Degradation of myocardial high-energy phosphates during twenty-four hours of cold storage. Effects of cardioplegic versus noncardioplegic arrest.
Purine nucleotide catabolism was examined during 24 hours of cold (0.5 degree C) storage of human transplant recipient hearts, baboon hearts, and dog hearts. The hearts were excised either after cold hyperkalemic cardioplegic arrest or after simple hypothermic arrest (25 degrees C). In human myocardium, hypothermia alone preserved the adenosine triphosphate pool markedly. Even after 24 hours of cold storage, adenosine triphosphate was still 9.5 +/- 2.5 mumol/gm dry weight (58% of the preischemic value). The major fraction of catabolites remained nucleotides: adenosine triphosphate plus adenosine diphosphate plus adenosine monophosphate decreased only from 99% +/- 1% (preischemic value) to 80% +/- 13% of the total purine content. The remaining catabolites were mainly nucleosides (adenosine 0.2% +/- 0.1% and inosine 19% +/- 13% of the total purine content). Cardioplegic arrest before cold storage did not change the pattern of purine nucleotide catabolism in any respect (p greater than 0.05). In baboon myocardium, hypothermia alone preserved the adenosine triphosphate content somewhat less than in human myocardium. Adenosine triphosphate content after 24 hours was 5.2 +/- 1.6 mumol/gm dry weight (40% of the preischemic value). The catabolism of adenosine triphosphate, however, did not proceed far beyond the level of adenosine monophosphate, so that the sum of nucleotides remained the same as in human hearts. Adenosine was 0.2% +/- 0.3% and inosine 17% +/- 4% of the total sum of purines. Also in the baboon heart, cardioplegia did not influence the pattern of catabolism significantly (p greater than 0.05). In the dog myocardium, hypothermia alone did not protect against severe catabolism of adenosine triphosphate. The adenosine triphosphate content at 24 hours of storage was 3.5 +/- 2.5 mumol/g dry weight (25% of the preischemic value). Catabolism of adenosine triphosphate proceeded far beyond the level of the nucleotides (63% +/- 17% of the total sum of purines), resulting in an accumulation of adenosine and inosine (5% +/- 4% and 30% +/- 13% of the total sum of purines) and even of hypoxanthine (1% +/- 1% of the total sum of purines). In the dog heart cardioplegic arrest inhibited adenosine triphosphate catabolism considerably. Adenosine triphosphate content at 24 hours was 8.1 +/- 1.8 mumol/gm dry weight (56% of the preischemic value); 83% +/- 5% of the total purine content remained present as nucleotides, and the nucleoside content was reduced to 2% +/- 3% for adenosine and 11% +/- 6% for inosine.(ABSTRACT TRUNCATED AT 400 WORDS)
Masuda
M
M
Laboratory of Experimental Cardiac Surgery, Katholieke Universiteit Leuven, Belgium.
Sukehiro
S
S
Möllhoff
T
T
Lu
H R
HR
Van Belle
H
H
Flameng
W
W
D000227:Adenine Nucleotides / Q000378:metabolism*; D000818:Animals; D002314:Cardioplegic Solutions; D004285:Dogs; D004734:Energy Metabolism; D006324:Heart Arrest, Induced / Q000379:methods*; D016027:Heart Transplantation; D006801:Humans; D007036:Hypothermia, Induced; D009206:Myocardium / Q000378:metabolism*; D009926:Organ Preservation / Q000379:methods*; D010215:Papio; D013997:Time Factors
D000227:Adenine Nucleotides; D002314:Cardioplegic Solutions