; b) o método gelo picado/sal coletou volumes maiores, sem aumento proporcional do nitrito; c) os valores do nitrito foram mais elevados no grupo cirúrgico utilizando os dois métodos; d) no grupo cirúrgico com clipe nasal ocorreu diminuição do nitrito em ambos os métodos. Conclusões: A metodologia do condensado do ar exalado pulmonar (CEP) foi eficiente na coleta respirando em ar ambiente. Os dois métodos de congelamento foram eficientes mostrando que é possível diminuir os custos, e, entre os dois métodos utilizados, o uso de gelo picado/sal mostrou melhor eficiência quanto ao volume da coleta do CEP em comparação com o uso de gelo seco.

Chronic Obstructive Pulmonary Disease (COPD) exacerbations play a central role in the disease natural history of the disease, affecting its overall severity, decreasing pulmonary function, worsening underlying co-morbidities, impairing quality of life (QoL) and leading to severe morbidity and mortality. Therefore, identification and correct assessment of COPD exacerbations is paramount, given it will strongly influence therapy success. For the identification of exacerbations, several questionnaires exist, with varying degrees of complexity. However, most questionnaires remain of limited clinical utility, and symptom scales seem to be more useful in clinical practice. In the assessment of exacerbations, the type and degree of severity should be ascertained in order to define the management setting and optimize treatment options. Still, a consensual and universal classification system to assess the severity and type of an exacerbation is lacking, and there are no established criteria for less severely ill patients not requiring hospital assessment. This might lead to under-reporting of minor to moderate exacerbations, which has an impact on patients' health status. There is a clear unmet need to develop clinically useful questionnaires and a comprehensive system to evaluate the severity of exacerbations that can be used in all settings, from primary health care to general hospitals.