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Sodium Glucose Transporter 2 (SGLT2) Inhibition does not Pro | 15869

<!DOCTYPE html> <html> <head> <meta charset="utf-8"> <meta name="viewport" content="width=device-width, initial-scale=1"> <title>Sodium Glucose Transporter 2 (SGLT2) Inhibition does not Pro | 15869</title> <meta name="keywords" content="Jespersen NR*, Lassen TR, Hjortbak MV, St&oslash;ttrup NB and B&oslash;tker HE, Ischemic-reperfusion injury; SGLT2- inhibition; Cardioprotection; Mitochondrial respiration"/> <meta name="description" content="Background: The Sodium Glucose Transporter 2 (SGLT2)-inhibitor, empagliflozin, reduces death from cardiovascular causes. We hypothesized that the mechanism..15869"/> <meta name="citation_publisher" content="Walsh Medical Media" /> <meta name="citation_journal_title" content="Cardiovascular Pharmacology: Open Access"> <meta name="citation_title" content="Sodium Glucose Transporter 2 (SGLT2) Inhibition does not Protect the Myocardium from Acute Ischemic Reperfusion Injury but Modulates Post- Ischemic Mitochondrial Function"> <meta name="citation_author" content="Jespersen NR" /> <meta name="citation_author" content="Lassen TR" /> <meta name="citation_author" content="Hjortbak MV" /> <meta name="citation_author" content="St&oslash;ttrup NB" /> <meta name="citation_author" content="B&oslash;tker HE" /> <meta name="citation_year" content="2017"> <meta name="citation_volume" content="6"> <meta name="citation_issue" content="2"> <meta name="citation_doi" content="10.4172/2329-6607.1000210"> <meta name="citation_issn" content="2329-6607"> <meta name="citation_online_date" content="2019/02/13" /> <meta name="citation_firstpage" content="1"> <meta name="citation_lastpage" content="3"> <meta name="citation_abstract" content="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 &times; 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 given 10 min prior to the acute myocardial infarction. Empagliflozin improved post-ischemic complex I+II respiration compared to the IR group. This improvement was similar to IPC. In contrast to the improved complex I respiration by IPC, empagliflozin mainly improved complex II respiration. Empagliflozin hearts had significantly higher respiration in oligomycin induced state 4 than the sham and IR group, indicating that empagliflozin modulates the inner mitochondrial membrane. Conclusion: In conclusion, empagliflozin yielded no acute cardioprotection in the isolated perfused non-diabetic rat heart. Empagliflozin mainly improved complex II respiration and increased permeability of the inner membrane, providing a potential explanation for the positive long-term effects observed in post infarction myocardial dysfunction. 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We hypothesized that the mechanism involved direct protection against Ischemia- Reperfusion (IR) injury and improved post-ischemic mitochondrial function.</p> <p><strong>Methods:</strong> 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 &times; 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).</p> <p><strong>Results:</strong> In contrast to IPC, empagliflozin did not reduce infarct size compared to the IR group, when given 10 min prior to the acute myocardial infarction. Empagliflozin improved post-ischemic complex I+II respiration compared to the IR group. This improvement was similar to IPC. In contrast to the improved complex I respiration by IPC, empagliflozin mainly improved complex II respiration. Empagliflozin hearts had significantly higher respiration in oligomycin induced state 4 than the sham and IR group, indicating that empagliflozin modulates the inner mitochondrial membrane.</p> <p><strong>Conclusion:</strong> In conclusion, empagliflozin yielded no acute cardioprotection in the isolated perfused non-diabetic rat heart. 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