Uveoscleral Routes Research Articles

Effects of atropine on aqueous humor dynamics in the vervet monkey ( Cercopithecus ethiops)

The effects of various doses of atropine on aqueous humor dynamies in vervet monkeys were studied by methods giving data for intraocular pressure, recipient venous pressure, gross facility of outflow, bulk flow of anterior chamber fluid into the general circulation and bulk flow into uveoscleral routes. Atropine (3 μg/ml) perfused through the anterior chamber enhanced uveoscleral flow by 0·41±0·08 μl/min and produced a corresponding reduction in flow into the general circulation. In control eyes, after the induction of anesthesia, there was an increase in the gross facility of outflow of 0·33±0·09 μl. min−1. mmHg−1. In atropine-treated eyes there was no significant increase in facility. Atropine (3 μg/ml) did not significantly change the rate of aqueous humor production, the intraocular pressure or the recipient venous pressure. Pseudofacility was not appreciably influenced by atropine.

Effects of atropine and pilocarpine on aqueous humour dynamics in cynomolgus monkeys ( Macaca irus)

The influence of anterior chamber infusion of atropine (10 μg/ml) on intraocular pressure, outflow facility, rate of aqueous humour formation, and the routes for aqueous humour drainage was studied in anaesthetized cynomolgus monkeys. [ 131 I]Albumin was used to determine the flow of aqueous humour from the atropine-treated eye; [ 125 I]albumin was used in the control eye. Atropine produced no significant changes in “gross” facility of outflow and aqueous humour drainage by vascular routes. It reduced the intraocular pressure 2·0 mmHg and raised the average rate of aqueous humour production from 2·28 to 2·54 μl/min. This rise was probably significant, P < 0·05. The average flow by way of uveo-scleral routes was raised from 0·90 to 1·07 μl/min; this rise was probably significant also, P < 0·05. A small dose of pilocarpine (5 μg/ml) known to have little or no effect on refraction and a variable effect on facility of outflow reduced the rate of uveo-scleral flow. Atropine inhibited this effect probably by preventing a localized contraction of the longitudinal fibres of the ciliary muscle. Autoradiography was used to demonstrate the effect of atropine and pilocarpine on the flow through uveo-scleral routes.

Formation and drainage of aqueous humour in cats

Radioactive albumin was used to determine the rate of aqueous humour production in cats and to study the routes for the bulk drainage of aqueous humour. The results show that more than 97% of the bulk flow of aqueous humour passes out by routes that drain into intrascleral veins and that less than 3% passes out by uveo-scleral routes. The average net rate of aqucous humour production was 14·4±0·9 μl/min. The “gross” facility of outflow was 1·56±0·20 μl/min/mmHg. The intraocular pressure was 17·4±1·3 mmHg at the start of the experiments and 19·2±1·5 mmHg at the end. The volume of the anterior chamber was about 0·72 ml. The intrascleral venous pressure (calculated from data for the mean intraocular pressure, rate of aqueous humour flow into the veins, and “gross” facility of outflow) was 8·1±0·6 mmHg, which value was in good agreement with previous values obtained by direct determinations. Thus, in cats, the intraocular pressure is determined mainly by the intrascleral venous pressure, the net rate of aqueous humour formation, and the outflow facility of those channels that deliver aqueous humour into the intrascleral veins, other channels being of minor importance.

Gross facility, facility of conventional routes, and pseudofacility of aqueous humor outflow in the cynomolgus monkey. The reduction in aqueous humor formation rate caused by moderate increments in intraocular pressure.

There is no doubt that to a large extent the aqueous humor is formed by a secretory mechanism that delivers fluid into the posterior chamber from the ciliary processes. The posterior chamber aqueous humor exchanges with the surrounding tissues,1and we do not know if this gives a net loss of aqueous humor volume or a gain before the fluid enters the anterior chamber by bulk flow. In the cynomolgus monkey the bulk outflow from this chamber, which may include some pinocytosis, occurs in part by way of Schlemm's canal into the general circulation (conventional outflow), and in part by way of uveoscleral routes into the episcleral tissues.2,3The outflow through the conventional routes is pressure dependent, that is, it increases with an increase in intraocular pressure; the uveoscleral drainage, on the contrary, is very little, if at all, influenced by a moderate increase in intraocular pressure above

The routes for bulk drainage of aqueous humour in the vervet monkey (Cercopithecus ethiops)

[ 131 I]Albumin and [ 125 I]-γ-globulin were used to mark the bulk flow of aqueous humour in young vervet monkeys. In living animals, at a mean intraocular pressure of about 13 mmHg, the not formation of aqueous humour was 0·96 ± 0·11 μl/min. The mean rate of outflow by conventional routes was 0·74 ± 0·12 μl/min and that by way of uveo-scleral routes was 0·23 ± 0·04 μl/min. After death, at an intraocular pressure artificially maintained at 14 mmHg, the rate of uveo-scleral flow was 1·13 ± 0·13 μl/min.

Conventional and uveo-scleral drainage of aqueous humour in the cynomolgus monkey (Macaca irus) at normal and high intraocular pressures

[ 131 I]Albumin and [ 125 I]-γ-globulin were used to mark the bulk flow of aqueous humour in young cynomolgus monkeys. In living animals, at a normal intraocular pressure of about 11 mmHg, the net formation of aqueous humour was 1·24 ± 0·13 μl/min. The rate of drainage by way of uveo-scleral routes was 0·44 ± 0·06 μl/min and by way of conventional routes was 0·80 ± 0·11 μl/min. At an intraocular pressure artificially raised to 22 mmHg by an extra inflow, the outflow from the anterior chamber by way of uveo-scleral routes was 0·63 ± 0·08 μl/min and by way of conventional routes was 4·18 ± 0·12 μl/min. It is suggested that, in the pressure region investigated, a change in intraocular pressure produces almost the same change in tissue pressure in the uvea and in the suprachoroid and that this explains why the outflow by way of uveo-scleral routes was so alike at the different pressures investigated. After death, at an intraocular pressure artificially raised to 14 mmHg by an inflow of about 5 μl/min, the mean outflow from the anterior chamber by way of uveo-scleral routes was 1·25 ± 0·17 μl/min.