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Aprotinin Reduces the Expression of P‐Selectin on the Surface of Platelet and Leukocyte‐Platelet Conjugates
Author(s) -
Inui Kiyoshige,
Shimazaki Yasuhisa,
Watanabe Takao,
Kuraoka Setsuo,
Uesho Kunihiro,
Uchida Tetsuro,
Shiono Satoshi
Publication year - 1998
Publication title -
artificial organs
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.684
H-Index - 76
eISSN - 1525-1594
pISSN - 0160-564X
DOI - 10.1046/j.1525-1594.1998.06181.x
Subject(s) - aprotinin , platelet , p selectin , superoxide , cardiopulmonary bypass , plasmin , chemistry , platelet activation , pharmacology , thrombin , immunology , medicine , biochemistry , enzyme
P‐Selectin, an adhesion molecule expressed on the surfaces of activated platelets and the vascular endothelium, mediates platelet binding to monocytes and neutrophils. Monocytes and neutrophils produce superoxide anion by activated platelets through p‐selectin. Aprotinin, a serine protease inhibitor, inhibits plasmin to activate platelets during cardiopulmonary bypass (CPB). A total of 25 patients were studied to clarify the effects of aprotinin on p‐selectin expression during CPB. Nine patients were not given aprotinin (control group), and 16 were given aprotinin of 2 million U in the priming solution (aprotinin group). The platelet count and soluble p‐selectin in the plasma, p‐selectin on the surface membranes of platelets, and leukocyte‐platelet conjugate levels were measured during and after CPB. The platelet count was maintained well in the aprotinin group. The increases of soluble p‐selectin in the plasma, platelet surface p‐selectin, and leukocyte‐platelet conjugates were less in the aprotinin group than in the control group (p < 0.05). In conclusion, aprotinin in patients undergoing CPB may reduce the early inflammatory reactions induced by p‐selectin.