- 作者: Wei-Luen Chang; Shoei-Sheng Lee; Ming-Jai Su
- 作者服務機構: 1 Institute of Pharmacology, College of Medicine, National Taiwan University, No. 1, Sec. 1, Jen-Ai Rd, Taipei, Taiwan; ; 2 Department of pharmacy, College of Medicine, National Taiwan University, Taipei, Taiwan
- 中文摘要: --
- 英文摘要: Pretreatment with thaliporphine before ischemia affords cardioprotective effects against reperfusion injury via antioxidant activity. This study evaluated whether thaliporphine administered at a certain period after myocardial ischemia conferred the same cardioprotection and assessed its possible new mechanism. The left main coronary artery of anaesthetized rats was occluded for 1 h and then reperfused for 2 h. Thaliporphine was administered at 10 min before reperfusion. Controls received saline only. Morphine, a nonselective opioid receptor agonist, was used as reference compound at 0.3 mg/kg. Thaliporphine at 0.05 and 0.5 mg/ kg were found to reduce the infarct size. Recovery of cardiac function was higher in thaliporphine (0.5 mg/ kg) group, as assessed by a significant improvement in the rates of pressure development ( + dp/dtmax). This compound also reduced plasma creatine kinase and cardiac MPO activity. These protective effects afforded by thaliporphine were diminished by the opioid receptor antagonists (naloxone or naltrexone) and by the mitochondrial KATP blocker 5HD. In comparison, morphine reduced infarct size and MPO activity in the myocardium but produced slightly improvement in cardiac function after ischemia-reperfusion. These results demonstrate that reperfusion therapy with thaliporphine protect cardiac injury through further mechanism via activation of opioid receptor and opening of mitochondrial KATP channels as morphine but with stronger activity.
- 中文關鍵字: --
- 英文關鍵字: cardioprotection, ischemia-reperfusion, KATP channel, morphine, opioid receptor, thaliporphine