Characterizing temperature-dependent photo-oxidation to explain the abrupt transition from thermal to non-thermal laser damage mechanisms at 413 nm

Abstract

Laser exposure duration dictates whether tissues subjected to short visible wavelengths (≤ 514 nm) are damaged by thermal (e.g. 0.1 s) or non-thermal (≥ 100 s) mechanisms. Somewhere between these extremes, an abrupt transition between the two damage mechanisms has been found for both in vitro and animal retinal models. Non-thermal (photochemical) damage is characterized by an inverse relationship between damage threshold irradiance and exposure duration (irradiance reciprocity). We have found that exposures of 60 – 90 s in an in vitro retinal model require radiant exposures well above the expected requirement for non-thermal damage, which thus led to damage by thermal mechanisms. Here we characterize and describe with computational modeling the temperature dependence of photo-oxidative processes between 37-45 °C.Laser exposure duration dictates whether tissues subjected to short visible wavelengths (≤ 514 nm) are damaged by thermal (e.g. 0.1 s) or non-thermal (≥ 100 s) mechanisms. Somewhere between these extremes, an abrupt transition between the two damage mechanisms has been found for both in vitro and animal retinal models. Non-thermal (photochemical) damage is characterized by an inverse relationship between damage threshold irradiance and exposure duration (irradiance reciprocity). We have found that exposures of 60 – 90 s in an in vitro retinal model require radiant exposures well above the expected requirement for non-thermal damage, which thus led to damage by thermal mechanisms. Here we characterize and describe with computational modeling the temperature dependence of photo-oxidative processes between 37-45 °C.