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

The sulfonylurea glibenclamide (Glib) abolishes the cardioprotective effect of ischemic preconditioning (IP), presumably by inhibiting mitochondrial K(ATP) channel opening in myocytes. Glimepiride (Glim) is a new sulfonylurea reported to affect nonpancreatic K(ATP) channels less than does Glib. We e...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 2001-06, Vol.103 (25), p.3111-3116
Main Authors: MOCANU, Mihaela M, MADDOCK, Helen L, BAXTER, Gary F, LAWRENCE, Christina L, STANDEN, Nicholas B, YELLON, Derek M
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Cardiology. Vascular system
Coronary heart disease
Diazoxide - pharmacology
Glyburide - pharmacology
Guanosine Triphosphate - pharmacology
Heart
Heart - drug effects
Heart - physiopathology
Heart Ventricles - cytology
Heart Ventricles - drug effects
Hemodynamics - drug effects
Hypoglycemic Agents - pharmacology
In Vitro Techniques
Intracellular Membranes - drug effects
Intracellular Membranes - physiology
Ischemic Preconditioning, Myocardial
Male
Medical sciences
Membrane Potentials - drug effects
Membrane Proteins - drug effects
Mitochondria, Heart - drug effects
Mitochondria, Heart - physiology
Myocardial Infarction - etiology
Myocardial Infarction - pathology
Myocardial Infarction - prevention & control
Myocardial Ischemia - complications
Myocardial Ischemia - prevention & control
Patch-Clamp Techniques
Potassium Channels
Rats
Rats, Sprague-Dawley
Sulfonylurea Compounds - pharmacology
Ventricular Function
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Summary:The sulfonylurea glibenclamide (Glib) abolishes the cardioprotective effect of ischemic preconditioning (IP), presumably by inhibiting mitochondrial K(ATP) channel opening in myocytes. Glimepiride (Glim) is a new sulfonylurea reported to affect nonpancreatic K(ATP) 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 K(ATP) channels. 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 micromol/L Diaz, (4) 10 micromol/L Glim, (5) 10 micromol/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
ISSN:0009-7322
1524-4539
DOI:10.1161/01.CIR.103.25.3111