EFFECTS OF COLD AND WARM BLOOD CARDIOPLEGIA ASSESSED BY MYOCARDIAL PHAND RELEASE OF METABOLIC MARKERS

The optimal temperature of blood cardioplegia remains controversial. I nterstitial myocardial pH was monitored online with a probe that was i nserted in the anterior wall of the left ventricle. Venous pH, lactate production, and creatine kinase and troponin T release were measured in coronary sinus blood obtained in 14 dogs after ischemic arrest peri ods of 5, 10, 20, and 40 minutes with warm (n = 7; mean myocardial tem perature, 35 degrees +/- 2 degrees C) and cold (n = 7; mean myocardial temperature, 12 degrees +/- 1 degrees C) blood cardioplegic protectio n. Blood cardioplegic solution was delivered at a rate of 100 mL/min d uring the 10 minutes between each ischemic arrest. The interstitial my ocardial pH decreased significantly (p < 0.05) from 7.1 +/- 0.3 to 6.5 3 +/- 0.3 after ischemia in animals perfused with warm blood cardiople gia and from 7.04 +/- 0.3 to 6.64 +/- 0.1 in those receiving cold bloo d cardioplegic protection; however, the difference between the groups was not significant (p > 0.05). Lactate production and creatine kinase and troponin T release increased significantly after ischemia, but th ere was no difference in the changes between the warm and cold blood c ardioplegia groups. In conclusion, ischemia caused significant changes in all variables measured, and these changes were directly proportion al to the duration of ischemia. However, there was no significant diff erence (p > 0.05) in the myocardial metabolic changes between the warm and cold blood cardioplegia groups in terms of the duration of ischem ic arrest studied. Thus, both warm and cold blood cardioplegia appear to confer a similar degree of myocardial protection, with similar meta bolic changes occurring after short periods of ischemic arrest.