• Journal of Chest Surgery
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• v.35 no.1
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• pp.11-19
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• 2002

Background: Ischemia-reperfusion myocardial injury is an important factor to determine the early and the late mortality of transplanted patients. Recently, modulation of the cytosolic NADH/NAD+ ratio by Pyruvate and aspartate was tested to Protect the heart from ischemia-reperfusion injury. Material and Method: We added pyruvate and aspartate to the University of Wisconsin solution, and evaluated their effect on myocardial protection. We used 16 piglet(age 1 to 3 days) hearts. Eight hearts were arrested with and stored in the University of Wisconsin solution(UW solution) for 24 hours(control group), and the other eight hearts were arrested with and stored in the modified UW solution added pyruvate(3mmol/L) and aspartate(2 mmol/L)(test group). All hearts underwent modified reperfusion with blood cardioplegic solution followed by conversion to a left-sided working model with perfusion from a support pig. And then, we measured stroke work index(SWI), high-energy phosphate stores, and myocardial water content of the hearts. SWI was calculated at left ventricular end-diastolic pressures of 3, 6, 9, and 12 mmHg after 60 and 120 minutes reperfusion, respectively, Result: At 60 minutes and 120 minutes after reperfusion, SWI was higher in the test group than in the control group significantly. The levels of AMP, ADP, ATP of the test group were also higher. But, the creatine phosphate level and myocardial water content were similar in the two groups. Conclusion: From these results, we could Prove that pyruvate and aspartate enhance cardiac contractility and high-energy phosphate stores after ischemia.

• Proceedings of the KTCVS Conference
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• 1995.10a
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• pp.19-19
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• 1995

• Journal of Chest Surgery
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• v.29 no.3
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• pp.255-262
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• 1996

The donor pool for heart transplants is severely limited and there is still a legal problem of brain death. This study assessed the function of hearts "absolute anoxic" for ten minutes after asphyxia by perfusing the hearts on a Langendorfr apparatus for 45 minutes with Krebs-Henseleit buffier at 37 t at 80 cm H2O. Forty isolated rat hearts were divided into four groups. Ten control hearts (group 1) were perfused on the circuit without intervening ischemia. Ten hearts (group 2) were harvested, quickly flushed with 5cc of cold University of Wisconsin solution, and stored in the same cold solution for 4 hours. Ten hearts (group 3) were excised, quickly flushed with 5 u of cold Stanford cardioplegic solution and stored in cold saline solution for 4 hours. Ten asphyxiated hearts (group 4) had warm ischemia for ten minutes and were perfused with 5u of cold Stanford cardioplegia containing 7,500 units of urokinase to dissolve intravascular clots, and stored in cold saline solution for 1.5 hours. Time of spontaneous defibrillation (TSD) after perfusion was significantly longer in group 2, group 3 and group 4 than in group 1. TSD in group 3 and group 4 was significantly longer in comparison to that of group 2. Left ventricular developed pressure(LVDP) at 15 minutes was significantly lower in group 3 and group 4 than in group 1 and group 2. In group 4, LVDP at 30 minutes and 45 minutes was significantly lower compared with that in group 1 . In conclusion, asphyxiated rat hear;ts which had absolute anoxia for 10 minutes after as hyxia showed relatively satisfactory cardiac function. function.