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March 1, 1986Arteriosclerosis An Official Journal of the American Heart Association IncOpen Access

Development of nonthrombogenicity of injured rabbit aortas despite inhibition of platelet adherence.

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Why the study?

Does inhibition of initial platelet adherence with PGI2 or dipyridamole influence the development of nonthrombogenicity in injured rabbit aortas?

Population

Rabbit model with injured aortas (removal of endothelium from normal aortas or injury to neointima)

Design

Preclinical

Follow-up

8 hours

Authors

HGH M GrovesMcMaster UniversityRKR L Kinlough-RathboneYork UniversityJMJ. F. MustardGeneral / Preventive / Lipids

Discussion

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Overview

Supports vessel passivation after platelet inhibition in rabbit injury models; leaves open translation to human antithrombotic strategies.

Structured PICO

Does inhibition of initial platelet adherence with PGI2 or dipyridamole influence the development of nonthrombogenicity in injured rabbit aortas?

P
Population
Rabbit model with injured aortas (removal of endothelium from normal aortas or injury to neointima)
I
Intervention
Infusion of PGI2 (850 ng/kg/min) or dipyridamole (12.5 mg/kg initially followed by 5 mg/kg/hr) for up to 8 hours
O
Outcome
Platelet accumulation on the subendothelium/surfaces after discontinuation of drug infusionsurrogate

Injured vessel walls can develop a nonthrombogenic surface over approximately 8 hours even when initial platelet adherence is pharmacologically prevented.

Cite This Study

Groves et al. (1986) studied this question.

synapsesocial.com/papers/6a764bd3177aa7007f06ddbchttps://doi.org/10.1161/01.atv.6.2.189
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Also Consider

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