Amerikanische Gesellschaft für Hirudotherapie

Saratin (an inhibitor of platelet-collagen interaction) decreases platelet aggregation and homocysteine-mediated postcarotid endarterectomy intimal hyperplasia in a dose-dependent manner

Comparative study published in Am J Surg (2004)

Zuletzt aktualisiert: June 18, 2026Geprüft von: ASH Editorial Board
Research article — evidence reviewArticle reference
Evidence: Observational studySpeichel-PharmakologieArzneimittelentwicklungDavis JA et al. · Am J Surg, 2004

Abstract

BACKGROUND: This study investigated Saratin's (Merck KGaA, Darmstadt, Germany) prevention of platelet adhesion and intimal hyperplasia at different doses and in the hyperhomocystinemia rat carotid endarterectomy (CEA) model. METHODS: Rats were divided into two groups: (1) platelet adhesion or (2) luminal stenosis because of intimal hyperplasia. At CEA, rats received 0, 0.5, 5.0, 10.0, or 20.0 microg Saratin on the artery. Post-CEA platelet aggregation was evaluated by standard error of the mean. Intimal hyperplasia group received either (1) control or (2) 4.5 g/kg DL-homocystine diets for two weeks followed by CEA and treated with diluent or 5.0 microg Saratin. Endpoints included platelet adhesion, intimal hyperplasia, plasma homocysteine (HCys), and its metabolic enzymes cystathionine beta-synthase (CBS) and methylenetetrahydrofolate reductase (MTHFR). RESULTS: Platelet adhesion: post-CEA, platelet adhesion was reduced by 63%, 67%, and 67% in Saratin doses > or =5.0 microg. Intimal hyperplasia: 5.0 microg Saratin in the HCys group decreased intimal hyperplasia by 45% compared with the non-Saratin-treated HCys group. Plasma HCys levels were not altered with Saratin treatment in the HCys groups nor were CBS or MTHFR. CONCLUSIONS: Saratin significantly inhibited platelet adhesion at > or =5.0 microg, and Saratin at 5.0 microg attenuated luminal stenosis in a hyperhomocysteinemic rat CEA model.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Publication typeComparative StudyJournal ArticleResearch Support, Non-U.S. Gov't
Indexed MeSH termsAnalysis of VarianceAnimalsBiopsy, NeedleCarotid StenosisDisease Models, AnimalDose-Response Relationship, DrugEndarterectomy, CarotidHomocystineImmunohistochemistryMalePlatelet Aggregation InhibitorsPlatelet Function Tests

Zusammenfassung

This study investigated Saratin's (Merck KGaA, Darmstadt, Germany) prevention of platelet adhesion and intimal hyperplasia at different doses and in the hyperhomocystinemia rat carotid endarterectomy (CEA) model.

Warum dies für die Hirudotherapie relevant ist

This study investigated Saratin (Merck KGaA, Darmstadt, Germany) applied locally at doses of 0–20.0 µg to rat carotid arteries after endarterectomy, evaluating effects on platelet adhesion and intimal hyperplasia in a hyperhomocysteinemic model. Saratin at ≥5.0 µg reduced post-endarterectomy platelet adhesion by 63–67%, and 5.0 µg decreased intimal hyperplasia by 45% in the hyperhomocysteinemic group without altering plasma homocysteine, CBS, or MTHFR. The abstract does not identify Saratin's biological origin or mention leeches, so no hirudotherapy or leech-secretome connection can be established from this article alone. Caveat: This is an animal (rat) study of a locally applied compound; it contains no leech-related data and its relevance to ASH's domain cannot be supported by the abstract.

Zitation

Saratin (an inhibitor of platelet-collagen interaction) decreases platelet aggregation and homocysteine-mediated postcarotid endarterectomy intimal hyperplasia in a dose-dependent manner.

Davis JA et al. · Am J Surg, 2004

DOI

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