It was found that intravenous administration of σ-receptor agonists (+)-SKF 10047 and (+)-bremazocine or κ2-agonist (-)-bremazocine resulted in increased tolerance of isolated perfused rat heart to ischemic and reperfusion damages. Both κ2- and σ-receptor stimulation prevented the development of reperfusion contracture, increased left ventricular developed pressure, the double product, +dP/dt and -dP/dt. Only σ-receptor agonists (d-SKF 10047 and d-bremazocine) prevented arrhythmias caused by reoxygenation. By contrast, only κ2-agonist (-)-bremazocine prevented development of reperfusion no-reflow phenomenon in vitro and increased tolerance of the heart to arrhythmogenic action of epinephrine in vivo. Of the three compounds tested, only (+)-SKF 10047 abolished reoxygenation cell membrane injuries. Thus activation of cardiac σ- and κ2-receptors might be useful for prevention of myocardial stunning. Stimulation of σ- and κ2-receptors can be used for protection of the heart against arrhythmogenic action of reperfusion and adrenergic agents, respectively. κ2-receptor agonists can be used for prevention of no-reflow phenomenon and σ-receptor agonist (+)-SKF 10047 -for protection against cardiac sarcolemma injury.
|Number of pages||7|
|Publication status||Published - 2001|
- Myocardial reperfusion
- Opioid receptors
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine