계명대학교 의학도서관 Repository

쥐의 심장에서 허혈성 후처치는 아편유사물질 수용체의 활성화에 의해서 사립체 투과 전이공 개방을 억제한다

Metadata Downloads
Author(s)
이용철장영호김진모김애라이성룡김윤년홍지희Yong Cheol LeeYoung Ho JangJin Mo KimAe Ra KimSeung Ryong LeeYoon Nyun KimJi Hee Hong
Keimyung Author(s)
Lee, Yong CheolJang, Young HoKim, Jin MoKim, Ae RaHong, Ji HeeLee, Seong RyongKim, Yoon Nyun
Department
Dept. of Anesthesiology & Pain Medicine (마취통증의학)
Dept. of Pharmacology (약리학)
Dept. of Internal Medicine (내과학)
Journal Title
대한마취과학회지
Issued Date
2008
Volume
54
Issue
3
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 reperfusion interspersed 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. (Korean J Anesthesiol 2008; 54: 320∼7) Key Words: ischemia, mitochondria, opioid receptor, postconditioning, reperfusion.
Alternative Title
Ischemic Postconditioning Inhibits Mitochondrial Permeability Transition Pore via Opioid Receptor Activation in
Intact Rat Heart
Keimyung Author(s)(Kor)
이용철
장영호
김진모
김애라
홍지희
이성용
김윤년
Publisher
School of Medicine
Citation
이용철 et al. (2008). 쥐의 심장에서 허혈성 후처치는 아편유사물질 수용체의 활성화에 의해서 사립체 투과 전이공 개방을 억제한다. 대한마취과학회지, 54(3), 320–327. doi: 10.4097/kjae.2008.54.3.320
Type
Article
ISSN
0302-5780
DOI
10.4097/kjae.2008.54.3.320
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/40127
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Anesthesiology & Pain Medicine (마취통증의학)
1. School of Medicine (의과대학) > Dept. of Internal Medicine (내과학)
1. School of Medicine (의과대학) > Dept. of Pharmacology (약리학)
공개 및 라이선스
  • 공개 구분공개
파일 목록

Items in Repository are protected by copyright, with all rights reserved, unless otherwise indicated.