Prevention of reperfusion injury in the neonatal heart with leukocyte-depleted blood.

Activated leukocytes release oxygen free radicals and cause microvascular occlusion. This experiment tests the hypothesis that reperfusion with leukocyte-depleted blood reduces injury after extended ischemic preservation. An in vitro model consisting of an isolated, working neonatal piglet heart and an adolescent support pig was used. Hearts were arrested with a cold crystalloid cardioplegic solution, excised, and stored in 4 degrees C saline for 12 hours. Two groups were compared. In group 1 piglets (n = 8), reperfused with whole blood, the maximum stroke work index was 0.91 +/- 0.29 x 10(3) erg/gm (mean +/- standard error of the mean). Group 2 piglets (n = 6), reperfused with blood depleted of leukocytes by a polyester filter, had a maximum stroke work index of 11.6 +/- 1.0 x 10(3) erg/gm. This difference was highly significant (p less than 0.0001). Group 1 exhibited severe injury with myofibrillar necrosis, mitochondrial disruption, nuclear chromatin clumping, and moderate interstitial edema. Group 2 had normal ultrastructure on electron microscopic examination. We conclude that reperfusion with leukocyte-depleted blood prevents reperfusion injury and results in excellent myocardial function after long-term heart preservation.