Effect of ticlopidine and prostaglandin E on endotoxin-induced pulmonary platelet sequestration in vivo.

Prostaglandin E1 has earlier been shown to decrease pulmonary platelet trapping (PPT) following shock. This experiment was performed to evaluate a new method to study PPT in vivo, and to study the effect of prostaglandin E1 and a new antiplatelet drug (ticlopidine) on PPT in rabbits after i.v. administration of endotoxin. Following platelet labeling with In-111, the rabbits were placed under a scintillation camera for continuous measuring of the activity distribution for 40 minutes. The first five minutes represented reference values, whereafter endotoxin E. coli was injected i.v. The following 2-4 minutes showed a sudden increase of radioactivity over the lungs and a simultaneous decrease over the heart, indicating PPT in the nontreated animals, followed by a slow decrease to almost preshock values during the following 30 minutes. Animals receiving prostaglandin E1 showed a significantly lower activity peak in the lungs after the administration of endotoxin, while the corresponding peak in ticlopidine-treated animals did not differ from that seen in the nontreated animals. In all groups, endotoxin caused a decrease in platelet count, but it was significantly lower in the PGE1-treated animals. The results have shown that this diagnostic model for PPT is reliable and may be used for evaluation of the effect on platelet aggregation in vivo of different drugs.