Real capillary walls are one endothelial cell thick, sealed by VE-cadherin tight junctions and a glycocalyx layer. In sepsis, circulating IL-6 and TNF-α bind endothelial receptors and trigger RhoA-mediated contraction of the cytoskeleton, pulling VE-cadherin junctions apart. This is capillary leak syndrome — the mechanism behind refractory hypotension and edema in septic shock.
Fluid movement across the wall follows the Starling–Landis equation:
J_v = K_f · [ (P_c − P_i) − σ·(π_c − π_i) ]
K_f = filtration coefficient (junction "leakiness")
σ = albumin reflection coefficient (1 = wall blocks albumin, 0 = fully open)
P_c, P_i = capillary / interstitial hydrostatic pressure
π_c, π_i = capillary / interstitial oncotic (protein) pressure
- Storm intensity raises the target junction permeability, which both increases Kf (small pores open, water leaks first) and lowers σ (large pores open, albumin follows).
- Once albumin leaks into the interstitium, πi rises and πc falls, collapsing the oncotic gradient that normally pulls fluid back in — a self-reinforcing "leaky bucket" that keeps filling the tissues even as the vessel empties.
- Anti-cytokine therapy (e.g. corticosteroids, IL-6 blockade) suppresses the target permeability, letting junctions reseal over a few seconds of simulated time.
- IV fluid resuscitation refills intravascular volume directly, but at high permeability much of it filters straight through the same leaky junctions — the clinical dilemma of treating septic shock with fluids alone.
- Mean arterial pressure is approximated from intravascular volume via a simplified Frank–Starling-style relation; it is illustrative, not a validated hemodynamic model.