<p>Sepsis frequently leads to cardiac dysfunction driven by oxidative stress (OS), inflammation, and conduction abnormalities. Nebivolol (NEB), a selective β1-blocker with vasodilatory and antioxidant properties, has shown organ-protective effects in sepsis, but its cardiovascular role remains unclear. This study investigated the effects of NEB in cecal ligation and puncture (CLP)-induced sepsis in rats. Thirty-two rats were assigned to four groups: Sham, NEB, CLP, and NEB + CLP. Hemodynamic parameters, ECG findings, cardiac and vascular OS markers, serum biochemistry, and histopathology were evaluated. CLP caused tachycardia, conduction disturbances, increased OS, and marked myocardial and aortic injury. NEB reduced heart rate, improved PR interval, and partially ameliorated oxidative and histological alterations. However, NEB did not improve blood pressure, myocardial edema, or aortic injury. NEB offered localized protection against sepsis-induced myocardial injury by modulating oxidative and inflammatory pathways. While these biochemical and histopathological improvements were significant, they were not accompanied by changes in systemic blood pressure or a complete reversal of all structural alterations during the acute phase. These findings support further investigation of NEB as a potential adjunctive therapy in sepsis.</p>

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Nebivolol as a potential adjunct therapy for sepsis-induced cardiac dysfunction: evidence from a rat model

  • Ruveyda Ummugulsum Unal,
  • Onural Ozhan,
  • Elif Sude Balkaya,
  • Azibe Yildiz,
  • Feyzi Dogru,
  • Mehmet Ertugrul Balkar,
  • Ayse Maden,
  • Ayse Yucekaya,
  • Zeynep Kucukakcali,
  • Hakan Parlakpinar

摘要

Sepsis frequently leads to cardiac dysfunction driven by oxidative stress (OS), inflammation, and conduction abnormalities. Nebivolol (NEB), a selective β1-blocker with vasodilatory and antioxidant properties, has shown organ-protective effects in sepsis, but its cardiovascular role remains unclear. This study investigated the effects of NEB in cecal ligation and puncture (CLP)-induced sepsis in rats. Thirty-two rats were assigned to four groups: Sham, NEB, CLP, and NEB + CLP. Hemodynamic parameters, ECG findings, cardiac and vascular OS markers, serum biochemistry, and histopathology were evaluated. CLP caused tachycardia, conduction disturbances, increased OS, and marked myocardial and aortic injury. NEB reduced heart rate, improved PR interval, and partially ameliorated oxidative and histological alterations. However, NEB did not improve blood pressure, myocardial edema, or aortic injury. NEB offered localized protection against sepsis-induced myocardial injury by modulating oxidative and inflammatory pathways. While these biochemical and histopathological improvements were significant, they were not accompanied by changes in systemic blood pressure or a complete reversal of all structural alterations during the acute phase. These findings support further investigation of NEB as a potential adjunctive therapy in sepsis.