1. What is the best perfusion temperature for coronary revascularization?
Richard M. Engelman, MDa,d,e, A.Bernard Pleet, MDb,e, John A. Rousou, MDa,d,e, Joseph E. Flack, MDa,d, David W. Deaton, MDa,d, Cheryl A. Gregory, RNa, Penelope S. Pekow, PhDc 
The Journal of Thoracic and Cardiovascular Surgery 
Volume 112, Issue 6, Pages (December 1996)
DOI: /S (96)
Copyright © 1996 Mosby, Inc. Terms and Conditions

2. Fig. 1
Schematic for fibrinolytic potential occurring during CPB is illustrated. Blood and artificial surface contact lead to activation of Hageman factor (factor XII) and conversion of prekallikrein to kallikrein. Both serve to degrade plasminogen into plasmin. Activated factor XII, through its initiation of clotting cascade promotes formation of thrombin from prothrombin. Disturbances affecting endothelial cell, such as myocardial ischemia and cardioplegia, promote formation of t-PA, which functions to support degradation of plasminogen to plasmin. An antifibrinolytic, PAI-1, is also formed from endothelium, and functions to interrupt degradation of plasminogen. Plasmin, in turn, acts on fibrinogen and fibrin to form degradation products, which are end stage of fibrinolysis. Interfering with activity of plasmin is α2-antiplasmin (α-2-ANTIPL). PAT interrupts activity of thrombin in forming fibrin from fibrinogen. Specifically measured in this analysis were studies marked with asterisk: t-PA antigen, PAI-1, PAT, plasminogen, prekallikrein and α2-antiplasmin.
The Journal of Thoracic and Cardiovascular Surgery  , DOI: ( /S (96) )
Copyright © 1996 Mosby, Inc. Terms and Conditions