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.