Glimepride, a novel sulfonylurea, does not abolish myocardial protection afforded by either ischemic preconditioning or diazoxide

M.M. Mocanu, Helen L. Maddock, G.F. Baxter, C.L. Lawrence, N.B. Standen, D.M. Yellon

    Research output: Contribution to journalArticle

    111 Citations (Scopus)

    Abstract

    Background: The sulfonylurea glibenclamide (Glib) abolishes the cardioprotective effect of ischemic preconditioning (IP), presumably by inhibiting mitochondrial KATP channel opening in myocytes. Glimepiride (Glim) is a new sulfonylurea reported to affect nonpancreatic KATP channels less than does Glib. We examined the effects of Glim on IP and on the protection afforded by diazoxide (Diaz), an opener of mitochondrial KATP channels. Methods and Results: Rat hearts were Langendorff-perfused, subjected to 35 minutes of regional ischemia and 120 minutes of reperfusion, and assigned to 1 of the following treatment groups: (1) control; (2) IP of 2x 5 minutes each of global ischemia before lethal ischemia; or pretreatment with (3) 30 µmol/L Diaz, (4) 10 µmol/L Glim, (5) 10 µmol/L Glib, (6) IP+Glim, (7) IP+Glib, (8) Diaz+Glim, or (9) Diaz+Glib. IP limited infarct size (18.5±1% vs 43.7±3% in control, P
    Original languageEnglish
    JournalCirculation
    Volume103
    Issue number25
    DOIs
    Publication statusPublished - 26 Jun 2001

    Fingerprint

    glimepiride
    Diazoxide
    Ischemic Preconditioning
    Glyburide
    Ischemia
    KATP Channels
    Muscle Cells
    Reperfusion
    Control Groups

    Bibliographical note

    The full text of this item is not available from the repository.

    Keywords

    • potassium
    • myocardial infarction
    • diabetes mellitus
    • ion channels

    Cite this

    Glimepride, a novel sulfonylurea, does not abolish myocardial protection afforded by either ischemic preconditioning or diazoxide. / Mocanu, M.M.; Maddock, Helen L.; Baxter, G.F.; Lawrence, C.L.; Standen, N.B.; Yellon, D.M.

    In: Circulation, Vol. 103, No. 25, 26.06.2001.

    Research output: Contribution to journalArticle

    Mocanu, M.M. ; Maddock, Helen L. ; Baxter, G.F. ; Lawrence, C.L. ; Standen, N.B. ; Yellon, D.M. / Glimepride, a novel sulfonylurea, does not abolish myocardial protection afforded by either ischemic preconditioning or diazoxide. In: Circulation. 2001 ; Vol. 103, No. 25.
    @article{fad20afe6237430e9c2d0f103d34c7c2,
    title = "Glimepride, a novel sulfonylurea, does not abolish myocardial protection afforded by either ischemic preconditioning or diazoxide",
    abstract = "Background: The sulfonylurea glibenclamide (Glib) abolishes the cardioprotective effect of ischemic preconditioning (IP), presumably by inhibiting mitochondrial KATP channel opening in myocytes. Glimepiride (Glim) is a new sulfonylurea reported to affect nonpancreatic KATP channels less than does Glib. We examined the effects of Glim on IP and on the protection afforded by diazoxide (Diaz), an opener of mitochondrial KATP channels. Methods and Results: Rat hearts were Langendorff-perfused, subjected to 35 minutes of regional ischemia and 120 minutes of reperfusion, and assigned to 1 of the following treatment groups: (1) control; (2) IP of 2x 5 minutes each of global ischemia before lethal ischemia; or pretreatment with (3) 30 µmol/L Diaz, (4) 10 µmol/L Glim, (5) 10 µmol/L Glib, (6) IP+Glim, (7) IP+Glib, (8) Diaz+Glim, or (9) Diaz+Glib. IP limited infarct size (18.5±1{\%} vs 43.7±3{\%} in control, P",
    keywords = "potassium, myocardial infarction, diabetes mellitus, ion channels",
    author = "M.M. Mocanu and Maddock, {Helen L.} and G.F. Baxter and C.L. Lawrence and N.B. Standen and D.M. Yellon",
    note = "The full text of this item is not available from the repository.",
    year = "2001",
    month = "6",
    day = "26",
    doi = "10.1161/01.CIR.103.25.3111",
    language = "English",
    volume = "103",
    journal = "Circulation",
    issn = "0009-7322",
    publisher = "American Heart Association",
    number = "25",

    }

    TY - JOUR

    T1 - Glimepride, a novel sulfonylurea, does not abolish myocardial protection afforded by either ischemic preconditioning or diazoxide

    AU - Mocanu, M.M.

    AU - Maddock, Helen L.

    AU - Baxter, G.F.

    AU - Lawrence, C.L.

    AU - Standen, N.B.

    AU - Yellon, D.M.

    N1 - The full text of this item is not available from the repository.

    PY - 2001/6/26

    Y1 - 2001/6/26

    N2 - Background: The sulfonylurea glibenclamide (Glib) abolishes the cardioprotective effect of ischemic preconditioning (IP), presumably by inhibiting mitochondrial KATP channel opening in myocytes. Glimepiride (Glim) is a new sulfonylurea reported to affect nonpancreatic KATP channels less than does Glib. We examined the effects of Glim on IP and on the protection afforded by diazoxide (Diaz), an opener of mitochondrial KATP channels. Methods and Results: Rat hearts were Langendorff-perfused, subjected to 35 minutes of regional ischemia and 120 minutes of reperfusion, and assigned to 1 of the following treatment groups: (1) control; (2) IP of 2x 5 minutes each of global ischemia before lethal ischemia; or pretreatment with (3) 30 µmol/L Diaz, (4) 10 µmol/L Glim, (5) 10 µmol/L Glib, (6) IP+Glim, (7) IP+Glib, (8) Diaz+Glim, or (9) Diaz+Glib. IP limited infarct size (18.5±1% vs 43.7±3% in control, P

    AB - Background: The sulfonylurea glibenclamide (Glib) abolishes the cardioprotective effect of ischemic preconditioning (IP), presumably by inhibiting mitochondrial KATP channel opening in myocytes. Glimepiride (Glim) is a new sulfonylurea reported to affect nonpancreatic KATP channels less than does Glib. We examined the effects of Glim on IP and on the protection afforded by diazoxide (Diaz), an opener of mitochondrial KATP channels. Methods and Results: Rat hearts were Langendorff-perfused, subjected to 35 minutes of regional ischemia and 120 minutes of reperfusion, and assigned to 1 of the following treatment groups: (1) control; (2) IP of 2x 5 minutes each of global ischemia before lethal ischemia; or pretreatment with (3) 30 µmol/L Diaz, (4) 10 µmol/L Glim, (5) 10 µmol/L Glib, (6) IP+Glim, (7) IP+Glib, (8) Diaz+Glim, or (9) Diaz+Glib. IP limited infarct size (18.5±1% vs 43.7±3% in control, P

    KW - potassium

    KW - myocardial infarction

    KW - diabetes mellitus

    KW - ion channels

    U2 - 10.1161/01.CIR.103.25.3111

    DO - 10.1161/01.CIR.103.25.3111

    M3 - Article

    VL - 103

    JO - Circulation

    JF - Circulation

    SN - 0009-7322

    IS - 25

    ER -