Component

Maintenance of normothermia by external heat support

Maintenance of normothermia by external heat support. Species, exposure and limitations are retained in each linked claim.

1 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

Where it participates (unsigned role)

  1. In stroke mice, dihydrocapsaicin infusion begun 90 minutes after the start of reperfusion produced hypothermia, decreased infarct volume by 87% and improved neurofunctional score, and the hypothermic and neuroprotective effects were absent in TRPV1 knockout mice or in mice maintained normothermic with heat support.

    Hypothermia induced by a drug rather than by physical cooling → Cerebral infarct volume source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/dihydrocapsaicin-research/24305062.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17", "start_char": 0, "end_char": 1711, "text_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17"}
    experimental_model
    Focal cerebral ischaemia-reperfusion in conscious wild-type and TRPV1 knockout mice with osmotic-pump infusion
    exposure
    Dihydrocapsaicin 1.25 mg/kg subcutaneously, begun 90 minutes after the start of reperfusion, with normothermia by external heat support as a control arm
    limitations
    The two control arms are what make this the strongest record here: the knockout shows the receptor is required, and the heat-support arm shows the temperature drop rather than receptor activation is what protects.
    nutrient_topic
    Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
    organism
    Mouse
    plain_language
    The stroke damage fell by almost nine tenths, and only when the animal was actually allowed to get cold.
    primary_references
    [dhc-p24305062] Pharmacologically induced hypothermia via TRPV1 channel agonism provides neuroprotection following ischemic stroke when initiated 90 min after reperfusion. (2014). https://pubmed.ncbi.nlm.nih.gov/24305062/ DOI: 10.1152/ajpregu.00329.2013
    tissue_or_cell_type
    Brain and cardiovascular system
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 309–320

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Focal cerebral ischaemia-reperfusion in conscious wild-type and TRPV1 knockout mice with osmotic-pump infusion · source_derived_draft · unverified_draft

    ### dhc-infarct-reduction In stroke mice, dihydrocapsaicin infusion begun 90 minutes after the start of reperfusion produced hypothermia, decreased infarct volume by 87% and improved neurofunctional score, and the hypothermic and neuroprotective effects were absent in TRPV1 knockout mice or in mice maintained normothermic with heat support. Condition category: machinery_impairment nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: The stroke damage fell by almost nine tenths, and only when the animal was actually allowed to get cold. organism: Mouse tissue_or_cell_type: Brain and cardiovascular system experimental_model: Focal cerebral ischaemia-reperfusion in conscious wild-type and TRPV1 knockout mice with osmotic-pump infusion limitations: The two control arms are what make this the strongest record here: the knockout shows the receptor is required, and the heat-support arm shows the temperature drop rather than receptor activation is what protects. exposure: Dihydrocapsaicin 1.25 mg/kg subcutaneously, begun 90 minutes after the start of reperfusion, with normothermia by external heat support as a control arm evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/24305062.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17", "start_char": 0, "end_char": 1711, "text_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17"} [dhc-p24305062] Pharmacologically induced hypothermia via TRPV1 channel agonism provides neuroprotection following ischemic stroke when initiated 90 min after reperfusion. (2014). https://pubmed.ncbi.nlm.nih.gov/24305062/ DOI: 10.1152/ajpregu.00329.2013
    Complete structured claim and evidence

In the sources

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

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