Sodium fluorescein and fluorescinated dextrans (FD) of selected molecular weights were combined and perfused into the anterior chamber of normal and inflamed eyes of cynomolgus monkeys. The eyes were dissected into iris, anterior and posterior uvea, anterior and posterior sclera, retina and intraocular fluids (excluding aqueous). Each tissue was homogenized and centrifuged and the supernatant was run through a gel-fltration column to separate the fluorescent tracers. Each of the resultant peaks was quantitated and facility of uveoscleral outflow was determined. In control eyes the calculated facility of uveoscleral outflow was very similar with all tracers (from 0·047-to 0·052 μl min-1 mmHg-1) and each tracer was found in highest concentration in the anterior sclera and anterior uvea. In inflamed eyes the calculated facility of uveoscleral outflow increased two- to five-fold with each tracer (0·12-; 0·17-; 0·29-; and 0·24 μl min-1 mmHg-1 with fluorescein, and the fluorescinated dextrans of MWs 4000, 40 000 and 150 000, respectively). Each tracer was found in the anterior sclera and uvea in inflamed eyes whereas the posterior sclera and uvea contained predominantly the higher molecular-weight tracers (MWs 40 000 and 150 000). It is concluded that iridocyclitis causes an increase in uveoscleral outflow by increasing the permeability of the anterior uvea to all tracers and fluid. Small tracers may then diffuse into uveal blood vessels or across the sclera, yielding lower values for uveoscleral outflow. Of the four tracers studied, the optimal tracer size for studying uveoscleral outflow in either normal or inflamed eyes is MW 40 000.
|Original language||English (US)|
|Number of pages||8|
|Journal||Experimental Eye Research|
|State||Published - Oct 1987|
Bibliographical noteFunding Information:
This work was SUl)l)orted by NIH grant EY-03277 ahd the ,lames S. Adams Research Scholar Award fi'om Research to Prevent Blindness (to Dr Pederson).
- Cynomolgus monkey
- uveoscleral outflow