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Joseph M. Forbess
Fumikazu Nomura
Takuya Miura
John E. Mayer, Jr
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Ann Thorac Surg 1995;60:1238-1244
© 1995 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Anti-CD11b Monoclonal Antibody Improves Myocardial Function After Six Hours of Hypothermic Storage

Joseph M. Forbess, MD, Takeshi Hiramatsu, MD, Fumikazu Nomura, MD, Takuya Miura, MD, G. King Farrington, PhD, Karen Sokolowski, Mark Bree, BS, John E. Mayer, Jr, MD

Department of Cardiovascular Surgery, Children's Hospital, Boston, and Repligen Corporation, Cambridge, Massachusetts

Accepted for publication June 19, 1995.

Background. The shortage of pediatric heart donors often necessitates considerable travel time and, as a result, prolonged donor heart ischemia. This excessive hypothermic storage may contribute markedly to myocardial dysfunction in the recipient.

Methods. We investigated the role of leukocyte-endothelial interactions in this dysfunction in an isolated, 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°C. Group M1/70 (n = 6) received at reperfusion 15 µg/mL of a monoclonal antibody F(ab`)2 fragment to CD11b, the {alpha}-subunit of the leukocyte adhesion molecule Mac-1. Group MB10.6 (n = 8) received 15 µg/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 the two control groups (p < 0.05).

Conclusions. These data implicate leukocyte-endothelial interactions mediated by the leukocyte adhesion molecule CD11b in myocardial dysfunction after long-term hypothermic ischemia. Specific antiadhesion strategies such as this may safely extend storage time for pediatric donor hearts.




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