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”.
Key words
Platelet - Aggregation - Pancreatitis - Canine
