Cardiovascular Pharmacology: Open Access

Hjortbak MV

Publications

• Short Communication
  Sodium Glucose Transporter 2 (SGLT2) Inhibition does not Protect the Myocardium from Acute Ischemic Reperfusion Injury but Modulates Post- Ischemic Mitochondrial Function
  Author(s): Jespersen NR*, Lassen TR, Hjortbak MV, Støttrup NB and Bøtker HEJespersen NR*, Lassen TR, Hjortbak MV, Støttrup NB and Bøtker HE
  
  Background: The Sodium Glucose Transporter 2 (SGLT2)-inhibitor, empagliflozin, reduces death from cardiovascular causes. We hypothesized that the mechanism involved direct protection against Ischemia- Reperfusion (IR) injury and improved post-ischemic mitochondrial function. Methods: We examined infarct size (series I) and mitochondrial respiration (series II) in four groups of isolated perfused hearts from male Wistar rats: Sham-operated hearts (Sham group), IR-injured hearts (IR group), hearts treated with ischemic preconditioning (IPC) by 2 × 5 min. cycles of IR prior to sustained ischemia (IPC group), and hearts co-perfused with 2.14 mg/l of empagliflozin 10 min. prior to sustained ischemia (EMPA group). Results: In contrast to IPC, empagliflozin did not reduce infarct size compared to the IR group, when give.. View More»
  DOI: 10.4172/2329-6607.1000210

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