title: Mechanisms of myocardial protection by adenosine-supplemented cardioplegic solution: myofilament and metabolic responses.
abstract: OBJECTIVE
  Adenosine supplementation of cardioplegic solutions in cardiac operations improves postarrest myocardial recovery after cardioplegic arrest and reperfusion; however, the mechanism of the action of adenosine remains unknown. We tested the hypotheses that adenosine-supplemented cardioplegic solution improves myofibrillar protein cooperative interaction and increases myocardial anaerobic glycolysis.
  
  
  METHODS
  The hearts of male Sprague-Dawley rats were randomized to undergo 120 minutes of cardioplegic arrest with 1 of 3 cardioplegic solutions: (1) St Thomas' Hospital No. 2 cardioplegic solution (St Thomas group), (2) St Thomas' Hospital No. 2 cardioplegic solution plus adenosine (100 micromol/L) (adenosine group), and (3) St Thomas' Hospital No. 2 cardioplegic solution plus adenosine (100 micromol/L) plus the nonspecific adenosine receptor antagonist 8-p -sulfophenyltheophylline (50 micromol/L) (sulfophenyltheophylline group). A fourth group of hearts underwent no cardioplegic arrest.
  
  
  RESULTS
  Systolic and diastolic functional recovery was improved in the adenosine group compared with that in the other two groups, independent of coronary flow. Adenosine supplementation of cardioplegic solution prevented the decrease in myofibrillar protein cooperative interaction seen after cardioplegic arrest and reperfusion (St Thomas and sulfophenyltheophylline groups). Adenosine-supplemented cardioplegic solution also caused significantly increased anaerobic glycolysis during cardioplegic arrest. These responses were blocked in the sulfophenyltheophylline group.
  
  
  CONCLUSIONS
  The changes in myocardial glycolytic activity and myofilament cooperativity coincided with functional recovery in the three cardioplegia groups and may represent mechanisms underlying protection with adenosine-supplemented cardioplegic solution.
authors.affiliation: University of Illinois College of Medicine at Chicago, Chicago, IL 60612, USA.
authors.forename: B G
authors.initials: BG
authors.lastname: Fogelson
authors.forename: S I
authors.initials: SI
authors.lastname: Nawas
authors.forename: W R
authors.initials: WR
authors.lastname: Law
mesh_terms: D008841:Actin Cytoskeleton / Q000187:drug effects* / Q000201:enzymology; D000241:Adenosine / Q000494:pharmacology*; D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D002314:Cardioplegic Solutions / Q000494:pharmacology*; D006019:Glycolysis / Q000187:drug effects*; D006321:Heart / Q000187:drug effects*; D008297:Male; D009206:Myocardium / Q000378:metabolism* / Q000648:ultrastructure; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D002314:Cardioplegic Solutions; D000251:Adenosine Triphosphatases; D000241:Adenosine