Acute Dapagliflozin Administration Ameliorates Cardiac Surgery-Associated Acute Kidney Injury in a Rabbit Model

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  • Matsuda Kensaku
    Department of Cardiovascular Surgery, Kyushu University Hospital
  • Mitsuo Hiroshi
    Department of Cardiovascular Surgery, Kyushu University Hospital
  • Nishijima Takuya
    Department of Cardiovascular Surgery, Kyushu University Hospital
  • Uchiyama Hikaru
    Department of Cardiovascular Surgery, Kyushu University Hospital
  • Nita Tobuhiro
    Department of Cardiovascular Surgery, Kyushu University Hospital
  • Matsunaga Shogo
    Department of Cardiovascular Surgery, Kyushu University Hospital
  • Fujimoto Noriko
    Department of Cardiovascular Surgery, Kyushu University Hospital
  • Ushijima Tomoki
    Department of Cardiovascular Surgery, Kyushu University Hospital
  • Ando Yusuke
    Department of Cardiovascular Surgery, Kyushu University Hospital
  • Kan-o Meikun
    Department of Cardiovascular Surgery, Kyushu University Hospital
  • Shinohara Gen
    Department of Cardiovascular Surgery, Kyushu University Hospital
  • Kimura Satoshi
    Advanced Aortic Therapeutics, Faculty of Medicine, Kyushu University Graduate School of Medicine
  • Sonoda Hiromichi
    Department of Cardiovascular Surgery, Kyushu University Hospital
  • Shiose Akira
    Department of Cardiovascular Surgery, Kyushu University Hospital

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<p>Background:  Several studies have shown that sodium-glucose cotransporter-2 inhibitors have a renoprotective effect on acute kidney injury (AKI), but their effect on cardiac surgery-associated AKI is unknown.</p><p>Methods and Results:  AKI was induced in 25 rabbits without diabetes mellitus by cardiopulmonary bypass (CPB) for 2 h and they were divided into 5 groups: sham; dapagliflozin-treated sham; CPB; dapagliflozin-treated CPB; and furosemide-treated CPB (n=5 in each group). Dapagliflozin was administered via the femoral vein before initiating CPB. Kidney tissue and urine and blood samples were collected after the surgical procedure. There were no differences in the hemodynamic variables of each group. Dapagliflozin reduced serum creatinine and blood urea nitrogen concentrations, and increased overall urine output (all P<0.05). Hematoxylin and eosin staining showed that the tubular injury score was improved after dapagliflozin administration (P<0.01). Dapagliflozin administration mitigated reactive oxygen species and kidney injury molecule-1 as assessed by immunohistochemistry (both P<0.0001). Protein expression analysis showed improvement of inflammatory cytokines and apoptosis, and antioxidant enzyme expression was elevated (all P<0.05) through activation of the nuclear factor erythroid 2-related factor 2 pathway (P<0.01) by dapagliflozin.</p><p>Conclusions:  Acute intravenous administration of dapagliflozin protects against CPB-induced AKI. Dapagliflozin may have direct renoprotective effects in renal tubular cells.</p>

収録刊行物

  • Circulation Journal

    Circulation Journal 88 (9), 1488-1498, 2024-08-23

    一般社団法人 日本循環器学会

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