Figure 5shows transverse cryostat sections from eyes that had been irradiated for various lengths of time in the absence or presence of PdTCPP. In the absence of the photosensitizer, the irradiated control retina showed good preservation of the laminar structure
(Fig. 5A) , whereas irradiation in the presence of the dye caused edema to various degrees
(Figs. 5B 5C 5D) . Likewise, a 2-minute irradiation resulted in vacuolization, particularly of the inner nuclear and outer plexiform layers
(Fig. 5B) . At 6 minutes, vacuolization had extended into the inner plexiform and ganglion cell layers
(Fig. 5C) . Irradiation for 30 minutes led to severe damage in virtually all retinal layers and thus to a complete loss of laminar organization
(Fig. 5D) . When studied with electron microscopy, irradiation for 30 minutes in the absence of the photosensitizer led to the formation of lamellar bodies throughout the retina, but the overall ultrastructure of retinal parenchyma and vessels appeared normal
(Fig. 6A) . However, in the presence of PdTCPP, irradiation for 2 minutes caused occlusion of small vessels
(Fig. 6B) , thrombus formation
(Fig. 6C) , and heavy damage to the vascular wall
(Figs. 6B 6C) . The neuropil of the inner plexiform layer looked normal
(Fig. 6B) , but damage in the inner nuclear layer was prominent with marked thinning of the glia limitans and swelling of Müller cells but not of the basement membrane
(Fig. 6C) . In regions of minor edema, Müller cells contained remnants of red blood cells (not shown). This indicates that, under certain circumstances, these glial cells are able to function as phagocytes. Taken together, the volume increase of the retina is due to both interstitial and cellular edema, the basement membrane contributing little if at all to fluid absorption. This situation is unlike the one in the optic nerve head, where the abundant extracellular matrix absorbs exudated fluid quite efficiently (cf.
Fig. 3A ).