The Effects of Cilostazol on Tissue Oxygenation upon an Ischemic-reperfusion Injury in the Mouse Cerebrum

摘要: Although cilostazol, an inhibitor of cyclic nucleotide phosphodiesterase 3 (PDE3), is known to exert a potent antiplatelet function by raising intracellular cAMP concentration, its effect on cerebral microcirculation upon ischemic insult not clearly understood. To examine effects cilostazol the global injury in brain, we first measured plasma leakage using modified Miles assay after mice had been subjected 60 min bilateral common carotid artery (BCCA) occlusion followed reperfusion for 4 h. Oral treatment with (30 mg/kg) significantly increased leakage. This result led us if recruits more capillaries leading increase surface area exchange and oxygen transport tissues. do so, simultaneously degrees tissue hypoxia vessel perfusion. Pimonidazol was injected intraperitoneally 1 h before sacrifice capillary patency assessed fluorescein isothiocyanate-labeled Lycopersicon esculentum lectin bound endothelial surface. Treatment markedly which accompanied reduction hypoxic area. caused flux proteins across barrier that may imply adverse role BCCA occlusion, this protein attributable turn brought about hypoxia. Taken together appears produce protective against ischemic-reperfusion injury.