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  • Title: [Clinical study of blood cardioplegia--for aerobic metabolism during aortic cross-clamping].
    Author: Okamura Y.
    Journal: Nihon Kyobu Geka Gakkai Zasshi; 1989 Feb; 37(2):287-96. PubMed ID: 2768907.
    Abstract:
    Blood cardioplegia is considered to be superior in oxygenating potential, buffering potential, oncotic, and other physiologic effects. In clinical cases, however, it is unproven whether aerobic metabolism can be obtained by using blood cardioplegia during aortic cross-clamping. Aerobic metabolism during aortic cross-clamping was therefore evaluated in patients with valvular heart disease who underwent relatively long periods of ischemic arrest. Myocardial metabolism of oxygen, lactate and pyruvate was studied in 14 patients under 126 +/- 41.2 min of cardiac arrest, and intramyocardial carbon dioxide tension (PmCO2) was also monitored continuously in 23 patients who received 121 +/- 29.8 min of aortic cross-clamping. After aortic cross-clamping, 4 degrees C St. Thomas solution was infused for immediate cooling, followed by blood cardioplegia for replenishment every 20-25 min. Blood cardioplegia and myocardial temperature were maintained within 15-20 degrees C by using an automatic cardiac hypothermia control system. Myocardial oxygen extraction during the pre-ischemic period was 26.8 +/- 13.3%. At 15 and 30 min after reperfusion, it was 30.0 +/- 10.8% and 33.8 +/- 8.2%, respectively. During ischemic arrest, myocardial oxygen extraction decreased, but the infusion of blood cardioplegia kept it above 14.0 +/- 9.3% at all times. As for lactate metabolism, although some cases showed lactate production even before the aortic cross-clamping, lactate extraction was attained in some cases during blood cardioplegia perfusion. Changes in excess lactate and redox potential of lactate and pyruvate (delta Eh) showed that aerobic metabolism could be obtained in 13/32 (41%) infusions of blood cardioplegia. PmCO2 at the aortic cross-clamp was 47.0 +/- 27.7 mmHg, and gradually rose during the ischemic arrest, but only as far as 68.4 +/- 64.8 mmHg at the time of cross-clamp release. PmCO2 decreased with each infusion of blood cardioplegia, and the decrease lasted up to 10 minutes. Though PmCO2 began to rise thereafter, the effect of blood cardioplegia continued as long as 20-25 min after the infusion. In conclusion, blood cardioplegia provides aerobic metabolism during aortic cross-clamping even in clinical setting, provided that cardiac hypothermia and delivery of cardioplegic solution are maintained appropriately.
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