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J Thorac Cardiovasc Surg 1997;114:1088-1096
© 1997 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

ISCHEMIC AND REPERFUSION INJURY OF CYANOTIC MYOCARDIUM IN CHRONIC HYPOXIC RAT MODEL: CHANGES IN CYANOTIC MYOCARDIAL ANTIOXIDANT SYSTEM

Received for publication March 11, 1997 Revisions requested May 15, 1997 Revisions received June 19, 1997 Accepted for publication June 25, 1997 Address for reprints: Koji Nakanishi, MD, Department of Cardiovascular Surgery, Okayama University Medical School, 2-5-1 Shikata-cho, Okayama 700, Japan.

Abstract

Objective: The objective was to evaluate the effect of left ventricular function on cyanotic myocardium after ischemia-reperfusion and to determine the effect of cyanosis on the myocardial antioxidant system. Methods: Cyanotic hearts (cyanotic group) were obtained from rats housed in a hypoxic chamber (10% oxygen) for 2 weeks and control hearts (control group) from rats maintained in ambient air. Isolated, crystalloid perfused working hearts were subjected to 15 minutes of global normothermic ischemia and 20 minutes of reperfusion, and functional recovery was evaluated in the two groups. Myocardial superoxide dismutase, glutathione peroxidase, glutathione reductase activity, and reduced glutathione content were measured separately in the cytoplasm and mitochondria at the end of the preischemic, ischemic, and reperfusion periods. Results: Mean cardiac output/left ventricular weight was not significantly different between the two groups. Percent recovery of cardiac output was significantly lower in the cyanotic group than in the control group (56.1% ± 5.7% vs 73.0% ± 3.1%, p = 0.001). Mitochondrial superoxide dismutase, mitochondrial and cytosolic glutathione reductase activity, and cytosolic reduced glutathione were significantly lower in the cyanotic group than in the control group at end-ischemia (superoxide dismutase, 3.7 ± 1.3 vs 5.9 ± 1.5 units/mg protein, p = 0.012; mitochondrial glutathione reductase, 43.7 ± 14.0 vs 71.0 ± 30.3 munits/mg protein, p = 0.039; cytosolic glutathione reductase, 13.7 ± 2.0 vs 23.2 ± 4.2 munits/mg protein, p < 0.001; and reduced glutathione, 0.69 ± 0.10 vs 0.91 ± 0.24 µg/mg protein, p = 0.037). Conclusions: Cyanosis impairs postischemic functional recovery and depresses myocardial antioxidant reserve during ischemia. Reduced antioxidant reserve at end-ischemia may result in impaired postischemic functional recovery of cyanotic myocardium.

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