AbstractCardiopulmonary bypass (CPB) causes bleeding and thrombotic complications, fluid retention and temporary dysfunction of every organ system. This morbidity of CPB is primarily do to activation of blood proteins and cells by contact with nonendothelial cell surfaces of the wound and biomaterials of the extracorporeal perfusion circuit. CPB is not possible without heparin, yet heparin is not an ideal anticoagulant and does not prevent activation of at least five plasma protein systems and five blood cells. Stimulation of these blood elements produces over 25 vasoactive substances that alter vascular tone, capillary permeability, and cardiac myocyte contractility. In addition, CPB produces showers of microemboli that pass filters to obstruct arterioles and precapillaries to produce necrosis of widely dispersed, small groups of cells. Attempts to develop nonthrombogenic synthetic materials have failed; only the endothelial cell is nonthrombogenic and achieves this property by active metabolic processes. Although some biomaterials are less thrombogenic than others, all activate blood elements to initiate clotting and the body's defense reaction. The concept of “blood anesthesia” envisions the use of reversible inhibitors of key blood reactions to temporarily prevent activation of blood elements during CPB. If the initial reactions of blood with nonendothelial surfaces are blocked, production of many vasoactive substances and microemboli by CPB is suppressed. This conserves blood elements that are normally consumed during CPB and makes them available after the inhibitor is reversed. Effective, reversible inhibitors of platelets are entering clinical trials; reversible inhibitors of other key blood relations are being developed and tested at a rapid rate. Within the next decade “blood anesthesia” for CPB promises to substantially reduce the morbidity associated with open heat
展开▼
