A P-31-NUCLEAR MAGNETIC-RESONANCE STUDY OF INTERMITTENT WARM BLOOD CARDIOPLEGIA

This study was designed to assess the effects of intermittent warm blo od cardioplegia on myocardial energy metabolites, intracellular pH, an d contractile function, The isolated blood-perfused pig hearts were di vided into three groups, After 30 minutes of control perfusion, the he arts in group 1 (n = 10) received 90 minutes of continuous warm (37 de grees C) blood cardioplegia; the hearts in group 2 (n = 9) received si x 5-minute periods of warm blood cardioplegia, interrupted by six 10-m inute episodes of ischemia (37 degrees C), The hearts were then reperf used for 30 minutes. The hearts in group 3 underwent 150 minutes of co ntrol perfusion without cardioplegia or ischemic episodes, Phosphorus 31-nuclear magnetic resonance spectra showed that a 10-minute interrup tion of warm blood cardioplegia decreased phosphocreatine levels and i ntracellular pH by approximately 47% (p < 0.01) and 0.12 unit (p < 0.0 5), respectively, and increased inorganic phosphate levels by approxim ately 87%, whereas resumption of cardioplegia for 5 minutes resulted i n almost 100% recovery of phosphocreatine and inorganic phosphate leve ls and intracellular pH, More important, subsequent interruptions did not result in any cumulative changes in phosphocreatine level, inorgan ic phosphate level, or intracellular pH beyond those changes observed after the initial cardioplegic interruption, Moreover, during reperfus ion there were no significant differences in adenosine triphosphate an d phosphocreatine levels among the three groups of hearts, Furthermore , hearts from groups 1 and 2 showed comparable recovery of contractile function. These results indicate that six 10-minute interruptions and six 5-minute restorations of warm blood cardioplegia caused only mild and reversible changes in myocardial energy metabolites and intracell ular pH and these changes were not cumulative. This study suggests tha t antegrade intermittent warm blood cardioplegia may provide as much m yocardial protection as does antegrade continuous warm blood cardiople gia in the normal heart.