Akademik Veri Yönetim Sistemi
Haseki Tip Bulteni, cilt.56, sa.3, ss.228-234, 2018 (Scopus)
Aim: During reperfusion of myocardial ischemia, damage can also be seen in the kidneys. Although many studies have been conducted on the underlying mechanisms, the basic mechanism of this interaction is still unknown. We think that this is oxidative/nitrosative damage caused by hypoperfusion. Nebivolol is a beta-blocker with nitric oxide (NO)-mediated effects. In this study, we aimed to investigate the NO-mediated effect of nebivolol on acute renal injury (ARI) developed after myocardial ischemia-reperfusion (IR). Methods: Adult male Sprague-Dawley rats were divided into three groups: sham-control, IR-control, and IR-nebivolol. Nebivolol (0.1 mg/ kg, intravenous) was administered within the 10 min of reperfusion. IR was performed by surgically anterior descending artery ligation. NO-mediated effects of nebivolol were assessed by hemodynamic, biologic and histologic studies. Results: Compared to the sham-control, changes in renal function were not statistically significant in the IR-control (p>0.05). Focal tubular damage findings were also observed in histologic sections. Decrease in superoxide dismutase (SOD) levels together with increase in nitrogen dioxide (NOx)/peroxynitrite (ONOO-) were also significant (p<0.05). On the contrary, consistent with focal tubular regeneration, elevated renal SOD levels together with reduced NOx/ONOO- levels were detected in IR-nebivolol (p<0.05). Conclusion: NO-mediated beneficial effects of nebivolol on ARI developing after myocardial IR were shown. The mechanism can be explained by the prevention of nitrosative damage and the protection of NO bioavailability.