ANTI-CD11B MONOCLONAL-ANTIBODY IMPROVES MYOCARDIAL-FUNCTION AFTER 6 HOURS OF HYPOTHERMIC STORAGE

Background. The shortage of pediatric heart donors often necessitates considerable travel time and, as a result, prolonged donor heart ische mia. This excessive hypothermic storage may contribute markedly to myo cardial dysfunction in the recipient. Methods. We investigated the rol e of leukocyte-endothelial interactions in this dysfunction in an isol ated, immature (mean age, 11.8 +/- 1.6 days) swine heart model using a monoclonal antibody against a leukocyte adhesion molecule. We studied a total of 20 hearts subjected to 6 hours of cardioplegic arrest at 4 degrees C. Group M1/70 (n 6) received at reperfusion 15 mu g/mL of a monoclonal antibody F(ab')(2), fragment to CD11b, the Lu-subunit of th e leukocyte adhesion molecule Mac-1. Group MB10.6 (n = 8) received 15 mu g/mL of the swine unreactive F(ab')(2) MB10.6, and the third group received saline vehicle. Results. Administration of M1/70 resulted in improved postischemic recovery of ventricular function compared with t he two control groups p < 0.05). Conclusions. These data implicate leu kocyte-endothelial interactions mediated by the leukocyte adhesion mol ecule CD11b in myocardial dysfunction after longterm hypothermic ische mia. Specific antiadhesion strategies such as this may safely extend s torage time for pediatric donor hearts.