A highly selective ATP-dependent potassium channel opener mimics ischaemic preconditioning protection in isolated human atrium.
MED SCI RES
651 - 654.
The K-ATP channel has been implicated in the mechanism of ischaemic preconditioning. We examined the effects of EMS 191095, a highly selective K-ATP channel opener, either alone or with glibenclamide (K-ATP channel blocker), on human atrium. Isolated human atrial trabecula superfused with oxygenated Tyrode's solution and paced at I Hz underwent one of four protocols prior to 90 min hypoxic substrate-free perfusion at 3 Hz (simulated ischaemia), followed by 120 min of reoxygenation with substrate at I Hz (reoxygenation). Preconditioning (PC) consisted of 3 min simulated ischaemia and 7 min reoxygenation. The experimental endpoint was recovery of contractile function, presented as percentage of baseline function. EMS (45.8% +/- 4.4) and PC (50.5% +/- 3.6) produced similar functional recoveries following 120 min reperfusion; significantly different to controls (20.8% +/- 3.5, p<0.05, ANOVA). Glibenclamide abolished the EMS protection (20.8% +/- 4.2). This results suggest that ischaemic preconditioning in humans may occur via a K-ATP channel opening effect.
|Title:||A highly selective ATP-dependent potassium channel opener mimics ischaemic preconditioning protection in isolated human atrium|
|Keywords:||K-ATP channel, myocardium, ischaemic preconditioning, atrium, IN-VITRO MODEL, INFARCT SIZE, CORONARY ANGIOPLASTY, K+ CHANNEL, RAT-HEART, ISCHEMIA, GLIBENCLAMIDE, MYOCARDIUM, BLOCKADE, LIMITATION|
|UCL classification:||UCL > School of Life and Medical Sciences > Faculty of Population Health Sciences > Institute of Cardiovascular Science|
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