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Progressive Loss of Fibronectin‐Mediated Opsonic Activity in Plasma Cryoprecipitate with Storage
Author(s) -
Blumenstock Frank A.,
Valeri C. Robert,
Saba Thomas M.,
Cho Eshin,
Melaragno Anthony,
Gray Alan,
Lewis Martin
Publication year - 1988
Publication title -
vox sanguinis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.68
H-Index - 83
eISSN - 1423-0410
pISSN - 0042-9007
DOI - 10.1111/j.1423-0410.1988.tb03887.x
Subject(s) - cryoprecipitate , opsonin , fibronectin , chemistry , andrology , immunology , medicine , phagocytosis , biochemistry , platelet , extracellular matrix
. Septic injured patients often manifest a deficiency of plasma fibronectin. Several studies have shown improvements in organ function in such patients following infusion of fibronectin‐rich plasma cryoprecipitate, while other studies found no improvement. One explanation for these differences may be the use of plasma crypoprecipitate which has been stored for various time intervals prior to its use as a source of fibronectin. This investigation tested the hypothesis that the opsonic activity of fibronectin in cryoprecipitate may decline with increased storage duration. Using a bioassay of opsonic activity, we evaluated human plasma cryoprecipitate that was stored at either ‐20 or ‐80°C for various intervals (2 weeks to 12 months) after its preparation from fresh donor plasma. Our findings demonstrated that the opsonic activity of fibronectin in cryoprecipitate declined with increasing time of storage. Significant loss (p < 0.05) of opsonic activity was first evident after 2 months of storage. Storage at ‐80°C did not prevent this decline in opsonic activity as compared to storage at ‐20 °C. Immunoblot analysis revealed extensive fragmentation of the dimeric fibronectin (440 kdaltons) and the presence of lower molecular weight fragments in 4‐ to 12‐month‐old plasma cryoprecipitate. Therefore, plasma cryoprecipitate of varying ages (storage time) when used as a source of fibronectin for replacement therapy to support phagocytic function in septic injured patients may result in different fibronectin‐mediated responses. The decline in activity may be due, in part, to fragmentation of the fibronectin molecule.