Maintenance of homeostasis in coagulation during cardiopulmonary bypass.
Cardiopulmonary bypass (CPB) represents a massive stimulus that overwhelms the body's homeostatic ability to buffer. Contact activation, the extrinsic cascade, and ongoing cellular interactions all must be considered to understand the coagulation dysfunction that occurs in CPB. Various aspects and the specific effects of these factors as well as their interrelationships are still poorly understood. Since we are dealing with a complex system, the way we approach our investigations must become more rather than less complex. Simply measuring peripheral blood levels of various proteins throughout CPB levels does not fit the important physiologic processes governing homeostasis, as production, clearance, redistribution, and dilution are all constantly at play. A recent study of prothrombin fragment F1.2 levels during CPB is provided as an illustration. Our increasing understanding of aprotinin's mechanisms of action has furthered our basic understanding of coagulation dysfunction in CPB. Further progress requires new thinking, more research, and increasingly complex approaches to the understanding of what drives homeostasis.
Spiess
B D
BD
Department of Anesthesiology, Northwest Hospital, Seattle, WA 98133, USA.
D000925:Anticoagulants / Q000494:pharmacology; D001777:Blood Coagulation / Q000502:physiology*; D001779:Blood Coagulation Factors / Q000502:physiology; D002315:Cardiopulmonary Bypass; D006493:Heparin / Q000494:pharmacology; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D010446:Peptide Fragments / Q000032:analysis; D011516:Prothrombin / Q000032:analysis
D000925:Anticoagulants; D001779:Blood Coagulation Factors; D010446:Peptide Fragments; C045879:prothrombin fragment 1.2; D011516:Prothrombin; D006493:Heparin