Prevention of acquired transient defect in platelet plug formation by
infused prostacyclin
TW Malpass, SR Hanson, B Savage, EA Hessel and LA Harker
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. In contrast, platelet-dense granules did not
undergo significant release. The bleeding times normalized rapidly
following bypass (8.5 +/- 1.4 min at 1 hr). The infusion of prostacyclin
(PGI2) into the bubble oxygenator during bypass (40--80 ng/kg/min)
prevented the prolongation in bleeding time (p less than 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. These results show that 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.
Volume 57,
Issue 4,
pp. 736-740,
04/01/1981
Copyright © 1981 by The American Society of Hematology
