Effect of Preconditioning on Reperfusion Arrhythmia

Although recent investigations have disclosed that preconditioning limits myocardial infarct size by activating adenosine receptors, it remains unclear how preconditioning modifies reper- fusion arrhythmias. The present study assessed effects of preconditioning on lethal reperfusion ar- rhythmia and examined possible roles of adenosine A? receptor activation, prostanoid production and bradykinin receptor activation in the cardioprotective effect of preconditioning. In an anesthetized open chest rat preparation, reperfusion arrhythmia was induced by 5 min of coronary occlusion and reperfusion with or without preconditioning by 2 min ischemia/5 min reperfusion. Prior to the coro- nary occlusion, rats were given no pharmacological agents, 8-phenyltheophylline (8-PT, lO mg/kg), pertussis toxin (20/μg/kg), aspirin-DL-lysin (18 mg/kg), or Hoe 140 (20 nmol/kg), a bradykinin receptor antagonist. The benefit of 8 PT, pertussis toxin, and Hoe140 was confirmed by the responses to exogenous administration of adenosine, acetylcholine, and bradykinin, respectively. The dose of aspirin-DL-lysin was shown to suppress thromboxane B? production of whole blood ex vivo by more than 90%. The incidence of ventricular tachycardia (VT) or ventricular fibrillation (VF) during reperfusion was 100% in the untreated control rats. However, in the preconditioned rats which were given no drug before the preconditioning, VT was observed in only 30% of subjects and no VF was induced (p