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Ann Thorac Surg 1980;30:58-63
© 1980 The Society of Thoracic Surgeons

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Articles

Platelet Loss during Experimental Cardiopulmonary Bypass and Its Prevention with Prostacyclin

From the Division of Cardiovascular and Thoracic Surgery, and the Department of Pharmacy Practice, University of Arizona Health Sciences Center, Tucson, AZ

Accepted for publication November 14, 1979.

^* Address reprint requests to Dr. Plachetka, Department of Pharmacy Practice, College of Pharmacy, University of Arizona, Tucson, AZ 85721

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.

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