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

Hypoxic Preconditioning Enhances Functional Recovery After Prolonged Cardioplegic Arrest

Daniel T. Engelman, MD, Chang-zhi Chen, MD, Masazumi Watanabe, MD, Pankaj Kulshrestha, MD, Dipak K. Das, PhD, John A. Rousou, MD, Joseph E. Flack, III, MD, David W. Deaton, MD, Richard M. Engelman, MD

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

Accepted for publication October 5, 1994.

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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