쥐의 심장에서 허혈성 후처치는 아편유사물질 수용체의 활성화에 의해서 사립체 투과 전이공 개방을 억제한다. (Ischemic Postconditioning Inhibits Mitochondrial Permeability Transition Pore via Opioid Receptor Activation in Intact Rat Heart)

서지정보

· 발행기관 : 대한마취통증의학회
· 수록지 정보 : Korean Journal of Anesthesiology / 54권 / 3호 / 320 ~ 327페이지
· 저자명 : 이용철, 장영호, 김진모, 김애라, 이성룡, 김윤년, 홍지희

초록

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 δ-opioid receptor antagonist), SB216763 (a glycogen synthase kinase 3β inhibitor, GSK-3β 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 δ-opioid receptor activation.GSK-3β is a downstream mediator of opioid receptors and an upstream mediator of mPTP opening in Post-C.

영어초록

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 δ-opioid receptor antagonist), SB216763 (a glycogen synthase kinase 3β inhibitor, GSK-3β 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 δ-opioid receptor activation.GSK-3β is a downstream mediator of opioid receptors and an upstream mediator of mPTP opening in Post-C.

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