ABSTRACT
It is fair to say that in 2003 we have a better understanding of glaucoma than did our counterparts of the early years of the last century, but that many of the questions from that era remain unanswered. Sometime during the middle to latter part of the last century the idea gradually became accepted that glaucoma was more than just the IOP compressing the optic nerve head.15 The role of many other factors, especially those involving peripheral and ocular blood flow, began to be considered and investigated, especially by the laboratories of Stephen Drance in Vancouver, BC and of his student Josef Flammer in Basel. Largely influenced by them, we, in 1994, set out to develop a multidisciplinary laboratory that would strive to develop non-pressure models of glaucoma.At first, the group focused on the ischemia to induce a glaucoma model. This, not surprisingly, has proved difficult, perhaps because we have isolated just one factor. We have chronically diminished optic nerve blood flow in monkeys by continuous administration of low dose endothelin-1 to the peri-optic neural space, sufficient to create ischemia but insufficient to induce infarction.These monkeys have mimicked some aspects of glaucoma by selective loss of temporal retinal ganglion cells and their axons, regional activation of the optic nerve and retinal glial tissues, and localized electrophysiological deficits.16
Interpretation of this work and of the many other studies of ocular blood flow is hampered by the lack of good technology that directly measures the velocity of blood flow in the pertinent vessels of the prelaminar and laminar regions of optic nerve in human subjects.17
