title: A 31P-nuclear magnetic resonance study of intermittent warm blood cardioplegia.
abstract: This study was designed to assess the effects of intermittent warm blood cardioplegia on myocardial energy metabolites, intracellular pH, and contractile function. The isolated blood-perfused pig hearts were divided into three groups. After 30 minutes of control perfusion, the hearts in group 1 (n = 10) received 90 minutes of continuous warm (37 degrees C) blood cardioplegia; the hearts in group 2 (n = 9) received six 5-minute periods of warm blood cardioplegia, interrupted by six 10-minute episodes of ischemia (37 degrees C). The hearts were then reperfused for 30 minutes. The hearts in group 3 underwent 150 minutes of control perfusion without cardioplegia or ischemic episodes. Phosphorus 31-nuclear magnetic resonance spectra showed that a 10-minute interruption of warm blood cardioplegia decreased phosphocreatine levels and intracellular pH by approximately 47% (p < 0.01) and 0.12 unit (p < 0.05), respectively, and increased inorganic phosphate levels by approximately 87%, whereas resumption of cardioplegia for 5 minutes resulted in almost 100% recovery of phosphocreatine and inorganic phosphate levels and intracellular pH. More important, subsequent interruptions did not result in any cumulative changes in phosphocreatine level, inorganic phosphate level, or intracellular pH beyond those changes observed after the initial cardioplegic interruption. Moreover, during reperfusion there were no significant differences in adenosine triphosphate and 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 intracellular pH and these changes were not cumulative. This study suggests that antegrade intermittent warm blood cardioplegia may provide as much myocardial protection as does antegrade continuous warm blood cardioplegia in the normal heart.
authors.affiliation: Institute for Biodiagnostics, National Research Council Canada, Winnipeg, Manitoba.
authors.forename: G
authors.initials: G
authors.lastname: Tian
authors.forename: B
authors.initials: B
authors.lastname: Xiang
authors.forename: K W
authors.initials: KW
authors.lastname: Butler
authors.forename: A M
authors.initials: AM
authors.lastname: Calafiore
authors.forename: A
authors.initials: A
authors.lastname: Mezzetti
authors.forename: T A
authors.initials: TA
authors.lastname: Salerno
authors.forename: R
authors.initials: R
authors.lastname: Deslauriers
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001769:Blood; D002314:Cardioplegic Solutions; D006324:Heart Arrest, Induced / Q000379:methods*; D006863:Hydrogen-Ion Concentration; D009682:Magnetic Resonance Spectroscopy; D009200:Myocardial Contraction / Q000502:physiology; D015425:Myocardial Reperfusion / Q000379:methods; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism*; D010710:Phosphates / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism; D013552:Swine; D013997:Time Factors
chemical_list: D002314:Cardioplegic Solutions; D010710:Phosphates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate