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      Niveles aumentados de estrés oxidativo se asocian a disfunción endotelial periférica y respuesta vascular pulmonar disminuida frente a vasodilatadores en pacientes con hipertensión pulmonar Translated title: Increased oxidative stress are associated with peripheral endothelial dysfunction and diminished vascular response to vasodilators in pulmonary hypertensive patients

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          Abstract

          Introducción: La Hipertensión arterial pulmonar (HP) se caracteriza por remodelado vascular y disfunción endotelial. Evidencia experimental muestra que el estrés oxidativo juega un rol importante en la patogénesis de la HP. El rol del estrés oxidativo, su relación con la función endotelial periférica y con la respuesta vascular pulmonar a vasodilatadores en pacientes con HP no está aclarada. Objetivo: evaluar parámetros de estrés oxidativo y función endotelial periférica en pacientes con HP y estudiar su relación con la respuesta vascular pulmonar frente a vasodilatadores. Métodos: estudio transversal. Se incluyeron 14 pacientes con HP y 14 controles pareados por edad y sexo. En todos los sujetos se midieron: niveles plasmáticos de malondialdehido (MDA), superóxi-do dismutasa ligada a endotelio (eSOD) y xantino oxidasa (eXO). Vasodilatación dependiente de endotelio mediada por flujo en arteria braquial fue usada como marcador de función endotelial (FDD). Función ventricular derecha y reactividad del lecho vascular pulmonar frente a iloprost inhalado fueron evaluadas ecocardiográficamente en los pacientes con HP Resultados: Los pacientes con HP presentaron FDD disminuida versus los controles (2,8 ± 0,6 vs 10,7% ± 0,6, p< 0,01). Niveles de MDA y eXO aumentados (0,61 ± 0,17 vs 0,34 ± 0,15μM, p<0,01 y 0,039 ± 0,005 vs 0,034 ± 0,004 U/mL1, p=0,02 respectivamente) y actividad de eSOD disminuida (235,55 ± 23 vs 461,41 ± 33 ABC, p<0,01). Iloprost mejora significativamente el gasto cardíaco derecho y disminuye la resistencia vascular pulmonar en los pacientes con HP y este cambio se correlaciona con la actividad de eSOD (Rho: 0,61, p<0,01) y FDD (Rho: 0,63, p=0,01). Conclusiones: Pacientes con HP presentan parámetros de estrés oxidativo elevados y disfunción endotelial periférica La respuesta hemodinámica frente al uso de Iloprost se correlaciona con estos parámetros sugiriendo un rol en la HP cuyo valor clínico deberá ser evaluado.

          Translated abstract

          Background: Pulmonary Arterial Hypertension (PAH) is characterized by endothelial dysfunction and vascular remodeling. Several lines of experimental evidence indícate that oxidative stress plays an important role in the pathogenesis of PAH. The role of oxidative stress and its relation with peripheral endothelial function and pulmonary vascular response to vasodilators remains unknown. Aim: To evalúate whether systemic oxidative stress and endothelial dysfunction markers are associated with the response of the pulmonary vascular bed to inhaled vasodilators in PAH patients. Methods: Cross-sectional study Fourteen patients with PAH and 14 age and gender-matched controls were in-cluded. Systemic oxidative stress was assessed through plasma malondialdehyde (MDA), xanthine oxidase (eXO) levéis and endothelial-bound superoxide dis-mutase (eSOD) activity Brachial artery endothelial-de-pendent flow-mediated vasodilation (FDD) was used to evalúate endothelial function. Right ventricular function and pulmonary vascular bed reactivity to inhaled vasodilators was determined with echocardiography in PAH patients. Results: Compared to controls, PAH patients showed impaired FDD (2.8 ± 0.6 vs 10.7% ± 0.6, p< 0.01), increased MDA and eXO levéis (0.61 ± 0.17 vs 0.34 ± 0.15μM, p<0.01 and 0.039 ± 0.005 vs 0.034 ± 0.004 U/ mL1, p=0.02 , respectively) and decreased eSOD activity 235.55 ± 23 vs 461.41 ± 33 AUC, p<0.01). Iloprost significantly improved right cardiac output (RCO) and decreased pulmonary vascular resistance. The amount of change in RCO after iloprost inhalation correlated significantly with baseline eSOD activity and FDD (Rho: 0.61, p<0.01 and Rho: 0.63, p=0.01 respectively). Conclusions: PAH patients show increased oxidative stress and endothelial dysfunction markers. Response to inhaled iloprost is closely related with baseline endothelial function and oxidative stress parameters, suggesting an important role of these elements that requires further clinical evaluation.

