Norepinephrine-Induced Delayed Cardioprotection against Stunning is at the Expense of a Higher Postishemic Arrhythmia Rate

Objective α 1 -adrenoceptor activation confers myocardial protection from ischemic injury. We tested whether norepinephrine mediates delayed cardioprotection against stunning and whether this alters postischemic arrhythmias. Methods New Zealand White rabbits were assigned to three groups: Control-group ( n = 7): no drugs. Norepinephrine-group ( n = 7): 75 μg norepinephrine/kg bodyweight (bw). Norepinephrine/prazosin-group ( n = 7):75 μg norepinephrine and 15 μg prazosin/kg bw. After 24 h, hearts were excised, perfused with buffer and subjected to 20 min of ischemia followed by 120 min of reperfusion. Results (a) Developed pressures (dP) ( P syst – P diast ) at the end of reperfusion: C: 51.2 ± 5.0%, NE: 71.7 ± 5.1% ( p < 0.05 vs. C), NEP: 50.7 ± 5.0%. (b) Ventricular extra beats (vebs) were detected throughout the experiments. C: 0.41 ± 0.15 vebs/min, NE: 1.06 ± 0.18 vebs/min ( p < 0.05 vs. C), NEP: 1.17 ± 0.3 vebs/min. Conclusion Norepinephrine confers delayed preconditioning against myocardial stunning via an α 1 -adrenoceptor mediated pathway. Norepinephrine-mediated preconditioning involves a beneficial effect towards stunning, but at the expense of a higher rate of postischemic ventricular arrhythmia.