It was shown previously that pressure-induced interruption of axonal transport at the optic nerve head is reversible after 8 hours of raised intraocular pressure (perfusion pressure of 25 to 35 mmHg). Here the authors report experiments on the nature, location, and reversibility of pressure-induced abnormalities of the optic nerve head, including interruption in axonal transport, in eyes subjected to a more extreme pressure insult (perfusion pressure less than 25 mmHg), including some insults that produced total ischemia. After 1/2 to 2 hours of intraocular pressure 10 mmHg greater than ophthalmic artery systolic blood pressure there was hydropic swelling and tissue necrosis in the anterior lamina cribrosa, the optic nerve head, and the retina. Organelle accumulation, identifying the locus of interruption in retrograde fast axonal transport, occurred exclusively within the posterior one-third of the lamina cribrosa. The degree of these changes and the number of axons involved related to the duration of the raised pressure in eyes studied 24 hours after this severe pressure insult. These tissue changes appeared to have been irreversible after a 4-hour insult and partly irreversible after a 1- or 2-hour insult. In eyes studied 2 weeks later diffuse axon atrophy was apparent across the extent of the optic nerve section after a 4-hour insult, and there was partial atrophy after a 1- or 2-hour insult. After 4 hours of slightly lower intraocular pressure levels (perfusion pressure of 10 to 20 mmHg) the irreversible nerve head injury was less extensive; after 4 hours of even lower pressure levels (perfusion pressures of 25 to 30 mmHg) no permanent nerve injury was identified. Thus at least some axons can survive total ischaemia for 2 hours, which is longer than the ganglion cells of the retina can survive ischaemia. A milder insult produces a partial injury that can be reversible after a much longer duration of the insult.
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience