Perfusion / vascular layer (mesenteric ischaemia, ischaemic colitis, NAFLD/MASLD metabolic overlap)

The perfusion / vascular layer rides a new Tier-3 primitive: a perfusion-viability switch — the R19 element in the viable basin with bias h = perfusion − demand. Chronic mesenteric ischaemia (intestinal angina) is the perfusion margin falling as a meal raises demand until it crosses to deficit, resolved by revascularisation. Acute mesenteric ischaemia (and ischaemic colitis) is a forced viable→ischaemic flip with a time-critical salvage window: reperfusion recovers the tissue only inside it. The NAFLD/MASLD overlap reuses the §12 type-2 homeostat unchanged, with the lipid-deposition layer declared a circulatory seam.

The third Tier-3 primitive is a perfusion-viability switch: the §2 R19 double well ds/dt = g·s − s³ + h resting in the viable basin at s = +√g, with the bias h = perfusion − demand (vendored single-source as perfusion_threshold / viability_margin / tissue_viable in the substrate). The first reading is chronic mesenteric ischaemia — intestinal angina: at a fixed marginal perfusion the reserve above the rescue threshold falls as metabolic demand rises, so a meal pushes the viability margin negative (post-prandial pain, food-aversion), and revascularisation (stent / bypass) lifts supply so the margin is positive across the demand range again. The second reading is acute mesenteric ischaemia (and its colonic counterpart, ischaemic colitis): a sudden occlusion drops perfusion past demand minus the spinodal and the tissue flips discontinuously into the ischaemic basin; the decisive feature is the salvage window — restoring flow recovers the tissue only if perfusion returns above demand + spinodal (a reserve window = 2·spinodal), so partial or late reperfusion stays infarcted (the time-critical revascularisation of clinical practice). The third reading is the NAFLD / MASLD metabolic overlap: it shares its insulin-resistance driver with the §12 diabetes axis, so rather than refit a parameter this layer reuses the §12 type-2 gain-loss homeostat unchanged, while the lipid-deposition step (hepatic triglyceride accumulation) is declared a circulatory seam handed across the firewall. The demand-driven margin collapse, the revascularisation rescue, the forced occlusion flip, the time-critical salvage window, and the s12 reuse are [V], the ischaemic-flip and rescue thresholds exact spinodal identities [F]; the absolute perfusion-pressure and metabolic-demand scales (model units), the structural infarction endpoint — transmural necrosis, perforation (need a tissue-injury layer) — and the hepatic lipid-deposition layer (circulatory's) are [O] with stated obstacles.

The first three Tier-3 primitives (relapsing inflammation, autocatalytic autodigestion, and — with the cancer kernel — metaplasia) covered the mucosa, the gland and the cell. This section opens the perfusion / vascular layer none of them touch: an intestinal tissue is viable only while its blood supply meets its metabolic demand, and the diseases of that balance — mesenteric ischaemia, ischaemic colitis, and the metabolic fatty-liver overlap — turn on a supply-versus-demand switch. Like every layer here it is not new dynamics: a perfused tissue is the §2 R19 switch ds/dt = g·s − s³ + h resting in the viable basin, with the bias h = perfusion − demand. Nothing is fitted; the thresholds are exact spinodal identities and the single anchor is one bisection.

The first reading is chronic mesenteric ischaemia — "intestinal angina". At a fixed marginal perfusion (a stenosed mesenteric artery), the reserve of supply above the rescue threshold falls as metabolic demand rises; a meal raises demand and pushes the margin negative, so pain follows eating and the patient becomes food-averse. The viability margin crosses from positive (viable) to negative (ischaemic) exactly as the post-prandial demand climbs:

The treatment is geometric, not pharmacological: revascularisation (stent or bypass) lifts the perfusion supply so the margin is positive again across the whole demand range — the post-prandial pain resolves because the meal no longer outruns the supply.

The second reading is acute mesenteric ischaemia (and its colonic counterpart, ischaemic colitis): a sudden occlusion drops perfusion below demand − spinodal (here a flip threshold of 0.215) and the tissue flips discontinuously from the viable basin into the ischaemic one. The clinically decisive feature is the salvage window: restoring flow recovers the tissue only if perfusion returns above demand + spinodal (a reserve window of 0.770); a partial or late reperfusion leaves it in the infarcted basin. The sweep shows viable tissue holding, then flipping, then failing to recover under partial flow:

The third reading is the NAFLD / MASLD metabolic overlap. Metabolic-associated fatty liver shares its insulin-resistance driver with the §12 diabetes axis — so rather than introduce a new parameter, this layer reuses the section-12 type-2 gain-loss homeostat unchanged (reuses_s12_type2_gain_loss = True). The lipid-deposition step itself (hepatic triglyceride accumulation, the cholesterol-delivery dynamics) is declared a circulatory seam, not modelled here: this package keeps only the perfusion-viability switch and the reused glucose homeostat, and hands the lipid layer across the firewall. This circulatory lipid-deposition seam is now wired in §27: the lipid load rests on the consumed circulatory hepatic perfusion, the handling staying circulatory’s [O].

Treatment (model reading). Mesenteric ischemia -- RESTORE perfusion: the model's lever is raising the splanchnic supply above the demand-dependent rescue threshold (demand + spinodal), i.e. revascularization (angioplasty/stent or bypass) for chronic 'intestinal angina', and URGENT revascularization for acute occlusion because re-perfusion recovers the tissue only within the salvageable ischemic window -- past structural infarction (cell death) no parameter move helps (resect dead bowel). Lowering the post-prandial demand (small frequent meals) raises the margin symptomatically. NAFLD/MASLD -- the metabolic lever is restoring insulin sensitivity (as type-2 diabetes) and reducing lipid load; the lipid-handling and fibrosis layer is a `circulatory` seam. GI bleeding / angiodysplasia are sibling-owned vascular events. Target directions [V]; absolute perfusion/demand scales, the infarct timescale, and the lipid layer [O].

The demand-driven collapse of the viability margin, the revascularisation rescue, the forced acute occlusion flip, the time-critical salvage window, and the reuse of the §12 type-2 homeostat are forced by the substrate [V], with the ischaemic-flip and rescue thresholds exact spinodal identities [F]. What stays open [O], each with its obstacle: the absolute perfusion-pressure and metabolic-demand scales (model units needing clinical calibration), the structural infarction endpoint — transmural necrosis, perforation — which needs a tissue-injury layer, and the hepatic lipid-deposition layer, which is circulatory's.