Arterial thrombosis

What acts on it

1. Several authors have reported that salicylate blocks and reverses aspirin inhibition of prostaglandin synthesis by platelets and arterial wall, but when rats were given sodium salicylate at 15 or 100 milligrams per kilogram two minutes before aspirin at 10 milligrams per kilogram, a significant antithrombotic effect of aspirin was observed in all cases regardless of prior salicylate administration with results similar to aspirin alone, so competition between salicylate and aspirin as reported in vitro does not appear to significantly affect the in vivo antithrombotic action in this model.

   Salicylate / salicylic acid → Arterial thrombosis source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/aspirin-research/6792646.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "55b09486e54c42e6ecdac3476a0ae8b9d9819f06b5b01a9fc33087fd621a9c82", "start_char": 0, "end_char": 767, "text_sha256": "55b09486e54c42e6ecdac3476a0ae8b9d9819f06b5b01a9fc33087fd621a9c82"}

   experimental_model

   Electrically induced carotid artery thrombosis in male rats with salicylate pretreatment

   exposure

   Sodium salicylate 15 or 100 milligrams per kilogram intravenously two minutes before aspirin 10 milligrams per kilogram

   limitations

   A direct in vivo test of an in vitro observation. One model, one species, and thrombus generation measured indirectly by downstream temperature.

   nutrient_topic

   Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid

   organism

   Rat

   plain_language

   The metabolite gets in the drug’s way in a test tube, but giving it first did not stop aspirin working in a rat.

   primary_references

   [asa-p6792646] Non-interference by salicylate with aspirin inhibition of arterial thrombosis in rats. (1981). https://pubmed.ncbi.nlm.nih.gov/6792646/ DOI: 10.1016/0161-4630(81)90052-5

   tissue_or_cell_type

   Carotid artery

   Aspirin: the serine it acetylates, the enzyme that acetylation creates, the dose that separates platelet from vessel wall, and the metabolite that is a different drug (2026-09-22) · lines 520–531

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Electrically induced carotid artery thrombosis in male rats with salicylate pretreatment · source_derived_draft · unverified_draft

   ### asa-antagonism-not-seen-in-vivo Several authors have reported that salicylate blocks and reverses aspirin inhibition of prostaglandin synthesis by platelets and arterial wall, but when rats were given sodium salicylate at 15 or 100 milligrams per kilogram two minutes before aspirin at 10 milligrams per kilogram, a significant antithrombotic effect of aspirin was observed in all cases regardless of prior salicylate administration with results similar to aspirin alone, so competition between salicylate and aspirin as reported in vitro does not appear to significantly affect the in vivo antithrombotic action in this model. Condition category: normal nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: The metabolite gets in the drug’s way in a test tube, but giving it first did not stop aspirin working in a rat. organism: Rat tissue_or_cell_type: Carotid artery experimental_model: Electrically induced carotid artery thrombosis in male rats with salicylate pretreatment limitations: A direct in vivo test of an in vitro observation. One model, one species, and thrombus generation measured indirectly by downstream temperature. exposure: Sodium salicylate 15 or 100 milligrams per kilogram intravenously two minutes before aspirin 10 milligrams per kilogram evidence_span: {"source_cache": "artifacts/aspirin-research/6792646.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "55b09486e54c42e6ecdac3476a0ae8b9d9819f06b5b01a9fc33087fd621a9c82", "start_char": 0, "end_char": 767, "text_sha256": "55b09486e54c42e6ecdac3476a0ae8b9d9819f06b5b01a9fc33087fd621a9c82"} [asa-p6792646] Non-interference by salicylate with aspirin inhibition of arterial thrombosis in rats. (1981). https://pubmed.ncbi.nlm.nih.gov/6792646/ DOI: 10.1016/0161-4630(81)90052-5

   Complete structured claim and evidence

2. Gpx3 deficiency increased platelet-dependent thrombosis after experimental vascular provocation.

   GPX3 → Arterial thrombosis source_derived_draftliterature_reviewed:direct_experimental
   Experimental context and source evidence

   cell_type

   arterial injury model

   experimental_model

   Gpx3 knockout

   limitations

   Does not establish a human selenium cutoff.

   organism

   mouse

   Selenium: literature corrections and mechanism additions · lines 702–712

   Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Gpx3 knockout · secondary_verified · secondary_verified

   ## gpx3-loss-increases-provoked-thrombosis GPX3-deficient mice formed more thrombus after vascular injury. Gpx3 deficiency increased platelet-dependent thrombosis after experimental vascular provocation. Organism: mouse Cell type: arterial injury model Experimental model: Gpx3 knockout Limitations: Does not establish a human selenium cutoff. Primary reference: [Glutathione Peroxidase-3 Deficiency Promotes Platelet-dependent Thrombosis in vivo](https://pmc.ncbi.nlm.nih.gov/articles/PMC3107543/)

   Complete structured claim and evidence