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Ann Thorac Surg 1995;59:428-432
© 1995 The Society of Thoracic Surgeons

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Articles

Hypoxic preconditioning enhances functional recovery after prolonged cardioplegic arrest

Department of Surgery, University of Connecticut School of Medicine, Farmington, Connecticut, USA

Accepted for publication October 5, 1994.

^* Address reprint requests to Dr Daniel T. Engelman, Surgical Research Center, University of Connecticut School of Medicine, 263 Farmington Ave, Farmington, CT 06030-1110.

The purpose of this study was to assess the ability of hypoxic preconditioning to improve myocardial salvage after prolonged hypothermic cardioplegic arrest. Isolated working rat hearts were arrested at 4°C with St. Thomas' Hospital cardioplegic solution and immersion stored for 4 or 6 hours. Two groups were studied, control and hypoxically preconditioned (HP) hearts. After 4 hours' preservation, aortic flow, coronary flow, and the first derivative of aortic pressure were 8.7 ± 1.6 mL/min, 17.8 ± 1.6 mL/min, and 2,064 ± 123 mm Hg/s, respectively, in control hearts (n = 11) and 25.7 ± 2.5 mL/min, 27.1 ± 2.5 mL/min, and 2,655 ± 93 mm Hg/s, respectively, in HP hearts (n = 11) (p < 0.05). After 6 hours' preservation, aortic flow, coronary flow, and the first derivative of aortic pressure were 3.5 ± 1.2 mL/min, 18.8 ± 0.4 mL/min, and 1,622 ± 226 mm Hg/s, respectively, in control hearts (n = 6) and 21.5 ± 3.2 mL/min, 25.5 ± 2.3 mL/min, and 2,439 ± 239 mm Hg/s, respectively, in HP hearts (n = 6) (p < 0.05). After 6 hours' preservation, adenine nucleotides and creatine phosphate levels were not significantly different between the two groups, but lactate dehydrogenase release was significantly increased (p < 0.05) in control versus HP hearts (4.66 ± 0.58 IU/L versus 1.98 ± 0.28 IU/L). We conclude that hypoxic preconditioning reduces cellular necrosis and preserves myocardial function after prolonged hypothermic cardioplegic arrest.

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