The relation of oxidative stress and apoptosis with the effect of global brain ischemia due to metabolic disorder on the histopathologic alterations of the lung

The important tissue damage occurs after brain ischemia and following reperfusion. The metabolic alterations due to sistemic effect from this damage can be exposed at the different organ with new mechanisms. The one of the main important organ is lung and free oxygene radicals from the cells of this organ play important role in this damage. The aim of this study was the investigation of the effects of respiratory asidosis as a critical determinant from metabolic alterations due to bilateral carotid artey occlusion which is a model for the brain ischemia on the damage after reperfusion and examination of their relation with oxidative stres coupling with apoptosis.4 group and 5 Male wistar rat (250 ± 50 gr) in each group were used in this study. After 48 hours, following 10 minutes ischemia for precondition group (PC), 20 minutes ischemia was used for the global ischemia (GI). Rats were waited for 48 hours after GI for the ischemic reperfusion (IR) effect. 10 ml blood for the gas analyses and hypovolemia were taken from femoral artery under the ketamin+xylasine anesthesia. Rats in all groups were sacrificed at the end of 96 hours which was total time for whole experiment. Their brain sections at the optic chiesma level were investigated for histochemical (H&), immunohistochemical (GFAP, S100ß, iNOS, eNOS, TUNEL) and morphometric analyses. The lung of the ischemic brain was processed for the similar analyses (H-E, MT, iNOS, eNOS, TUNEL).There was significant changes with ischemic brain which showed gliosis (GFAP, S100ß) with oxidative stres and free radicals (iNOS, eNOS) related to apoptosis (TUNEL). The histopathologic damage of the lung was evaluated by morphometry with histological parameters. There was minimal alterations between sham and preconditioning group. However, these groups were significantly different from global ischemia and ischemic reperfusion groups for the damage. Interstisyel edema, vascular conjestion, intraalveoler hemorhagia, neutrophil infiltration and alveol destruction were found with H-E examination. There was also inflamatuar cells in connective tissue by Masson Triachrom staining. The damage in the lung as a distance organ was similar to ischemic reperfusion damage of the brain which related to the free radicals from oxidative stres (iNOS, eNOS). Increase of the free radical caused the induction of the apotosis (TUNEL) and the activation of the cell death.Our results showed that the histopathological alterations of the lung after the damage of the ischemic reperfusion in the brain were originated from the infiltration of the cells producing free oxygene radicals and inducing apoptosis as a mechanism which cause cell deathKey word: Brain, Ischemia, Reperfüsion, Lung, NOS, Apoptosis