Effects of adenosine infusion with or without leukocyte depletion on recovery after hypothermic ischemia in neonatal lamb hearts.

OBJECTIVE

Leukocytes have been shown to have an important role in ischemia/reperfusion injury. Adenosine also reduced this ischemia/reperfusion injury. There is an interaction between adenosine and leukocyte via receptor mediated function. To determine whether beneficial effects of adenosine on reperfusion injury is mediated by changes in leukocyte function, we studied the effects of adenosine with and without leukocyte depletion during reperfusion on the functional recovery of the neonatal myocardium after cold cardioplegic arrest.

MATERIALS AND

METHODS

We infused adenosine (350 micromol/l) during the first 20 min of reperfusion for adenosine treated group and adenosine-leukocyte treated group. The other two groups were perfused with leukocyte treated blood or untreated blood. All the groups were subjected to 2 h of cold cardioplegic ischemia (n = 8 in each group). At 30 min of reperfusion, LV function was measured. Coronary blood flow and oxygen consumption (MVO2) were also measured to evaluate the metabolic recovery.

RESULTS

Adenosine treated, adenosine-leukocyte treated, and leukocyte treated groups showed better functional recovery than the control group (maximum developed pressure: control = 74.6 +/- 5.6%, adenosine treated = 97.6 +/- 9.5%, adenosine-leukocyte treated = 98.5 +/- 5.6%, leukocyte treated = 82.5 +/- 6.0%. P < 0.05). Both adenosine treated and adenosine-leukocyte treated groups showed better recovery than leukocyte treated group (P < 0.05). Coronary blood flow was higher in adenosine-leukocyte treated group compared to other groups (P < 0.05). MVO2/beat was higher in adenosine treated, adenosine-leukocyte treated, and leukocyte treated groups than control group (P < 0.05).

CONCLUSION

Adenosine, with or without leukocyte depletion, had similar beneficial effect on recovery of systolic and diastolic functions, which involved other mechanisms in addition to the leukocyte inhibitory effect.