title: Moderate glucose deprivation preconditions myocardium against infarction.
abstract: Glucose-free perfusion preconditions myocardium against the consequences of subsequent ischemia. We investigated whether mitochondrial ATP-sensitive potassium (mK (ATP)) channels are involved in preconditioning by glucose deprivation, and whether moderate glucose deprivation also preconditions myocardium. Isolated rat hearts underwent 30 min of no-flow ischemia followed by 1 h reperfusion. Controls were not further treated. Three groups were preconditioned by perfusion with 0, 40 or 80 mg/dl (0, 2.22, 4.44 mmol/l) glucose (correction of osmotic pressure by addition of urea) for 10 min followed by 10 min perfusion with normal buffer (150 mg/dl, or 8.33 mmol/l glucose) before the ischemia reperfusion protocol. In one group, 100 micromol/l of the mK (ATP) channel blocker 5-HD was added to the glucose-free perfusate. Two groups were treated with 5-HD or urea before ischemia without preconditioning. Left ventricular developed pressure and maximum ischemic contracture (82 +/- 21 mmHg) were similar in all groups. Mean left ventricular developed pressure was 100 +/- 16 mm Hg under baseline conditions, and poorly recovered to 8 +/- 11 mm Hg during reperfusion. Preconditioning with 0 and 40 mg/dl glucose containing buffer reduced infarct size from 41 +/- 10% (control) to 23 +/- 12% (p = 0.02) and 26 +/- 8% (p = 0.011). The 5-HD blocked preconditioning by glucose deprivation (38 +/- 9%, p = 0.04) while 80 mg/dl glucose, 5-HD and urea had no effect on infarct size (39 +/- 9%; 38 +/- 13%; 37 +/- 8%; p = 1.0 each). We conclude that transient severe glucose deprivation and moderate glucose deprivation preconditions the isolated rat heart. Preconditioning by complete glucose deprivation depends on the opening of mK (ATP) channels.
authors.affiliation: Klinik für Anästhesiologie, Universitätsklinikum Düsseldorf, Düsseldorf, Germany. ebeld@uni-duesseldorf.de
authors.forename: D
authors.initials: D
authors.lastname: Ebel
authors.forename: S
authors.initials: S
authors.lastname: Redler
authors.forename: B
authors.initials: B
authors.lastname: Preckel
authors.forename: W
authors.initials: W
authors.lastname: Schlack
authors.forename: V
authors.initials: V
authors.lastname: Thämer
mesh_terms: D000818:Animals; D005947:Glucose / Q000494:pharmacology*; D009203:Myocardial Infarction / Q000378:metabolism*; D015425:Myocardial Reperfusion / Q000379:methods; D015428:Myocardial Reperfusion Injury / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D009924:Organ Culture Techniques; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000378:metabolism*; D051381:Rats; D014508:Urea / Q000494:pharmacology
chemical_list: D026902:Potassium Channel Blockers; D015221:Potassium Channels; D014508:Urea; D005947:Glucose