Pathogenesis of block of rapid orthograde axonal transport by elevated intraocular pressure

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Abstract

The subject was investigated in 40 rhesus monkeys. The perfusion pressure (PP) in the eye was altered by changing the blood pressure (BP) and/or intraocular pressure (IOP). Rapid orthograde axoplasmic transport was studied by intravitreal injection of 100 μCi of [3H]leucine and light microscopic autoradiography. The study was planned to determine whether the presence and degree of rapid orthograde axoplasmic flow blockage relate more closely to the level of IOP (suggesting a mechanical basis) or of PP (suggesting an ischemic mechanism). It proved technically impossible to maintain IOP and PP at desired levels for the necessary period (6–712hr)—this difficulty has never been admitted in the literature. Several biological and technical variables also confounded the interpretation of the data, e.g. non-availability of a reliable technique to ascertain the exact PP in the vessels of the optic nerve head, lack of information on the blood flow and the nutritive capability of a given PP, possible artefacts by the perfusion pump used to alter BP, and marked limitations of routine microscopic autoradiography in quantifying exactly the axoplasmic flow blockage. As a result an intensive and sustained study offers only inconclusive results, and cannot resolve the controversy as to whether the axoplasmic flow blockage is due to ischemia or mechanical compression of the nerve fibers in the optic nerve head. Although no single observation is absolutely decisive one way or the other, the sum total of the various evidence put together is somewhat suggestive that the axonal blockage is probably mediated by ischemic mechanism.

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This paper was presented in abridged form at the International Glaucoma Committee Meeting in Nara (Japan) in May 1978.

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