Plasma membrane disruption underlies injury of the corneal endothelium by ultrasound

The nature and the extent of acute injury to corneal endothelial cells caus ed by exposure to ultrasound radiation were characterized, as well as the l ong-term reaction of these cells to this form of injury. It was found that the degree of lethal cell injury induced by ultrasound scaled with exposure intensity and duration. Immediate changes in plasma membrane permeability were induced by ultrasound exposure. This ultrasound-induced permeability c hange was, however, transient in many cells, allowing them to trap and reta in a normally impermeant tracer, fluorescein dextran, in cytosol. Microvill i were present on ultrasound treated cells in far greater density than on c ontrol cells, characteristic of exocytosis-based resealing. Cultures contai ning a majority of transiently permeabilized endothelial cells were morphol ogically indistinguishable from untreated control cultures, and the fluores cein dextran-labeled cells in these populations locomoted and divided norma lly. We conclude that cell death due to ultrasound exposure can occur rapid ly via a necrotic mechanism that can be attributed to mechanically induced damage to the plasma membrane. However, not all cells injured become necrot ic: some survive and appear to behave normally after exposure. Conditions t hat favor plasma membrane disruption resealing, e.g. that result in sub-let hal rather than lethal cell injury, map mitigate the reduction in corneal e ndothelial cell density consequent on phacoemulsification and aspiration su rgery. (C) 1999 Academic Press.