Intracellular trapping of adenosine during myocardial ischemia by L-homocysteine.
Experiments were carried out to test the hypothesis whether adenosine produced by ATP catabolism during ischemia can be trapped with L-homocysteine and be re-utilized during reperfusion. During intraatrial infusion of L-homocysteine (100 mg/kg/h), the ischemic accumulation of adenine nucleosides and oxypurines in dog myocardium was found to be less than 50% of that during control ischemia. A high proportion of adenosine was recovered as S-adenosyl-L-homocysteine. On reperfusion, S-adenosyl-L-homocysteine. On reperfusion, S-adenosyl-L-homocysteine tissue content remained high. After 3 hours of reperfusion approximately 50% of the accumulated S-adenosyl-L-homocysteine were still found in the tissue. Infusion of L-homocysteine did not cause an accumulation of S-adenosyl-L-homocysteine in the nonischemic myocardial tissue. L-homocysteine treatment caused a further depletion of ATP during reperfusion after 30 minutes of ischemia, which can be interpreted as a toxic effect. We conclude that L-homocysteine is indeed able to trap adenosine produced by ATP breakdown, but the reaction is not readily reversible and is therefore not useful for quick restoration of postischemic ATP levels.
D000227:Adenine Nucleotides / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001826:Body Fluids / Q000378:metabolism*; D003327:Coronary Disease / Q000378:metabolism*; D004285:Dogs; D005260:Female; D006710:Homocysteine / Q000494:pharmacology*; D007424:Intracellular Fluid / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009705:Nucleosides / Q000378:metabolism
D000227:Adenine Nucleotides; D009705:Nucleosides; D006710:Homocysteine; D000255:Adenosine Triphosphate