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Influence of aspirin and carbacyclin on bovine platelet function
G H Rao1, D G Ericson, D J Weiss
1Department of Laboratory Medicine and Pathology, University of Minnesota Medical School, Minneapolis.
Insights
Bovine platelets show compromised responses to common agonists, suggesting cows are not ideal models for artificial heart thrombogenicity studies. Further research is needed to understand these differences in platelet function.
Area of Science:
- Biomedical Engineering
- Comparative Physiology
- Hematology
Background:
- Total artificial hearts (TAH) research often utilizes animal models.
- Understanding platelet response is crucial for evaluating biomaterial thrombogenicity.
Purpose of the Study:
- To investigate the functional differences between human and bovine platelets.
- To assess the suitability of cows as a model for TAH-related thrombogenicity studies.
Main Methods:
- Comparative analysis of human and bovine platelet aggregation in response to agonists like epinephrine, arachidonate, and adenosine diphosphate (ADP).
- Evaluation of platelet cyclo-oxygenase inhibition by aspirin and response to prostaglandin E1 (PGE1) and carbacyclin (U55185).
Main Results:
- Bovine platelets failed to aggregate with epinephrine and arachidonate.
- Prostaglandin E1 (PGE1) inhibited bovine platelet response to ADP, an effect not reversed by epinephrine.
- Aspirin and carbacyclin (U55185) inhibited bovine platelet function, indicating compromised cyclo-oxygenase pathways.
Conclusions:
- Bovine platelets exhibit severely compromised responses to various agonists compared to human platelets.
- The observed platelet dysfunctions and inability to spread properly suggest cows may not be suitable models for evaluating artificial organ thrombogenicity.
Abstract:
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 mumol/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 authors' 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.