Ischemic Postconditioning Inhibits Mitochondrial Permeability Transition Pore via Opioid Receptor Activation in Intact Rat Heart / 대한마취과학회지
Korean Journal of Anesthesiology
;
: 320-327, 2008.
Article
in Korean
| WPRIM
| ID: wpr-151688
ABSTRACT
BACKGROUND:
Ischemic postconditioning (Post-C), brief cycles of myocardial ischemia and reperfusion during the early phase of reperfusion, is considered as a novel adjunct strategy to protect myocardium.However, the exact mechanism remains unclear and should be determined.METHODS:
The hearts of male Wistar rats were subjected to 30 min ischemia and 2 hrs reperfusion.Control rats had no intervention either before or after left coronary artery occlusion.Post-C was elicited by 6 cycles of 10s reperfusioninterspersed by 10s ischemia immediately after onset of reperfusion.Subsets of postconditioning rats were treated with drugs as followings; naloxone (non-selective opioid receptor antagonist), naltrindole (a delta-opioid receptor antagonist), SB216763 (a glycogen synthase kinase 3beta inhibitor, GSK-3beta inhibitor), or atractyloside (a mitochondrial permeability transition pore opener, mPTP opener).RESULTS:
Post-C significantly reduced infarct size (15.9 +/- 2.4%, P = 0.003) compared to control (29.9 +/- 3.7%).The anti-infarct effect by Post-C was blocked by both naloxone (25.5 +/- 3.9%, P = 0.044) and naltrindole (26.9 +/- 2.3%, P = 0.022).Infarct size limiting effect by Post-C was also abolished by atractyloside (30.6 +/- 3.6%, P = 0.003).In SB216763 with naloxone treated animals, the infarct size was decreased (17.4 +/- 3.2%, P = 0.007) but not in SB216763 with atractyloside treated animals (27.4 +/- 2.6%) compared to control.CONCLUSIONS:
These data suggest that Post-C may protect myocardium by inhibiting mPTP opening via delta-opioid receptor activation.GSK-3beta is a downstream mediator of opioid receptors and an upstream mediator of mPTP opening in Post-C.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Permeability
/
Atractyloside
/
Reperfusion
/
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
/
Rats, Wistar
/
Myocardial Ischemia
/
Receptors, Opioid
/
Coronary Vessels
/
Glycogen Synthase Kinases
/
Glycogen Synthase Kinase 3
Limits:
Animals
/
Humans
/
Male
Language:
Korean
Journal:
Korean Journal of Anesthesiology
Year:
2008
Type:
Article
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