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

Thörne, Johan LU ; Jönsson, Bo-Anders LU ; Norgren, Lars LU and Strand, Sven-Erik LU (1986) In Circulatory Shock 20(1). p.61-69
Abstract
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... (More)
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 (Less)
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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Circulatory Shock
volume
20
issue
1
pages
61 - 69
publisher
John Wiley & Sons Inc.
external identifiers
  • scopus:0022509490
ISSN
0092-6213
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Emergency medicine/Medicine/Surgery (013240200), Radiation Physics, Lund (013034000), Surgery (Lund) (013009000)
id
16c5ec57-bfd9-4f7c-b4e5-de88f4ca040f (old id 1103728)
date added to LUP
2016-04-01 15:47:18
date last changed
2021-01-03 11:13:12
@article{16c5ec57-bfd9-4f7c-b4e5-de88f4ca040f,
  abstract     = {{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}},
  author       = {{Thörne, Johan and Jönsson, Bo-Anders and Norgren, Lars and Strand, Sven-Erik}},
  issn         = {{0092-6213}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{61--69}},
  publisher    = {{John Wiley & Sons Inc.}},
  series       = {{Circulatory Shock}},
  title        = {{Effect of ticlopidine and prostaglandin E on endotoxin-induced pulmonary platelet sequestration in vivo}},
  volume       = {{20}},
  year         = {{1986}},
}