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It has been postulated that the delivery of radiotherapy at ultra-high doserates ("FLASH") reduces normal tissue toxicities by depleting them of oxygen.The fraction of normal tissue and cancer cells surviving radiotherapy dependson dose and oxygen levels in an exponential manner and even a very smallfraction of tissue at low oxygen levels can determine radiotherapy response.The effect of FLASH on radiation-induced normal and tumour tissue cell killingwas studied by simulating oxygen diffusion, metabolism, and radiolytic oxygendepletion over domains with simulated capillary architectures. Twoarchitectural models were used: 1.) randomly distributed capillaries and 2.)capillaries forming a regular square lattice array. The resulting oxygenpartial pressure distribution histograms were used to simulate normal andtumour tissue cell survival using the linear quadratic model of cell survival,modified to incorporate oxygen-enhancement ratio (OER) effects. Tumour cellsurvival was found to be increased by FLASH as compared to conventionalradiotherapy, with a 0-1 order of magnitude increase for expected levels oftumour hypoxia, depending on the relative magnitudes of radiolytic oxygendepletion and tissue oxygen metabolism. Interestingly, for the random capillarymodel, the impact of FLASH on well-oxygenated (normal) tissues was found to bemuch greater, with an estimated increase in cell survival by up to 10 orders ofmagnitude, even though reductions in mean tissue partial pressure were modest,less than 7 mmHg for the parameter values studied. The presence of very smallnearly hypoxic regions in otherwise well-perfused normal tissues with high meanoxygen levels resulted in a greater proportional sparing of normal tissue thantumour cells during FLASH irradiation, possibly explaining empirical normaltissue sparing and iso-tumour control results.

Modeling the impact of spatial oxygen heterogeneity on radiolytic oxygen depletion during FLASH radiotherapy