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          Most cited references 29

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          Isoprostanes and lung vascular pathology.

           Joop Janssen (2008)
          Isoprostanes are products of peroxidative attack of membrane lipids. As such, they accumulate to substantial levels in conditions of oxidative stress, including many pulmonary vascular diseases such as acute lung injury and pulmonary hypertension, and are increasingly being used as indicators of disease state and severity. However, our group and others have hypothesized that they are more than inert markers, but may also act as signal transduction molecules. As isomers of prostaglandins, they can exert powerful biological effects on many lung cell types through actions on prostanoid receptors. In this review, we collect many lines of evidence that point to causal roles for the isoprostanes in those disease states.
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            Endothelial modulation of pulmonary vascular tone.

             Tri Dinh (1992)
            Pulmonary endothelial cells normally synthesize prostacyclin (PGI2) and nitric oxide (NO), which are both potent vasodilators. Although PGI2 is largely used to treat patients with severe pulmonary hypertension, its role in the physiology and pathophysiology of the pulmonary circulation is still debated. NO, which is now considered as the endogenous nitrovasodilator, is perhaps more involved than PGI2 in the mechanisms that modulate pulmonary vascular tone in health and disease. There is evidence to suggest that background release of NO contributes to the normally low pulmonary vascular tone in normoxia. Although there are theoretical grounds to hypothesize that hypoxia reduces the synthesis of NO, lack of the latter does not seem to account for the acute hypoxic pulmonary vasoconstriction. Instead, there is evidence to suggest that NO activity is increased in order to modulate the pulmonary vasopressor response to acute alveolar hypoxia. However, more consistent, concerning the role of NO, are data gathered from studies performed in chronic hypoxic conditions. Both experimental data and studies performed in man demonstrate impairment of NO synthesis and/or release in chronic hypoxic pulmonary hypertension. The impaired NO production, whilst reducing the ability of the pulmonary vasculature to relax, also favours the occurrence of excessive pulmonary vasoconstriction. Lack of NO synthesis might also permit mitogenesis and proliferation of various cell types within the vascular wall. We hypothesize that functional alterations of pulmonary endothelium are likely to affect both reactivity and growth of pulmonary vessels. In this respect, NO probably has a pivotal role in modulating pulmonary vascular tone and controlling pulmonary vascular remodelling in health and disease.
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              Testing endothelial function using ultrasound.

              Endothelial dysfunction appears to be a key early event in a number of important cardiovascular disease states, including atherosclerosis and hypertension. Testing endothelial function in vivo has proved challenging. Although the endothelium releases a number of products, no single blood test has yet proved useful to determine normal endothelial function or early abnormalities. The most common test of endothelial function used to date in vivo depends on measuring endothelium-dependent dilatation in response to pharmacologic or physiologic stimuli. This depends mostly on the endothelial ability to release nitric oxide (NO), not only a potent vasodilator but also an inhibitor of platelet aggregation, monocyte adhesion, and smooth muscle proliferation. Over the past decade, endothelium-dependent dilatation has been tested using high-resolution external vascular ultrasound. The major advantage of this method is that it is completely noninvasive, accurate, and reproducible. The major disadvantage is that the coronary arteries cannot be imaged directly with ultrasound, and therefore the test is usually applied to peripheral arteries, such as the brachial or femoral conduit vessels. Using such ultrasound techniques, many groups have documented endothelial dysfunction in children and young adults at risk for atherosclerosis and have performed a variety of studies concerning reversibility of early arterial damage, using potentially important antiatherogenic strategies.
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                Author and article information

                Contributors
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                Journal
                rchcardiol
                Revista chilena de cardiología
                Rev Chil Cardiol
                Sociedad Chilena de Cardiología y Cirugía Cardiovascular (Santiago )
                0718-8560
                2010
                : 29
                : 3
                : 291-298
                Affiliations
                [1 ] Pontificia Universidad Católica de Chile Chile
                [2 ] Universidad de Chile Chile
                Article
                S0718-85602010000300002
                10.4067/S0718-85602010000300002
                Product
                Product Information: website
                Categories
                CARDIAC & CARDIOVASCULAR SYSTEMS

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