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Myocardial Damage Induced by Uncontrolled Reoxygenation

Department of Cardiovascular Surgery University Hospital of Vaud Lausanne, Switzerland 1 S Paolo Hospital, University of Milan Milan, Italy

For reprint information contact: Antonio F Corno, MD, FRCS Tel: 41 21 314 2280 Fax: 41 21 314 2278 email: antonio.corno{at}chuv.hospvd.ch University Hospital of Vaud, , Department of Cardiovascular Surgery, Rue du Bugnon 46, Lausanne CH1011, Switzerland.

To evaluate myocardial impairment induced by uncontrolled reoxygenation, the effects of hypoxia-reoxygenation were compared with ischemia-reperfusion in isolated rat hearts. After stabilization, 2 groups (n = 8) of Langendorff-perfused rat hearts were exposed to 40 minutes of ischemia (10% of baseline flow) or hypoxia (10% of baseline oxygen content) followed by a sudden return to baseline conditions (reperfusion or reoxygenation). The O₂ content was identical for the two groups during baseline conditions, O₂ shortage, and O₂ readmission. Metabolic (lactate production) and functional parameters (heart rate, peak systolic pressure, left ventricular developed pressure, maximal contraction and relaxation rates, end-diastolic pressure, coronary perfusion pressure) were recorded at the end of stabilization, after O₂ deficiency, and after 2 minutes of reoxygenation. Systolic function was significantly depressed after ischemia (p < 0.0001) but completely recovered to baseline values after 2 minutes of reperfusion. In contrast, systolic function was less severely depressed after hypoxia but failed to return to baseline after 2 minutes of reoxygenation. Diastolic function, unchanged during ischemia-reperfusion, remained significantly impaired during hypoxia-reoxygenation.

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