TY - JOUR
T1 - Platelet Loss during Experimental Cardiopulmonary Bypass and Its Prevention with Prostacyclin
AU - Plachetka, John R.
AU - Salomon, Neal W.
AU - Larson, Douglas F.
AU - Copeland, Jack G.
N1 - Funding Information:
From the Division of Cardiovascular and Thoracic Surgery, and the Department of Pharmacy Practice, University of Arizona Health Sciences Center, Tucson, AZ. Supported by a University of Arizona Biomedical Research Support Grant.
PY - 1980
Y1 - 1980
N2 - Prostacyclin (PGI2), a newly discovered short-acting prostaglandin that inhibits platelet aggregation, was evaluated as an agent for prevention of cardiopulmonary bypass–induced thrombocytopenia. Ten adult, splenectomized greyhounds were divided into three treatment groups prior to beginning 120 minutes of partial cardiopulmonary bypass. Group 1 animals received 300 units of heparin per kilogram of body weight, Group 2 animals received 300 units of heparin per kilogram plus PGI2, 1.5 μg per minute, and Group 3 animals received 300 units of heparin per kilogram plus PGI2 3.0 μg per minute. Bypass and PGI2 infusion were started simultaneously. Mean platelet counts of each group at 5 minutes were approximately 40% of prebypass levels. Additional platelet loss was seen in Groups 1 and 2 at 30, 60, and 120 minutes. However in Group 3, platelet counts at 30 and 60 minutes were essentially unchanged from prebypass levels. At 30, 60, and 120 minutes of cardiopulmonary bypass, the differences between Groups 1 and 3, and 2 and 3 are highly significant (p < 0.01). We conclude that PGI2 is an effective agent for preserving platelet levels during experimental cardiopulmonary bypass. Furthermore, it is possible that platelet loss during cardiopulmonary bypass may be caused, in part, by an imbalance between PGI2 and thromboxane A2, which results in excessive platelet adhesion and aggregation.
AB - Prostacyclin (PGI2), a newly discovered short-acting prostaglandin that inhibits platelet aggregation, was evaluated as an agent for prevention of cardiopulmonary bypass–induced thrombocytopenia. Ten adult, splenectomized greyhounds were divided into three treatment groups prior to beginning 120 minutes of partial cardiopulmonary bypass. Group 1 animals received 300 units of heparin per kilogram of body weight, Group 2 animals received 300 units of heparin per kilogram plus PGI2, 1.5 μg per minute, and Group 3 animals received 300 units of heparin per kilogram plus PGI2 3.0 μg per minute. Bypass and PGI2 infusion were started simultaneously. Mean platelet counts of each group at 5 minutes were approximately 40% of prebypass levels. Additional platelet loss was seen in Groups 1 and 2 at 30, 60, and 120 minutes. However in Group 3, platelet counts at 30 and 60 minutes were essentially unchanged from prebypass levels. At 30, 60, and 120 minutes of cardiopulmonary bypass, the differences between Groups 1 and 3, and 2 and 3 are highly significant (p < 0.01). We conclude that PGI2 is an effective agent for preserving platelet levels during experimental cardiopulmonary bypass. Furthermore, it is possible that platelet loss during cardiopulmonary bypass may be caused, in part, by an imbalance between PGI2 and thromboxane A2, which results in excessive platelet adhesion and aggregation.
UR - http://www.scopus.com/inward/record.url?scp=0018832761&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0018832761&partnerID=8YFLogxK
U2 - 10.1016/S0003-4975(10)61203-9
DO - 10.1016/S0003-4975(10)61203-9
M3 - Article
C2 - 6994666
AN - SCOPUS:0018832761
SN - 0003-4975
VL - 30
SP - 58
EP - 63
JO - Annals of Thoracic Surgery
JF - Annals of Thoracic Surgery
IS - 1
ER -