Component

Template bleeding time

Template bleeding time. Species, exposure and limitations are retained in each linked claim.

1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

Where it participates (unsigned role)

  1. Two hours after 150 or 300 milligrams of aspirin, 81 to 100% inhibition of vein-wall prostacyclin synthesis was demonstrated with 86% inhibition still evident in one subject at eight hours, while platelet thromboxane B2 production was completely inhibited for more than 24 hours, leading to the conclusion that there is little difference between the initial inhibitory response of platelet cyclooxygenase and that of vessel-wall cyclooxygenase to these doses, and that the prolonged bleeding time after aspirin is not a consequence of selective inhibition of platelet thromboxane production.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/aspirin-research/7003384.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b54b61e084b6ec232b9c86ef5de713b0d5a57def2525eb6d3d50e5d7768e5c38", "start_char": 0, "end_char": 1148, "text_sha256": "b54b61e084b6ec232b9c86ef5de713b0d5a57def2525eb6d3d50e5d7768e5c38"}
    experimental_model
    Vein segments and platelets sampled from five subjects before and after aspirin, with radioimmunoassay of stable metabolites
    exposure
    150 or 300 milligrams of oral aspirin
    limitations
    Five subjects, and the vein segments are surgically obtained rather than sampled in situ. Its conclusion is the opposite of the low-dose study in this collection and the doses differ tenfold.
    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
    Human
    plain_language
    At ordinary tablet doses the vessel wall is hit about as hard as the platelet.
    primary_references
    [asa-p7003384] Inhibition of prostacyclin and platelet thromboxane A2 after low-dose aspirin. (1981). https://pubmed.ncbi.nlm.nih.gov/7003384/ DOI: 10.1056/nejm198101083040203
    tissue_or_cell_type
    Vein wall and platelets

    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 377–388

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Vein segments and platelets sampled from five subjects before and after aspirin, with radioimmunoassay of stable metabolites · source_derived_draft · unverified_draft

    ### asa-no-selectivity-at-higher-dose Two hours after 150 or 300 milligrams of aspirin, 81 to 100% inhibition of vein-wall prostacyclin synthesis was demonstrated with 86% inhibition still evident in one subject at eight hours, while platelet thromboxane B2 production was completely inhibited for more than 24 hours, leading to the conclusion that there is little difference between the initial inhibitory response of platelet cyclooxygenase and that of vessel-wall cyclooxygenase to these doses, and that the prolonged bleeding time after aspirin is not a consequence of selective inhibition of platelet thromboxane production. 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: At ordinary tablet doses the vessel wall is hit about as hard as the platelet. organism: Human tissue_or_cell_type: Vein wall and platelets experimental_model: Vein segments and platelets sampled from five subjects before and after aspirin, with radioimmunoassay of stable metabolites limitations: Five subjects, and the vein segments are surgically obtained rather than sampled in situ. Its conclusion is the opposite of the low-dose study in this collection and the doses differ tenfold. exposure: 150 or 300 milligrams of oral aspirin evidence_span: {"source_cache": "artifacts/aspirin-research/7003384.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b54b61e084b6ec232b9c86ef5de713b0d5a57def2525eb6d3d50e5d7768e5c38", "start_char": 0, "end_char": 1148, "text_sha256": "b54b61e084b6ec232b9c86ef5de713b0d5a57def2525eb6d3d50e5d7768e5c38"} [asa-p7003384] Inhibition of prostacyclin and platelet thromboxane A2 after low-dose aspirin. (1981). https://pubmed.ncbi.nlm.nih.gov/7003384/ DOI: 10.1056/nejm198101083040203
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards