Thromb Haemost 1986; 55(02): 197-200
DOI: 10.1055/s-0038-1661521
Original Article
Schattauer GmbH Stuttgart

Platelet Function in Experimentally Induced Pancreatitis in the Dog

R M Jacobs
1   The Department of Veterinary Pathobiology, The Ohio State University, Columbus, Ohio, USA
,
R J Murtaugh
2   The Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio, USA
,
R H Fertel
3   The Department of Pharmacology, The Ohio State University, Columbus, Ohio, USA
› Author Affiliations
Further Information

Publication History

Received 30 July 1985

Accepted 21 January 1986

Publication Date:
18 July 2018 (online)

Summary

Evidence suggests that changes in prostaglandins and disseminated intravascular coagulation accompany pancreatitis. Both may induce changes in platelet function. We wished to determine if experimentally induced pancreatitis in the dog was associated with altered platelet number and function, and whether there were concomitant changes in prostaglandins. Evidence for disseminated intravascular coagulation in the dogs with pancreatitis were red blood cell fragmentation, increased platelet turnover indicated by macro-platelets and the transient presence of fibrin degradation products in urine. There were no significant changes in platelet count. The platelets from dogs with pancreatitis showed a functional defect characterized by significantly decreased aggregation in response to adenosine diphosphate, arachidonic acid, and collagen. Release of adenosine triphosphate from platelets was reduced in collagen-stimulated aggregation. There were no changes in the plasma concentrations of thromboxane B2, 6-Keto-PGF1a, and PGE2. This defect may have been due to the generation of fibrin degradation products and platelet “exhaustion”.

 
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