Applied Mathematics and Computation 189 (2007) 734745 www.elsevier.

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Modelling aqueous humor outow through trabecular meshwork

Ram Avtar, Rashmi Srivastava
*
Department of Mathematics, Harcourt Butler Technological Institute, Kanpur 208 002, India

Abstract A simple model of aqueous outow through the trabecular meshwork in eye has been developed. The model considers the meshwork as an annular cylindrical ring with uniform thickness of homogenous, isotropic, viscoelastic material, swollen with continuously percolating aqueous humor through it. It incorporates a strain-dependent permeability function into Darcys law which is coupled to the force balance for the bulk material. A simple analytical expression relating aqueous ux to pressure dierential is developed which shows how strain-dependent permeability can lead to reduction in hydraulic conductivity (aqueous outow facility) with increasing intraocular pressure (IOP) as observed in experiments by ophthalmologists. Analytical expressions for the displacement, uid pressure and dilatation in the trabecular meshwork have been obtained. 2006 Elsevier Inc. All rights reserved.
Keywords: Aqueous humor; Trabecular meshwork; Intraocular pressure; Biphasic

1. Introduction Aqueous humor occupying the anterior chamber leaves it via the uveoscleral drainage system and the conventional outow system. Most of the uid, approximately 85%, drains away to the blood streams through the conventional outow pathway which consists of in series: the uveal and corneoscleral meshwork, the juxtacanalicular meshwork (JCM), the inner endothelial wall of the Schlemms canal, the Schlemms canal and the collector channels and the aqueous veins. The part comprised of rst three layers altogether is known as the trabecular meshwork. An obstruction to the aqueous outow results in the accumulation of aqueous humor in the anterior chamber raising the intraocular pressure (IOP). Increased IOP, sustained for a long time, can damage the optic nerve in the eye and can lead to blindness [1,24]. Despite many years of research, mainly devoted to the identication of principal site of the outow resistance in the aqueous outow system and to the investigations of its origin and its possible role in the development of a pathological state known as glaucoma [2], we still do not know how the majority of aqueous outow resistance is generated which implies that we do not understand the fundamental factors controlling
*

Corresponding author. E-mail address: rashmiirs@redimail.com (R. Srivastava).

0096-3003/$ - see front matter 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.amc.2006.11.109

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IOP. For those glaucoma therapies directed towards lowering the intraocular pressure through the enhancement of aqueous humor outow, a better understanding of the outow network, changes in which can lead to ocular hypertension and glaucoma and that of mechanism of aqueous outow resistance increase is required. Both experimental and theoretical approaches should be adopted by researchers to elucidate the aqueous drainage mechanism in various components of the outow network. There have been numerous attempts to identify the primary site and the underlying cause of outow resistance in the aqueous outow system. McEwens [3] calculations of ow resistance based on the dimensions of the ow passage in the inner aspects of the meshwork indicated that both the uveal meshwork and corneoscleral meshwork do not generate signicant resistance consistent with Grants [4] nding that removal of uveal meshwork had little eect on the outow facility. Grant [5] later demonstrated that 75% of the resistance resided between the anterior chamber and aqueous veins. In humans, the pores in the inner wall endothelium of Schlemms canal generate perhaps 10% of the total ow resistance. Schlemms canal itself only generates signicant ow resistance when it is substantially collapsed, and the collector channels and aqueous veins have been shown to have negligible ow resistance. It has been suggested that the apparently open spaces in the JCM are lled with an extracellular matrix gel, and that such a gel lled JCM is likely to be the major source of ow resistance in the normal eye [6]. The source of outow resistance in the aqueous outow system of normal or glaucomateous eyes has not been denitely established although each of the components of the outow pathways has been analyzed to determine whether they might generate signicant ow resistance. Under the circumstances of confusing conclusions regarding the aqueous outow mechanism derived from experimental studies, a mathematical analysis of the aqueous outow may facilitate the denite conclusion. Several mathematical models of the aqueous outow in the trabecular meshwork, the juxtacanalicular meshwork and Schlemms canal have been developed to explore the outow mechanisms in the respective components of the outow network. But these models have limitations due to many assumptions and simplications. Despite numerous studies [4,5,9] of the aqueous outow, the origin of outow resistance in the meshwork and increase in it with IOP elevation in some cases is not clearly known. In order to select an ideal therapy for reducing the outow resistance increase observed in open angle glaucoma, knowledge of causes of abnormalities in the tissue and that of mechanism of outow resistance increase is required. Poiseuille ow [3] models as well as various empirical models have been applied to describe aqueous ow through the trabecular meshwork. Tandon and Avtar [7] presented a biphasic continuum model for aqueous ow through the meshwork using small strain expansion and obtained approximate solution by an iterative technique. The models proposed earlier are not sucient to describe the outow phenomenon. The microstructure of trabecular meshwork can be described as composed of cellular conglomerates embedded in a porous brous extracellular matrix and interstices of the matrix are lled with aqueous uid. It is like a bi-phasic material, comprised mainly of aqueous humor enclosed within an elastic matrix of elastin and collagen bres. Johnson and Grant [8] and several other investigators [9,10] observed from their experimental studies that striking structural changes occurred in the meshwork in response to alterations in the intraocular pressure. An elevation in the IOP above the normal level may produce compression in the meshwork diminishing the ow regions. Aqueous humor owing through the meshwork will interact with its solid phase giving rise to a drag force, i.e. a force exerted by aqueous humor on the solid phase as it passes through the tissue. A rise in IOP forces more aqueous uid to ow out through the meshwork, which, in turn, exerts a greater drag force on the solid matrix causing compression in the meshwork. The compression caused by the increased IOP may decrease the intrinsic permeability, which depends upon the dilatation of the solid phase. This concept is supported by Lai and Mow [11]. Once a uid pressure is applied, the viscous drag caused by the uid owing through the tissues causes it to compact in a non-uniform manner, thereby decreasing the permeability. The behavior of aqueous humor, thus, depends upon the intrinsic interaction between the deformation of the solid matrix and the motion of the interstitial aqueous uid. From a uid mechanical point of view, there are two primary mechanisms for the transport of aqueous humor across the meshwork. (i) The interstitial aqueous uid may transport through the poroelastic, permeable meshwork under the inuence of a pressure dierential across the meshwork.

