Protective efficiacy of taurine against pulmonary edema progression: experimental study

Re-expansion pulmonary edema (RPE) is an acute, rare and potentially lethal complication [1,2]. Its beginning is sudden and dramatic. The mechanism is not yet fully understood [1]. Some authors suggest that it may occur after rapid re-inflation of a collapsed lung [1]. It was reported by other authors that it may relate to surfactant depletion or may result from hypoxic capillary damage, leading to increased capillary permeability [1,3]. In RPE, unilateral lung injury is initiated by cytotoxic oxygen metabolites and temporally associated with an influx of polymorphonuclear neutrophils [1]. These toxic oxygen products are the results of re-oxygenation of a collapsed lung. Treatment of re-expansion pulmonary edema is basically preventive [4].The RPE is a disease process that is characterized by diffuse inflammation in the lung parenchyma and resultant permeability edema [2]. The involvement of inflammatory mediators in RPE has been the subject of intense investigation, and oxidant-mediated tissue injury is likely to be important in the pathogenesis of RPE [2]. In response to various inflammatory stimuli, lung endothelial cells, alveolar cells, and airway epithelial cells, as well as alveolar macrophages, produce reactive oxygen species (ROS) [2,5]. Free oxygen radicals increase after pulmonary re-expansion and, it can enhance the production of these toxic species [2,5]. As the antioxidant defense system, various enzymes and low-molecular weight ROS scavengers are present in the lung tissue and epithelial lining fluid [2,5].Taurine, 2-amino ethane sulfonic acid, is a normal constituent of the human diet and is a ubiquitous powerful antioxidant [6]. It prevents tissue injury mainly through antioxidation [6]. Taurine was revealed to be beneficial in preventing experimental lead-induced oxidative damage, diabetic neuropathy, CCl4-induced oxidative stress, caeurelein-induced acute pancreatitis, and early changes in experimental diabetic kidney through antioxidant mechanism