Hypoxic preconditioning enhances functional recovery after prolonged cardioplegic arrest

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. Thomasʹ Hospital cardioplegic solution and immersion stored for 4 or 6 hours. Two groups were studied, control and hypoxically preconditioned (HP) hearts. After 4 hoursʹ 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 hoursʹ 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 hoursʹ 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.