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Eur J Cardiothorac Surg 2003;23:66-73
© 2003 Elsevier Science NL

Electromechanical impairment of human auricle and rat myocardial strip subjected to exogenous oxidative stress

^a Departments of Anesthesiology and Critical Care, Tel Aviv Sourasky Medical Center and the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
^b Department of Cardiothoracic Surgery, Tel Aviv Sourasky Medical Center and the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
^c Department of Pathology, Tel Aviv Sourasky Medical Center and the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv Israel
^d Department of Cardiology, Tel Aviv Sourasky Medical Center and the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
^e Department of Post-Anesthesia Care and Animal Research Laboratory, Tel Aviv Sourasky Medical Center and the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel

Received 24 March 2002; received in revised form 2 October 2002; accepted 21 October 2002.

* Corresponding author. Tel.: +972-3-697-3237; fax: +972-3-692-5749
e-mail: draviw{at}tasmc.health.gov.il

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 (n=64) 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 µM+XO 3 mU ml^-1 (X+XO-human, X+XO-rat), or (4) exited from post 2 h-ischemic livers and contained 100 µM allopurinol (human or rat IR+allopurinol groups). Results: Unlike the unchanged electromechanical performance in the control and IR+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+XO-enriched Krebs. The basal amplitudes of contraction in these four latter groups increased twofold (P<0.01). XO activity was similarly low in the control and in the IR+allopurinol groups, but four- to 45-fold (P<0.001) higher in the IR and the X+XO groups, both in the rat and human organs. The reduced glutathione was reduced by 50% (P<0.01) in either preparation in the IR and the X+XO groups compared to the control and IR+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.

Key Words: Auricle • Human • Rat • Myocardium • Reperfusion • Injury

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