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Oral cicaprost reduces platelet and neutrophil activation in experimental hypercholesterolemia.

Abstract
Oral treatment of cholesterol-fed rabbits with the PGI2 mimetic cicaprost largely reduces hypercholesterolemia-induced platelet and neutrophil hyperreactivity. In addition, cicaprost prevents atherosclerosis-induced platelet desensitization for PGI2. These effects persist after cicaprost treatment is withdrawn. Since platelets and leukocytes are supposed to contribute to atherogenesis, this suggests a favourable effect of long-term oral PGI2 substitution in hypercholesterolemia.
AuthorsT Hohlfeld, A Weber, K Schrör
JournalAgents and actions. Supplements (Agents Actions Suppl) Vol. 37 Pg. 289-96 ( 1992) ISSN: 0379-0363 [Print] Switzerland
PMID1632303 (Publication Type: Journal Article)
Chemical References
  • Platelet Aggregation Inhibitors
  • Adenosine Diphosphate
  • Collagen
  • Cholesterol
  • Epoprostenol
  • cicaprost
Topics
  • Adenosine Diphosphate (pharmacology)
  • Administration, Oral
  • Animals
  • Cholesterol (blood)
  • Collagen (pharmacology)
  • Epoprostenol (administration & dosage, analogs & derivatives, pharmacology)
  • Hypercholesterolemia (blood)
  • Lymphocyte Activation (drug effects)
  • Male
  • Neutrophils (drug effects)
  • Platelet Activation (drug effects)
  • Platelet Aggregation (drug effects)
  • Platelet Aggregation Inhibitors (pharmacology)
  • Rabbits

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