Pii: S1010-7940(02)00729-7

Objective: Animal myocardial dysfunction induced by remote ischemia-reperfusion (IR) was shown to be partly accomplished via a direct effect of the pro-oxidant xanthine oxidase (XO). This direct remote effect was not tested in humans. We now assessed the performance of human auricles in the presence of solutions containing XO and/or allopurinol and compared them to those of rat myocardial strips. Methods: Human and rat specimens ðn 1⁄4 64Þ were separately exposed for 2 h to Krebs–Henseleit solution that either (1) exited from rat livers that were earlier perfused for 2 h (control-human or control-rat), (2) exited from livers that were earlier made ischemic for 2 h (IR-human, IR-rat), (3) contained xanthine (X) 3.8 mM 1 XO 3 mU ml (X 1 XO-human, X 1 XO-rat), or (4) exited from post 2 h-ischemic livers and contained 100 mM allopurinol (human or rat IR 1 allopurinol groups). Results: Unlike the unchanged electromechanical performance in the control and IR 1 allopurinol auricles and strips, the rates of contraction, maximal force of contraction and working index of either preparation were reduced by 75–98% (P , 0:01) when exposed to the IR reperfusate or to the X 1 XO-enriched Krebs. The basal amplitudes of contraction in these four latter groups increased twofold ðP , 0:01Þ. XO activity was similarly low in the control and in the IR 1 allopurinol groups, but fourto 45-fold ðP , 0:001Þ higher in the IR and the X 1 XO groups, both in the rat and human organs. The reduced glutathione was reduced by ,50% ðP , 0:01Þ in either preparation in the IR and the X 1 XO groups compared to the control and IR 1 allopurinol groups. Conclusions: Remotely and exogenously originated oxidative burst directly induces electromechanical dysfunction and disrupts oxidant/ antioxidant balance in human auricles as it does in the rat myocardial strip. q 2002 Elsevier Science B.V. All rights reserved.