Abstract

Despite the widespread use of ventricular tissue in the investigation involving hydroxyl radical Aim: (OH*) injury, one of the most potent mediators in ischemia-reperfusion injury, little is known about the impact on atrial myocardium. In this study we thus compared the OH*-induced injury response between atrial and right ventricular muscles from both rabbits and dogs under identical experimental conditions. Methods: Small, contracting ventricular and atrial rabbit and dog trabeculae were directly exposed to OH*, and contractile properties were examined and quantified. Results: A brief OH* exposure led to transient rigor like contracture with marked elevation of diastolic tension and depression of developed force. Although the injury response showed similarities between atrial and ventricular myocardium, there were significant differences as well. In rabbit atrial muscles, the development of the contracture and its peak was much faster as compared to ventricular muscles. Also, at the peak of contracture, both rabbit and dog atrial muscles show a lesser degree of contractile dysfunction. Conclusion:These results indicate that both atrial and ventricular muscles develop a rigor-like contracture after acute OH*-induced injury, and atrial muscles showed a lesser degree of contractile dysfunction. Comparison of dog versus rabbit tissue shows that the response was similar in magnitude, but slower to develop in dog tissue.

Highlights

  • Ischemic heart disease is one of the leading causes of death in developed countries

  • The results of this study show that direct acute exposure of OH* to clinically relevant levels of reperfusion injury leads to a transient rigor like contracture in both atrial and ventricular myocardium

  • The development of the injury contracture occurred much faster compared to the response in ventricular muscles

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Summary

Introduction

Ischemic heart disease is one of the leading causes of death in developed countries. Timely and effective reperfusion is one of the treatment strategies for limiting the size of the infarct. Reperfusion injury is a serious pathological process that is induced by the restoration of blood flow to previously ischemic tissue. When ischemic myocardium is reperfused, and oxygen reintroduced, there is a sudden burst of oxygen free radical production. Of these oxygen free radicals, the hydroxyl radical (OH*) is one of the most aggressive species, and is involved in the pathogenesis of ischemia-reperfusion injury (IR injury). IR injury is observed in many clinical situations including acute heart failure, stroke, and myocardial infarction (Gao et al, 1996; Zeitz et al, 2002). There is abundant information available regarding the ventricular myocardial response to OH*, but little is known about the contractile response of atrial myocardium to OH*-induced injury

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