PREVENTION OF ACQUIRED TRANSIENT DEFECT IN PLATELET PLUG FORMATION BY INFUSED PROSTACYCLIN

  • 1 January 1981
    • journal article
    • research article
    • Vol. 57  (4) , 736-740
Abstract
Cardiopulmonary bypass in baboons produced transient severe platelet dysfunction (bleeding times prolonged to 27.8 .+-. 1.4 min compared with 3.9 .+-. 0.7 baseline) that was associated with a parallel release of platelet .alpha.-granule proteins into plasma (platelet factor 4 and .beta.-thromboglobulin levels of 28.8 .+-. 9.3 and 20.0 .+-. 1.8 ng/ml, respectively), and their clearance into urine with a reciprocal depletion from circulating platelets. Platelet-dense granules did not undergo significant release. The bleeding times normalized rapidly following bypass (8.5 .+-. 1.4 min at 1 h). The infusion of prostacyclin (PGI2) into the bubble oxygenator during bypass (40-80 ng/kg per min) prevented the prolongation in bleeding time (P < 0.01 compared with untreated control values), but did not block the release of .alpha.-granule proteins. Dosages outside this range were associated with prolonged bleeding times. Transient platelet dysfunction occurring during cardiopulmonary bypass represents activation of platelets independent of .alpha. or dense granule release and is blocked by potent short-acting inhibition of platelet function using PGI2 infused into the oxygenator apparatus at optimal therapeutic doses.