Platelet and neutrophil activation in cardiopulmonary bypass

Abstract

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 A 2, 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 E 1 appears to prevent both neutrophil and platelet alterations.