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刺激κ-阿片受体诱导的延迟性心肌保护作用 被引量:1

κ-Opioid Receptor Stimulation Induced Delayed Cardioprotection
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摘要 本研究利用-κ阿片受体激动剂U50488H预处理(U50488Hpretreatment,UP)大鼠,在离体Langendorff灌流心脏和缺血/复灌模型上观察-κ阿片受体激动剂诱发的延迟性心肌保护作用,研究结果表明U50488H预处理大鼠24h后,可明显改善心肌缺血后的复灌期内LVEDP的抬高,以及LVDP和±dP/dtmax的下降(P<0.05);其作用可被κ阿片受体选择性拮抗剂Nor-binaltorphimine(nor-BNI)所阻断。结论:刺激-κ阿片受体诱导了延迟性心肌保护作用。 The aim of the present studies was to determine whether U50488H, a specific K-opioid receptor agonist, could induce dalayed cardioprotecfion against myocardical ischemia / reperfusion injury and to explore the underlying mechanisms. Isolated perfused rat hearts were subjected to 30 rain of ischemia followed by 120 rain reperfusion. Left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (LVDP) and maximal velocity of contraction and relaxation (±dP/dtmx) were improved when U50488H was administered 24h before ischemia (P〈0.05). In conclusion, K-opioid receptor stimulation could induce delayed cardioprotection against myocardial ischemia and reperfusion.
出处 《金华职业技术学院学报》 2006年第3期76-79,共4页 Journal of Jinhua Polytechnic
关键词 K-阿片受体 心肌缺血 复灌 K-opioid receptor , myocardial ischemia reperfusion
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  • 1Ryan M. Fryer,Anna K. Hsu,Yigang Wang,Michele Henry,Janis Eells,Garrett J. Gross. PKC-δ inhibition does not block preconditioning-induced preservation in mitochondrial ATP synthesis and infarct size reduction in rats[J] 2002,Basic Research in Cardiology(1):47~54
  • 2Takayuki Miki,Michael V. Cohen,James M. Downey. Opioid receptor contributes to ischemic preconditioning through protein kinase C activation in rabbits[J] 1998,Molecular and Cellular Biochemistry(1-2):3~12

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