Alterations of the coagulation potential of heparinized blood after using an extracorporeal circulation have been studied by means of a toluidine blue-calcium chloride reagent. This technique was originally used to detect the effect of activation by contact on the coagulation mechanism in heparinized blood. It has been shown that it also detects, in the presence of heparin, the clotpotentiating effect of blood cell contents liberated in vitro by mechanical trauma to blood.
Variable destruction of platelets, red cells, and white cells occurred in heparinized sheep blood recirculated in a heart-lung machine in vitro. This was accompanied by increased clotting potential. Complete coagulation was prevented by heparin and fibrinogen levels remained unaltered.
Similar enhancement of the coagulation potential and destruction of blood cells were detected in the blood of heparinized patients and sheep after perfusion for open-heart surgery. The coagulation changes were usually transient, and impaired coagulation associated with significant fibrinogen loss was detected in most samples taken after the neutralization of heparin.
It is suggested that the coagulation changes are due to activation by contact of the coagulation mechanism during perfusion and to the clot-accelerating effect of blood cell contents. The results support the hypothesis that coagulation defects and fibrinogen loss after using an extracorporeal circulation are due, at least in part, to intravascular coagulation. This is thought to occur, especially during neutralization of heparin, while the coagulation mechanism is hyperactive.
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