Intraocular pressure is set by a fluid balance between how fast the ciliary body makes aqueous humor and how fast it leaves the eye. At steady state this is the Goldmann equation:
IOP = (F − F_u) / C + P_v
F = aqueous humor production rate (µL/min)
F_u = pressure-independent uveoscleral outflow (µL/min)
C = trabecular outflow facility (µL/min per mmHg)
P_v = episcleral venous pressure (mmHg)
Aqueous is secreted by the ciliary processes, crosses the posterior and anterior chambers, and drains two ways: most of it (F − F_u) is pressure-driven flow through the trabecular meshwork into Schlemm's canal and the episcleral veins — this pathway's conductance is C, so raising IOP pushes more fluid through it, exactly like current through a resistor obeying Ohm's law. The rest, F_u, leaves through the uveoscleral pathway (between ciliary muscle bundles into the suprachoroidal space) at a rate that does not depend on IOP.
- Inflow rate F — ciliary body secretion. Beta-blockers and carbonic-anhydrase inhibitors reduce F.
- Outflow facility C — trabecular meshwork conductance. In primary open-angle glaucoma the meshwork stiffens and clogs with debris, C falls, and IOP rises even though F is unchanged. Cholinergics (pilocarpine) and trabecular procedures raise C.
- Episcleral venous pressure Pv — the downstream back-pressure the trabecular pathway drains against; it sets the floor IOP can never go below regardless of C.
- Uveoscleral outflow Fu — prostaglandin analogs (latanoprost) are first-line glaucoma therapy specifically because they increase this pressure-independent term.
The particles you see are colour-coded by which pathway carries them: teal particles exit through the trabecular meshwork grid at the iridocorneal angle, amber particles slip out through the uveoscleral gap near the ciliary body root. When C is lowered, meshwork particles back up in the anterior chamber before finding a pore — a direct visual of how meshwork resistance, not overproduction, is the dominant cause of chronically elevated IOP in glaucoma.