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[Attempt at preventing hyperacute xenogenic rejection by isotopic suppression of IgM in the recipient].

Hyperacute xenogeneic rejection is partly initiated by the binding of performed natural antibodies on the recipient's vascular endothelium. In this study, isotypic suppression of IgM in the recipient was conducted in the guinea pig-to-rat combination. Anti-IgM HIS 40 and 56 monoclonal antibodies were injected intraperitoneally in rats (n = 3) (Group 1). Control animals were rats (n = 13) treated by PBS (Group 2). Guinea pig hearts were implanted heterotopically in all rats. Depletion of circulating IgM in the recipient was assessed by ELISA. The circulating and splenic B-lymphocyte population was scanned by FACS analysis. Isotypic suppression was very effective for the depletion of circulating IgM in Group 1 rats (alpha < 0.01) as assessed by ELISA. Similarly, the rate of circulating and splenic B-lymphocytes was significantly decreased in treated animals (alpha < 0.01). However, the graft survival in Group 1 (14 +/- 6.9 min) was not different from that observed in Group 2 (15.4 +/- 5 min). Isotypic suppression of IgM in the recipient did not delay hyperacute xenogenic rejection in the guinea pig-to-rat combination. The prevention of hyperacute rejection must therefore be based on the various mechanisms of this phenomenon.