Influence of Aspirin and Carbacyclin on Bovine Platelet Function

Cows, calves, and sheep are the animals of choice for in vivo studies on total artificial hearts. In this study, the response of human and bovine platelets to agonists and antagonists was followed. Epinephrine and arachidonate failed to cause aggregation of bovine platelets. Exposure of bovine platelets to prostaglandin E1 (PGE1) resulted in inhibition of response to the action of adenosine diphosphate (ADP). Although epinephrine restored the response of PGE1 treated human platelets, it failed to restore the sensitivity of bovine platelets to the action of ADP. Exposure of bovine platelets to aspirin (100.0 μmol/L) or administration to calves intravenously (10.0 mg/kg) inhibited platelet cyclo-oxygenases. Infusion of carbacyclin (U55185) inhibited the ex vivo platelet response to the action of ADP. Results of this study demonstrate that the response of bovine platelets to agonists such as epinephrine, arachidonate, and the endoperoxide mimetic, U46619, is severely compromised. The authorsʼ observations in this study, as well as earlier findings demonstrating the inability of bovine platelets to fully spread on a surface, suggests that the cow may not be an appropriate “model” for evaluating thrombogenicity caused by artificial organs and implants.