advertisement

---

Gullstrand Meeting

Upsalla, June 2002

The Gullstrand Glaucoma Meeting is organized every year during spring (this year late spring) in Uppsala, Sweden by Albert Alm (helped by Paul Kaufman). There are some 6-8 speakers that present an update on their topic of expertise followed by an extensive discussion. Here follow two selected Top-Ten/Five reports.

Top-Ten on Aqueous Humor Flow

  Jay McLaren

• Aqueous humor flows through the anterior chamber at a rate of 3.0 ± 0.8 µl/min (mean ± SD) in the morning and 1.3 ± 0.4 µl/min during sleep, as measured by fluorescein dilution in a normal population.
• The circadian changes in aqueous humor flow are most likely driven by the circadian activity of the sympathetic nerves and circulating epinephrine. Corticosteroids enhance the flow-stimulating effect of epinephrine.
• Three classes of drugs suppress aqueous humor formation. These are: b-adrenergic antagonists, a₂-adrenergic agonists, and carbonic anhydrase inhibitors.
• b-adrenergic antagonists reduce flow during the day by 40%, to about the same flow rate as during sleep. They do not suppress the already-diminished flow during sleep.
• a₂-adrenergic agonists decrease flow during the day by 33% and during sleep by 27%. Carbonic anhydrase inhibitors decrease flow during the day by 19% (topical) and 25% (systemic), and during sleep by 16% (topical) and 24% (systemic).
• b- and a₂-adrenergic receptors in the ciliary epithelium are linked to Na,K-ATPase activity; b stimulation increases movement of sodium into the aqueous humor and a₂ stimulation decreases sodium movement. Water is drawn osmotically with sodium and becomes aqueous humor. During the day, its transfer rate (aqueous humor formation rate) decreases as b receptors are blocked or as a₂ receptors are stimulated.
• Carbonic anhydrase in the ciliary epithelium catalyzes the production of bicarbonate from carbon dioxide and water, and bicarbonate movement to aqueous humor osmotically draws water that becomes aqueous humor. Carbonic anhydrase inhibitors reduce aqueous humor flow by slowing this reaction and reducing the production and transfer rate of bicarbonate.
• Aqueous humor flow does not increase or decrease with either chronic or transient increases or decreases in intraocular pressure through a moderate range.
• Aqueous humor flow rate decreases with age by about 4% per decade of life.
• Substances are washed out of the anterior chamber by aqueous humor flow with a half-life of about 46 minutes, and substances such as fluorescein that distribute between the anterior chamber and cornea disappear with a half-life of about 4.5 hours.

Top-Five on Ischemia

 Jack Cioffi

• Chronic Ischemia Model - We have developed a model of chronic optic nerve ischemia, based on local endothelian application which has been applied in multiple animals from rats to non-human primates. This model results in approximately 30% decrease in bloodflow to the anterior optic nerve, and the eyes have been evaluated in vivo and post-mortem.
• Temporal Optic Nerve Preferential Axonal Loss - There is a preferential loss of the temporal optic nerve axons in our model of chronic ischemia in the primate eye.
• Glial Elements May Be The Important Intermediary - We have proposed that glial cells are a potential link between induced ischemia and dysfunction/death of the optic nerve fibers.
• Increased Temporal Susceptibility - We know that the temporal optic nerve is more susceptible to damage in Glaucomatous Optic Neuropathy associated with high intraocular pressure. This is the first evidence that a purely ischemic insult also causes preferential temporal loss.
• Temporal Optic Nerve Differences - The questions remains, what is unique about the temporal optic nerve making it more susceptible to several different mechanisms of damage?