In vivo pretreatment with selective μ-opioid receptor agonist DAMCO (0.1 mg/kg intravenously 15 min before heart isolation) increased tolerance of the isolated perfused rat heart to ischemic (45 min) and reperfusion (60 min) damages in vitro. This prior stimulation of μ-opioid receptors led to significant improvement of postreperfusion contractile function, significant prevention of reoxygenation destruction of cardiac cells and a decrease in the incidence of reperfusion arrhythmias. All these cardioprotective effects of μ-receptor activation were completely eliminated by pretreatment with the opioid receptor antagonist naloxone (0.1 mg/kg intravenously 10 min before DAMGO injection) or by pretreatment with the KATP-channel blocker glibenclamide (0.3 mg/kg intravenously 30 min before DAMGO injection). It is concluded that μ-opioid receptor activation can be an approach to prevent ischemic/reperfusion damage of the heart. Cardioprotective effects of μ-receptor activation can be mediated via KATP-channels.
|Состояние||Опубликовано - 2001|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine