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)
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.
Resumen
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.
Por qué esto importa para la hirudoterapia
Este estudio investigó la Saratina (Merck KGaA, Darmstadt, Alemania) aplicada localmente en dosis de 0–20,0 µg a arterias carótidas de rata tras endarterectomía, evaluando los efectos sobre la adhesión plaquetaria y la hiperplasia intimal en un modelo de hiperhomocisteinemia. La Saratina a dosis ≥5,0 µg redujo la adhesión plaquetaria posendarterectomía entre un 63 y un 67 %, y 5,0 µg disminuyó la hiperplasia intimal en un 45 % en el grupo con hiperhomocisteinemia, sin alterar la homocisteína plasmática, la CBS ni la MTHFR. El resumen no identifica el origen biológico de la Saratina ni menciona sanguijuelas, por lo que no puede establecerse ninguna conexión con la hirudoterapia o el secretoma de sanguijuela a partir de este artículo por sí solo. Advertencia: se trata de un estudio animal (rata) sobre un compuesto de aplicación local; no contiene datos relacionados con sanguijuelas y su relevancia para el ámbito de la ASH no puede fundamentarse a partir del resumen.
Citación
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
Contexto clínico relacionado
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Añadido a la biblioteca ASH: May 27, 2026 · Última actualización del sitio: 18 de junio de 2026