Summary
Although snake venom enzymes such as reptilase do not cause viscous metamorphosis,
platelet secretion or clot retraction; when batroxobin and calcium are added to citrated
blood significant platelet force development occurs. When this batroxobin-calcium
system was applied to the study of platelet function during cardiopulmonary bypass
(CPB), force development was found to be completely inhibited. After heparin reversal
by protamine sulfate, significant recovery of force occurred. The present investigation
was performed to evaluate the role of heparin in reducing force development during
CPB. At concentrations above 0.10 U/ml, heparin totally suppressed force development
in normal plasma. Addition of protamine sulfate to heparinized plasma caused complete
recovery of force development. These concentrations of heparin had little effect on
platelet aggregation by ADP or collagen. Possible direct effects of heparin on fibrin
assembly and structure were studied by adding varying amounts of heparin to plasma
and then inducing clot formation with batroxobin. At 1 U/ml, heparin reduced the size
of fibrin fibers by 33%. Higher heparin concentrations had no additional effect. These
results indicate that heparin may be responsible for a significant component of the
decreased platelet force noted during cardiopulmonary bypass. To test whether heparin’s
effect could be due to suppression of thrombin activity, the effects of the antithrombin
hirudin on force development were measured. Hirudin also inhibited force development
in a concentration dependent manner. Thus, heparin’s reduction of platelet force development
may be due, at least in part, to suppression of thrombin activity.
