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Top-Ten Glaucoma Meeting Basel: A sick eye in a sick body?
October 18-19, 2001, Basel, Switzerland
Josef Flammer
- Astrocyte activation is a key factor in the development of glaucomatous optic neuropathy, especially for tissue remodelling.
- Optic nerve head astrocytes express MHC-II molecules and NOS-2. The same type of gene expression in astrocytes can be induced in vitro by both mechanical stress and ischemia.
- NO and Endothelin-1 are involved in the regulation of both aqueous humor homeostasis and ocular blood flow regulation.
- The increased production of NO· in astrocytes, together with the increased production of O2·¯ in neural axons, leads to the damaging ONOO· (peroxynitrite).
- Endothelin in the plasma of normal- and high-tension glaucoma patients is increased to a level that may influence ocular perfusion. Such an increase of endothelin concentration is not specific to glaucoma, but also occurs in other diseases, especially in patients with autoimmune diseases.
- Perfusion of the retina and choroid in healthy subjects is autoregulated. Retinal blood flow is (among other things) regulated by pO2 and pCO2, while chorioidal blood flow is regulated by pCO2 and NO.
- Glaucoma patients with progressive damage despite decreased IOP have disturbed autoregulation of ocular perfusion, similar to that observed in healthy vasospastic subjects.
- On average, vasospastic patients tend to have prolonged sleep-onset latency, less thirst, and a lower body mass index.
- Sleep apnea is an established risk factor for glaucomatous damage.
- Leukocytes in the circulating blood of glaucoma patients have increased numbers of DNA breaks and a characteristic altered gene expression.
