Cal acute inflamatory cells in RPE (HEx400), (d) severe pulmonary edema
Cal acute inflamatory cells in RPE (HEx400), (d) severe pulmonary edema with alveolar damage and scattered typical acute inflamatory cells in RPE (HEx200).expansion of a collapsed lung increases the microvascular permeability and causes reexpansion pulmonary edema [5,14]. Neutrophils and their products have been implicated in the development of this phenomenon [14]. There is a large body of evidence that reactive oxygen species produced during RPE play a key role in lung damage andTable 2: Oxidative stress related parameters of the groups.endothelial dysfunction [15]. It was suggested that antioxidants might play a role in the treatment of RPE. Taurine is known to be a potent antioxidant and a membranestabilizing agent. Therefore; we investigated whether taurine PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28607003 has a possible beneficial effect in RPE in rats.GroupsnMDA (nmol/g) Mean ?Std. Deviation 1,45 ?0,21 1,78 ?0,12 1,63 ?0,SOD (U/g) Mean ?Std. Deviation 654,48 ?98,48 585,32 ?97,14 655,32 ?112,11 ,GPx Mean ?Std. Deviation 24,94 ?1,94 20,44 ?1,53 23,85 ?2,CG RPEG TG10 10Contrtol group (CG), RPEG Reexpancion Pulmonary Group and Taurine groups (TG) lung tissues. MDA; Malondialdehyde, SOD; Superoxide SC144 solubility Dismutase. : p < 0,001, RPEG compared with CG; : p < 0,05, TG compared with RPEG, : p < 0,05, TG compared with CG.Page 4 of(page number not for citation purposes)Journal of Cardiothoracic Surgery 2008, 3:http://www.cardiothoracicsurgery.org/content/3/1/Previous studies demonstrated that administration of taurine, vitamin C, and vitamin E partially protected from oxidative damage and while all substances had antioxidant effects, only taurine showed morphological protection in surviving cells [16]. Other studies have demonstrated that addition of taurine to St. Thomas' cardioplegic solution, improved cardiac function recovery for prolonged hypothermic rat heart preservation by suppressing DNA oxidative stress and cell apoptosis [17]. Besides this, another study have emphasized that treatment with taurine reduces iron-mediated myocardial oxidative stress, preserves cardiovascular function, and improves survival in iron-overloaded mice. Oudit et al revealed the role of taurine in protecting reduced glutathione levels that provides an important mechanism by which oxidative stress-induced myocardial damage can be curtailed [18]. All these studies made us choose taurine to use as a potent antioxidant against RPE. Sivrikoz et al reported that lung is the largest reservoir for monocytes, macrophages and PNLs. In their study, lymphocyte (++) dominance was found semi-quantitatively at the end of the pnomothorax. Together with reexpancion, lymphocyte levels were increased (+++) and PNLs started to remigrate to the area. They empahsized that the reperfusion achieved during reexpancion increases the production of free radicals by activating the inflammatory cells in addition to increasing the oxygen supply to the tissue [1]. Saito et al revealed that they therefore believe ROS produced by xanthine oxidase in endothelial and alveolar type II cells, plays a major role in the pathogenesis of RPE [19]. Doerschunk et al demonstrated that histological examination of the injured right lungs in control animals has focal areas of edema; hemorrhage in both the alveolar spaces and the interstitium. There was lymphatic dilatation and edema within the bronchovascular bundle. They founded that alveolar macrophages containing cytoplasmic granules were more in number than PML which are sparse in the injured lung [5].
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