Abstract

PurposeTo estimate the threshold radiant exposure for 1090 nm IRR and the time evolution of lens damage; To determine the temperature time evolution in the eye during the previously found threshold exposure, and the associated heat diffusion; To investigate if 1090 nm IRR induces cataract photochemically considering irradiance exposure time reciprocity.MethodsThe 6‐weeks‐old albino rats were anesthetized intraperitoneally, ten min before exposure. The pupils of both eyes were dilated with tropicamide. Five min after pupil dilation, the animals were unilaterally exposed to 1090 nm IRR within the pupil area. Temperature was recorded with thermocouples placed in the selected positions of the eye. At the planned post‐exposure time, the animal was sacrificed and the lenses were extracted for measurements of forward light scattering and macroscopic imaging.ResultsThe in vivo exposure to 197 W/cm2 1090 nm IRR required a minimum 8 s for cataract induction with a delayed onset of approx 16 h. The same radiant exposure was found to cause a temperature increase of 10°C at the limbus and 26°C close to the retina. The in vivo exposure to 96 W/cm2 1090 nm IRR with exposure time up to 1 h resulted in an average temperature elevation of 7°C at the limbus with the cornea humidified and no significant light scattering was induced one week after exposure.ConclusionsAn in vivo exposure to 197 W/cm2 IRR at 1090 nm within the pupil for 8 s induces cataract with a time delay. This threshold exposure causes a temperature rise of 10°C at the anterior segment of the rat eye. IRR at 1090 nm produces thermal cataract, probably by indirect heat conduction from absorption in tissues surrounding the lens. There is no cataract development given that the limbal temperature increase is below 8ºC.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call