Component

Serum thromboxane B2 after whole blood clotting

Serum thromboxane B2 after whole blood clotting. Species, exposure and limitations are retained in each linked claim.

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

Read recorded mechanisms Open recursive mind map

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.

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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

What acts on it

  1. Single doses of 6 to 100 milligrams of aspirin produced a linear inhibition of platelet thromboxane B2 production ranging from 12 to 95% after 24 hours, and a daily dose of 0.45 milligrams per kilogram for 7 days produced cumulative and virtually complete inhibition without significantly reducing urinary excretion of prostaglandin E2, prostaglandin F2-alpha or 6-keto-prostaglandin F1-alpha in both men and women, an effect maintained unaltered through one month of therapy with no cumulative inhibition of renal prostaglandin synthesis, while furosemide-induced renal prostacyclin synthesis and renin release were unaffected.

    Aspirin / acetylsalicylic acid → Serum thromboxane B2 after whole blood clotting source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/aspirin-research/7045161.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "58bb82650f675f1ba3dd21b6dcf3d83b71a56c437a687f72d2af9dcdc07abadb", "start_char": 0, "end_char": 1963, "text_sha256": "58bb82650f675f1ba3dd21b6dcf3d83b71a56c437a687f72d2af9dcdc07abadb"}
    experimental_model
    Radioimmunoassay of serum thromboxane B2 and urinary prostaglandin excretion in 46 healthy subjects given single or repeated oral aspirin
    exposure
    Single doses of 6 to 100 milligrams, and 0.45 milligrams per kilogram daily for 7 days and up to one month
    limitations
    The dose-ranging design across 46 subjects is what makes the selectivity claim testable. Urinary prostaglandin excretion is an indirect measure of renal synthesis.
    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
    A very small daily dose wipes out platelet thromboxane and leaves the kidney untouched.
    primary_references
    [asa-p7045161] Selective cumulative inhibition of platelet thromboxane production by low-dose aspirin in healthy subjects. (1982). https://pubmed.ncbi.nlm.nih.gov/7045161/ DOI: 10.1172/jci110576
    tissue_or_cell_type
    Platelets and kidney
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    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 364–375

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radioimmunoassay of serum thromboxane B2 and urinary prostaglandin excretion in 46 healthy subjects given single or repeated oral aspirin · source_derived_draft · unverified_draft

    ### asa-cumulative-and-selective Single doses of 6 to 100 milligrams of aspirin produced a linear inhibition of platelet thromboxane B2 production ranging from 12 to 95% after 24 hours, and a daily dose of 0.45 milligrams per kilogram for 7 days produced cumulative and virtually complete inhibition without significantly reducing urinary excretion of prostaglandin E2, prostaglandin F2-alpha or 6-keto-prostaglandin F1-alpha in both men and women, an effect maintained unaltered through one month of therapy with no cumulative inhibition of renal prostaglandin synthesis, while furosemide-induced renal prostacyclin synthesis and renin release were unaffected. Condition category: biomarker_context 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: A very small daily dose wipes out platelet thromboxane and leaves the kidney untouched. organism: Human tissue_or_cell_type: Platelets and kidney experimental_model: Radioimmunoassay of serum thromboxane B2 and urinary prostaglandin excretion in 46 healthy subjects given single or repeated oral aspirin limitations: The dose-ranging design across 46 subjects is what makes the selectivity claim testable. Urinary prostaglandin excretion is an indirect measure of renal synthesis. exposure: Single doses of 6 to 100 milligrams, and 0.45 milligrams per kilogram daily for 7 days and up to one month evidence_span: {"source_cache": "artifacts/aspirin-research/7045161.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "58bb82650f675f1ba3dd21b6dcf3d83b71a56c437a687f72d2af9dcdc07abadb", "start_char": 0, "end_char": 1963, "text_sha256": "58bb82650f675f1ba3dd21b6dcf3d83b71a56c437a687f72d2af9dcdc07abadb"} [asa-p7045161] Selective cumulative inhibition of platelet thromboxane production by low-dose aspirin in healthy subjects. (1982). https://pubmed.ncbi.nlm.nih.gov/7045161/ DOI: 10.1172/jci110576
    Complete structured claim and evidence

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.

    Aspirin / acetylsalicylic acid → Prostacyclin synthesis by the vessel wall source_derived_draftungraded
    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

  2. Excretion of leukotriene E4 was increased by a mean of 361% during aspirin-induced asthma episodes, but the degree of increase for individual patients did not correlate with the degree of bronchospasm or with inhibition of platelet thromboxane B2 formation, so although endogenous synthesis of potent bronchoconstrictor leukotrienes increases during aspirin-induced bronchospasm it appears unlikely that direct shunting of unmetabolised arachidonate into leukotriene synthesis represents the mechanism of aspirin-induced asthma.

    Urinary leukotriene E4 excretion → Aspirin-induced bronchospasm source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/aspirin-research/1309376.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "115a13f9e08205c2b6ea376e5a1fcb90cc6887b277041acc114908c7d85f6e05", "start_char": 0, "end_char": 1427, "text_sha256": "115a13f9e08205c2b6ea376e5a1fcb90cc6887b277041acc114908c7d85f6e05"}
    experimental_model
    Urinary leukotriene E4 measured during aspirin-induced asthma episodes across a range of provoking doses
    exposure
    Aspirin doses from 30 to 365 milligrams in individual aspirin-sensitive patients
    limitations
    Tests the shunting hypothesis by asking whether the leukotriene rise tracks the bronchospasm, which it does not. Urinary leukotriene E4 is a whole-body measure rather than an airway one.
    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
    The leukotrienes do rise, but how much they rise says nothing about how badly the patient wheezes.
    primary_references
    [asa-p1309376] Increased excretion of leukotriene E4 during aspirin-induced asthma. (1992). https://pubmed.ncbi.nlm.nih.gov/1309376/
    tissue_or_cell_type
    Airway and urine

    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 559–570

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Urinary leukotriene E4 measured during aspirin-induced asthma episodes across a range of provoking doses · source_derived_draft · unverified_draft

    ### asa-shunting-does-not-track Excretion of leukotriene E4 was increased by a mean of 361% during aspirin-induced asthma episodes, but the degree of increase for individual patients did not correlate with the degree of bronchospasm or with inhibition of platelet thromboxane B2 formation, so although endogenous synthesis of potent bronchoconstrictor leukotrienes increases during aspirin-induced bronchospasm it appears unlikely that direct shunting of unmetabolised arachidonate into leukotriene synthesis represents the mechanism of aspirin-induced asthma. 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 leukotrienes do rise, but how much they rise says nothing about how badly the patient wheezes. organism: Human tissue_or_cell_type: Airway and urine experimental_model: Urinary leukotriene E4 measured during aspirin-induced asthma episodes across a range of provoking doses limitations: Tests the shunting hypothesis by asking whether the leukotriene rise tracks the bronchospasm, which it does not. Urinary leukotriene E4 is a whole-body measure rather than an airway one. exposure: Aspirin doses from 30 to 365 milligrams in individual aspirin-sensitive patients evidence_span: {"source_cache": "artifacts/aspirin-research/1309376.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "115a13f9e08205c2b6ea376e5a1fcb90cc6887b277041acc114908c7d85f6e05", "start_char": 0, "end_char": 1427, "text_sha256": "115a13f9e08205c2b6ea376e5a1fcb90cc6887b277041acc114908c7d85f6e05"} [asa-p1309376] Increased excretion of leukotriene E4 during aspirin-induced asthma. (1992). https://pubmed.ncbi.nlm.nih.gov/1309376/
    Complete structured claim and evidence

In the sources

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