Protective Effects of Fluvoxamine against Ischemia/Reperfusion Injury in Isolated, Perfused Guinea-Pig Hearts

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  • Muto Tatsuya
    College of Pharmacy, Kinjo Gakuin University Meitetsu Hospital Pharmacy
  • Usuda Haruki
    College of Pharmacy, Kinjo Gakuin University
  • Yamamura Aya
    College of Pharmacy, Kinjo Gakuin University
  • Yoshida Koji
    College of Pharmacy, Kinjo Gakuin University
  • Ohashi Ai
    College of Pharmacy, Kinjo Gakuin University
  • Mitsui-Saitoh Kumiko
    College of Pharmacy, Kinjo Gakuin University Faculty of Sports and Health Science, Nagoya Gakuin University
  • Sakai Junichi
    College of Pharmacy, Kinjo Gakuin University Faculty of Sports and Health Science, Nagoya Gakuin University
  • Sugimoto Yumi
    Laboratory of Pharmacology, Department of Clinical Pharmacy, Yokohama College of Pharmacy
  • Mizutani Hideki
    College of Pharmacy, Kinjo Gakuin University
  • Nonogaki Tsunemasa
    College of Pharmacy, Kinjo Gakuin University
  • Hotta Yoshihiro
    College of Pharmacy, Kinjo Gakuin University Department of Pharmacology, Aichi Medical University School of Medicine

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Serotonin (5-hydroxytryptamine; 5-HT) is known to be activated during ischemia–reperfusion and triggers contractile dysfunction and pathological apoptosis. Here, the beneficial effects of the selective serotonin reuptake inhibitor (SSRI) fluvoxamine was demonstrated on ischemia–reperfusion injury in guinea-pig hearts perfused using the Langendorff technique. The recovery (%) of left ventricular developed pressure (LVDP) by fluvoxamine (5×10−8 M) was 95.4% (control: 32%), which was consistent with the inhibition of mitochondrial Ca2+([Ca2+]m) uptake induced by changes in the Ca2+ content and acidification of the perfusate, and similar to reperfusion following global ischemia in Langendorff-perfused hearts. Fluvoxamine inhibited the increase in [Ca2+]m induced by changes in the Ca2+ content of the perfusate in perfused preparations of mitochondria, which was similar to the results obtained with the mitochondrial permeability transition pore (MPTP) opener atractyroside. The terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL)-positive cells were significantly less in fluvoxamine-treated hearts than in control hearts, with decreases in caspase-3 activity. These results suggest that SSRI inhibits opening of the MPTP by preventing [Ca2+]m overload-induced apoptosis related to the endogenous accumulation of 5-HT in ischemia–reperfusion hearts.

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