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Ann Thorac Surg 1990;49:32-34
© 1990 The Society of Thoracic Surgeons
Thrombosis Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania USA
* Address reprint requests to Dr Colman, Thrombosis Research Center, Temple University School of Medicine, 3400 N Broad St, Philadelphia, PA 19140.
My colleagues and I have employed a simulated extracorporeal circuit to help define blood cell changes during clinical cardiopulmonary bypass. Platelet count decreases sharply due to temporary adhesion to the circuit. Platelets degranulate, synthesize and release thromboxane A2, and lose the ability to aggregate with adenosine diphosphate and epinephrine. These changes are also due to the loss of α 2-adrenergic and fibrinogen receptors. The neutrophil count decreases to a lesser extent, but neutrophils also are stimulated to secrete latoferrin and elastase concomitant with activation of plasma kallikrein. Although lidocaine can inhibit the neutrophil activation and prostacyclin can inhibit the platelet stimulation, prostaglandin E1 appears to prevent both neutrophil and platelet alterations.
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