The platelet in cardiopulmonary bypass
Abstract
Platelets are the smallest of the blood cells and are known to be activated during cardiopulmonary bypass. They play a role in many associated complications. Both quantitative and qualitative platelet defects have been demonstrated, resulting in microvascular hemorrhage and thromboembolism. As their interactions with endothelium and other blood cells are unraveled, the important contribution they make toward the systemic inflammatory response to operation seen in cardiopulmonary bypass is increasingly evident. In this review, we consider platelet activation during cardiopulmonary bypass, the resultant clinical effects, and potential approaches to therapy and prevention.
Platelets are 1.5- to 3.5-mm diameter anucleated circulating cells derived from precursor megakaryocytes. Adult humans have 150 to 400 × 109 platelets per liter of blood. Their daily turnover is around 35 × 109 cells per liter of blood volume. The majority of the body’s platelets are in the circulation with 25% to 30% being sequestrated in the spleen at any one time. The average survival time of human platelets in the circulation is 9 to 11 days.
Unactivated platelets are discoid in shape. Their cytoplasm contains organelles, a cytoskeleton consisting of microtubules and microfilaments, and granules. The surface membrane of the platelet expresses various glycoprotein molecules. Invaginations of the cell wall form a passageway between the exterior and the interior of the platelet and are known as the surface-connected canalicular system
Resting platelets are discoid in shape. On activation changes occur in the internal cytoskeleton causing the platelet to become spheroid in shape. Along with this, constitutively present surface molecules are reorganized (eg, glycoprotein IIb and IIIa), which form a fibrinogen-binding complex. Simultaneously there is movement of cytoplasmic granules toward the surface of the cell. These granules fuse with the platelet surface extruding their contents. Platelet factor-4, β-thromboglobulin, and von Willebrand factor are secreted in this manner from α-granules. At the same time molecules that were an integral part of the granule membranes are now expressed on the surface of the activated platelet. P-selectin derived from α-granules and CD63 derived from lysosomes are two such molecules. On activation platelets also generate large quantities of microparticles containing phospholipids such as phosphatidylserine.