Physical mechanism of normal-tissue sparing at ultra-high dose rate

Identify the mechanism by which mean dose rates above roughly $4000\ \mathrm{rad}/\mathrm{s}$ ($1\ \mathrm{rad} = 100\ \mathrm{erg}/\mathrm{g}$), delivered in under $200\ \mathrm{ms}$, raise normal-tissue tolerance at fixed total dose (typically $1000\ \text{to}\ 3000\ \mathrm{rad}$ single fraction) without a matching rise in tumour tolerance. Candidate classes: transient radiolytic oxygen depletion, inter-track radical-radical recombination altering peroxidation yields, differential iron and labile metal pools, immune and vascular responses. An answer is a quantitative model reproducing the measured sparing as a function of dose, dose rate, pulse structure and tissue oxygen tension.

A model whose parameters are fixed by independent chemical and physiological measurements and that predicts, without refitting, the sparing measured across electron, proton and photon FLASH experiments in several tissues.