RETINAL DAMAGE FROM HIGH INTENSITY LIGHT

The results of the preceding papers raise the question as to the mechanism involved in retinal damage from exposure to high intensity light. After reviewing the data obtained from histochemical techniques and tissue electrophoresis in particular, it should be stressed that the reported results and interpretations have to be studied carefully since there is a lack of adequate comparison in this relatively unexplored field. The observed changes in the proteinogram of the retina by tissue agar electrophoresis, for instance, have to be examined very critically. I t should be realized that with this method alterations were recorded at the site of a calculated thermal density of 1.0 X 104 cal/cm* and this even if no loss by absorption would have occurred within the zone between center and 2 mm distance. However, it remains to explore the basis of this observation to rule out alterations in membrane changes rather than true protein denaturation. Another observation requiring caution is ,the reduction of B wave amplitude in ERG recordings after light exposure. I t should be stressed that this alteration should not be equaited with functional defect, since the two might not be related at all. Moreover, direct thermocouple measurements as a means of accurate temperature recording in biological structures presents a serious problem. The insertion of a thermocouple into biological structures in itself gives rise to artefacts of reflectance, absorption, and conduction, at the very site in the tissue where measurements are being carried out. The relative size of the thermocouples with respect to image size of the incident light beam on the retina and with regard to the dimensions of the biological structures is of great importance. Temperature rise and thermal conduction within the retina and choroid is an extremely rapid process and can easily be missed or underrated if the response time of the measuring device is of the same order as the time of actual