AQUEOUS HUMOR

 Physiological properties:

1. Volume 0.31ml 
2. Refractive index 1.333 
3. PH 7.2 
4. Hyperosmotic 
5. Rate of formation 1.5 to 4.5 µl/min

Volume: The aqueous humour is a clear watery fluid filling the anterior chamber (0.25 ml) and posterior chamber (0.06 ml) of the eyeball. 

Functions of aqueous humour are: 

1. It maintains proper intraocular pressure. 
2. It plays an important metabolic role by providing substrates and by removing metabolites from the avascular cornea and lens.
3. It maintains optical transparency. 
4. Brings oxygen to the cornea, lens & iris.
5. maintaining IOP 
6. It takes the place of lymph that is absent within the eyeball. Refractive index of aqueous humour is 1.336. 

Composition:

Constituents of normal aqueous humour are on :. 

1. Water 99.9 and solids 0.1% which include :

• Proteins (colloid content). Because of blood aqueous barrier the protein content of aqueous humour (5-16 mg%) is much less than that of plasma (6-7 gm%). However, in inflammation of uvea (iridocyclitis) the blood-aqueous barrier is broken and the protein content of aqueous is increased (plasmoid aqueous). 
• Amino acid constituent of aqueous humour is about 5 mg/kg water. 
• Non-colloid constituents in millimols /kg water are glucose (6.0), urea (7), ascorbate (0.9), lacticacid (7.4), inositol (0.1), Na+ (144), K+ (4.5), Cl— (10), and HCO3 — (34). 
• Oxygen is present in aqueous in dissolved state.

Note: 

Thus, composition of aqueous is similar to plasma except that it has:

• High concentrations of ascorbate, pyruvate and lactate;
• Low concentration of protein, urea and glucose. 

Aqueous humour: anterior chamber versus posterior chamber. The composition of aqeuous humour in anterior chamber differs from that of the aqueous humour in posterior chamber because of metabolic interchange. The main differences are : 

HCO3 — in posterior chamber aqueous is higher than in the anterior chamber. 

Cl— concentration in posterior chamber is lower than in the anterior chamber. 

Ascorbate concentration of posterior aqueous is slightly higher than that of anterior chamber aqueous.

 Production:Aqueous humour is derived from plasma within the capillary network of ciliary processes. 

The normal aqueous production rate is 2.3 µl/min. The three mechanisms diffusion(10%), ultrafiltration(20)% and secretion (active transport)(70%) play a part in its production at different levels. The steps involved in the process of production are summarized below: 

1. Ultrafiltration: First of all, by ultrafiltration, most of the plasma substances pass out from the capillary wall, loose connective tissue and pigment epithelium of the ciliary processes. Thus, the plasma filtrate accumulates behind the non-pigment epithelium of ciliary processes. 

2. Secretion: The tight junctions between the cells of the non-pigment epithelium create part of blood aqueous barrier. Certain substances are actively transported (secreted) across this barrier into the posterior chamber. The active transport is brought about by Na+-K+ activated ATPase pump and carbonic anhydrase enzyme system. Substances that are actively transported include sodium, chlorides, potassium, ascorbic acid, amino acids and bicarbonates. 

3. Diffusion: Active transport of these substances across the non-pigmented ciliary epithelium results in an osmotic gradient leading to the movement of other plasma constituents into the posterior chamber by ultrafiltration and diffusion. Sodium is primarily responsible for the movement of water into the posterior chamber

Control of aqueous formation: The diurnal variation in intraocular pressure certainly indicates that some endogenous factors do influence the aqueous formation. The exact role of such factors is yet to be clearly understood. Vasopressin and adenyl-cyclase have been described to affect aqueous formation by influencing active transport of sodium. Ultrafiltration and diffusion, the passive mechanisms of aqueous formation, are dependent on the level of blood pressure in the ciliary capillaries, the plasma osmotic pressure and the level of intraocular pressure. 

Drainage of aqueous humour Aqueous humour flows from the posterior chamber into the anterior chamber through the pupil against slight physiologic resistance. From the anterior chamber the aqueous is drained out by two routes: 

1. Trabecular (conventional) outflow: Trabecular meshwork is the main outlet for aqueous from the anterior chamber. Approximately 90 percent of the total aqueous is drained out via this route. Free flow of aqueous occurs from trabecular meshwork up to inner wall of Schlemm's canal which appears to provide some resistance to outflow. Mechanism of aqueous transport across inner wall of Schlemm’s canal. It is partially understood. Vacuolation theory is the most accepted view. According to it, transcellular spaces exist in the endothelial cells forming inner wall of Schlemm's canal. These open as a system of vacuoles and pores, primarily in response to pressure, and transport the aqueous from the juxtacanalicular connective tissue to Schlemm’s canal. From Schlemm's canal the aqueous is transported via 25-35 external collector channels into the episcleral veins by direct and indirect systems. A pressure gradient between intraocular pressure and intrascleral venous pressure (about 10 mm of Hg) is responsible for unidirectional flow of aqueous. 

2. Uveoscleral (unconventional) outlow: It is responsible for about 10 percent of the total aqueous outflow. Aqueous passes across the ciliary body into the suprachoroidal space and is drained by the venous circulation in the ciliary body, choroid and sclera. The drainage of aqueous humour is summarized in the flowchart

Maintenance of intraocular pressure 

The intraocular pressure (IOP) refers to the pressure exerted by intraocular fluids on the coats of the eyeball. The normal IOP varies between 10 and 21 mm of Hg (mean 16 ± 2.5 mm of Hg). The normal level of IOP is essentially maintained by a dynamic equilibrium between the formation and outflow of the aqueous humour. Various factors influencing intraocular pressure can be grouped as under: 

(A) Local factors :

1. Rate of aqueous formation influences IOP levels. The aqueous formation in turn depends upon many factors such as permeability of ciliary capillaries and osmotic pressure of the blood. 

2. Resistance to aqueous outflow (drainage). From clinical point of view, this is the most important factor. Most of the resistance to aqueous outflow is at the level of trabecular meshwork. 

3. Increased episcleral venous pressure may result in rise of IOP. The Valsalva manoeuvre causes temporary increase in episcleral venous pressure and rise in IOP.

(B) General factors: 

1. Heredity. It influences IOP, possibly by multifactorial modes. 

2. Age. The mean IOP increases after the age of 40 years, possibly due to reduced facility of aqueous outflow. 

3. Sex. IOP is equal between the sexes in ages 20- 40 years. In older age groups increase in mean IOP with age is greater in females. 

4. Diurnal variation of IOP. Usually, there is a tendency of higher IOP in the morning and lower in the evening (Fig. 9.7). This has been related to diurnal variation in the levels of plasma cortisol. Normal eyes have a smaller fluctuation (< 5 mm of Hg) than glaucomatous eyes (> 8 mm of Hg). 

5. Postural variations. IOP increases when changing from the sitting to the supine position. 

6. Blood pressure. As such it does not have longterm effect on IOP. However, prevalence of glaucoma is marginally more in hypertensives than the normotensives. 

7. Osmotic pressure of blood. An increase in plasma osmolarity (as occurs after intravenous mannitol, oral glycerol or in patients with uraemia) is associated with a fall in IOP, while a reduction in plasma osmolarity (as occurs with water drinking provocative tests) is associated with a rise in IOP. 

8. General anaesthetics and many other drugs also influence IOP e.g., alcohol lowers IOP, tobacco smoking, caffeine and steroids may cause rise in IOP. In addition there are many antiglaucoma drugs which lower IOP.