State, Not Scar · source record · workpaper

Workpaper: latch-state evidence by vessel type, caliber, and persistence (study VASO-S001)

This site (AI-authored project work held in the repository) · 2026

AI-verified citationSRC-VASO-S001

AI-authored study workpaper

This source is the citable container for study VASO-S001 — the full pre-registered criteria, sourced table, and limitations are on the study page. Only the study's aggregate findings carry ledger weight.

identifier / locator: Criteria frozen 2026-09-01 (hash fe5e031b8b8f); table collected 2026-09-01
verification note: Every row cell carries its own citation and verification label on the study page; the aggregate findings are the only ledger-bearing grain.
reliability notes: Secondary synthesis under frozen criteria; the study never grades a claim — the panel judges what it means.
Every row was built from the published abstract; no full text was accessible to the collection, as the study's limitations record.

Evidence drawn from this source

Undermines· moderateVASO-E019

Study table: energetic cost has never been measured in any arteriole, so the economy argument rests entirely on conduit arteries

what the source states: Across sixteen rows spanning 1981-2022, contemporaneous energetic measurement — oxygen consumption, lactate release, or ATP turnover — appears only in large tonic arterial preparations (swine and porcine carotid, at zero transmural pressure), and in no arteriole or resistance microvessel of any bed. No located study satisfies all four conditions the study set: skeletal-muscle arteriole or smaller, physiological temperature and transmural pressure, maintained force or diameter, and a contemporaneous energetic or cycling measurement. The frozen literal queries aimed at microvascular energetics returned nothing, as did two further searches run specifically for arteriole-level oxygen consumption and ATP economy.
what we infer: The energetic feasibility step under VASO-C020 — that a knot can be held cheaply — is an extrapolation across both vessel class and caliber, not a borrowed-and-demonstrated mechanism. The extrapolation may still be correct; what the ledger can now say is that nobody has measured it where the hypothesis needs it, and that this is a gap in the literature rather than a gap in this case's reading of it.
limitations: Absence of a demonstration is not a demonstration of absence; the study's own limitations record that discovery ran against PubMed, Europe PMC and Crossref, which cover the older non-indexed energetics literature poorly.

This site (AI-authored project work held in the repository) (2026)AI-verified citationVASO-C020

Undermines· moderateVASO-E020

Study table: in pressurized skeletal-muscle arterioles, maintained constriction tracks maintained activation rather than the latch signature

what the source states: Three rows are pressurized skeletal-muscle resistance vessels — rat cremaster and gracilis — in which LC20 phosphorylation was measured against diameter. In all three, maintained constriction is accompanied by maintained or rising phosphorylation rather than by force held while activation falls: 27.7% at 30 mmHg rising to 39.6% at 120 mmHg (Zou, Ratz & Hill 1995, at 34 degrees C in roughly 100-micrometre arterioles); a monophasic rise correlated with instantaneous wall tension (Zou, Ratz & Hill 2000); and 40% already at 10 mmHg rising to about 55% at 80 mmHg with no further change to 140 mmHg (Moreno-Dominguez et al. 2013, which attributes the sustained constriction to Rho-kinase-mediated Ca2+ sensitization and actin polymerization). The 2000 paper states that spontaneous arteriolar tone "represents a state of maintained smooth muscle activation that requires increases in [Ca2+]i and myosin light-chain phosphorylation."
what we infer: This is the first record in the case bearing directly on the tissue compartment VASO-C020 names, and it does not fit the latch picture: at arteriole caliber the published measurements show sustained activation, not an economical dephosphorylated hold. It is a mismatch rather than a refutation — none of the three studies was designed as a latch test, all held their stimulus present throughout, and none measured energetic cost. What it removes is the assumption that the arteriole compartment is simply unexamined; it has been examined with the right molecular readout, and what was found there points at a different mechanism for holding constriction.
limitations: All three rows were built from published abstracts; full texts were not accessible, so temperature is recorded for only one of the three and endothelial status for none.
Myogenic tone is by construction a response to a maintained stimulus, so these studies could not have shown input-free persistence even if it exists.

This site (AI-authored project work held in the repository) (2026)AI-verified citationVASO-C020

Qualifies· moderateVASO-E021

Study table: latch behaviour is not generic across vascular smooth muscle, and the divergence was never followed downstream

what the source states: Paired rows from rabbit femoral and saphenous artery record sustained isometric stress at falling intracellular calcium in the femoral (1.3e5 N/m2 at 10 min, MLC phosphorylation 42%) against a 40% stress loss in its own muscular branch (0.8e5 N/m2, phosphorylation 28%), which the authors attribute to expressed motor proteins that do not support latch-bridge formation, together with greater MLC phosphatase. The pressurized follow-up reports the same asymmetry in diameter behaviour. Forward citation chaining from both 2006 papers located no study extending the comparison into arterioles or the microcirculation.
what we infer: VASO-C010 states a capability, and the capability is real — but the ledger should no longer be read as saying that vascular smooth muscle generically latches. The one published comparison between a vessel and its own downstream branch found the behaviour present in the parent and absent one branch order later, which makes vessel type and motor-protein phenotype load-bearing variables rather than incidental ones. That nobody has run the comparison further down is the specific gap VASO-R004's paired-caliber design now exists to close.
limitations: One publication and one laboratory supply both arms of the comparison; the femoral/saphenous divergence has not been independently replicated, and the study records the two 2006 papers as non-independent.
The saphenous artery is a named conduit artery, not a resistance microvessel, so it constrains how far downstream the finding can be read.

This site (AI-authored project work held in the repository) (2026)AI-verified citationVASO-C010