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(ii) The deformation of elastic solid matrix caused by the drag force directly aects the aqueous outow phenomenon. A measure of the ease with which the ow of aqueous humor occurs through the aqueous outow system is the hydraulic conductivity which is interpreted as outow facility in ophthalmology. It has been well established that aqueous outow facility decreases with a rise in the IOP [12]. As mentioned earlier, most of the outow resistance is encountered in the trabecular meshwork. The outow facility of the aqueous outow system is, therefore, mainly determined by the meshwork. The factors involved in the process of aqueous percolation through the meshwork play a role in determining the outow facility, which is important determinant of the IOP. In addition to the pressure dierential drop across the meshwork, and elasticity of the meshwork, several other physiological factors such as the ciliary muscle contraction, the intrinsic contractility of the trabecular meshwork and scleral spur cells, the cellular volume, extracellular matrix status, protein concentration, nervous control have been observed to aect the aqueous outow facility. An increase in the ciliary muscle contraction results in distension of trabecular meshwork with subsequent reduction in outow [21]. But the mechanism of the ciliary muscle contraction in reducing outow resistance is not well understood [12]. The contraction of the trabecular meshwork cells and scleral spur cells, decreases the permeability of the trabecular meshwork because the size of the intercellular space is reduced. Similarly when trabecular meshwork cells and scleral spur cells relax, the opposite eect appears and the permeability of tissue increases [21]. Whether contractility of trabecular meshwork and scleral spur cells also play a role in old and glaucomatous human eyes is not known [19]. Similarly, volume regulatory properties would be aected as well. The survey of ophthalmic literature shows that there is a lot of confusion regarding the importance of protein concentration in generating ow resistance in the aqueous outow pathway. Some studies [1618,20] have shown that soluble protein in the aqueous humor of bovine eye can inuence the aqueous outow resistance. In 1901, Troneoso [22] suggested that glaucoma is caused by an excess of protein in aqueous humor. Johnson et al. [23] conrmed that plasma-derived proteins in the aqueous humor of the trabecular meshwork can generate a signicant fraction of aqueous outow resistance. In 1997, Sit et al. [18] concluded that outow facility would be controlled by a resistance causing mechanism other than the bulk level of aqueous humor proteins. Finally some aspects of trabecular meshwork physiology and their signicance in tissue permeability and outow facility are still unknown. The model considers coupled dynamical interaction between the aqueous outow and mechanical deformation in the meshwork. The aqueous outow in the meshwork is described by the Darcys law. The straindependent permeability is incorporated in the Darcys law. In this work, the trabecular meshwork is modelled as a thin wall of a cylinder surrounding the anterior chamber. The inner side of the cylinder represents the anterior chamber. The trabecular meshwork as a whole consists of a series of at perforated sheets or lamellae lying one on the top of the other, connective tissues containing collagen and elastin bres, a ground substances and the endothelial cells. Thus, the trabecular meshwork lled with aqueous humor may be described as a biphasic matrix comprising the solid and uid phases. 2. Mathematical model of ltration ow through trabecular meshwork tissue The mathematical model is based on the theory for consolidation of porous elastic materials due to Kenyon [13] and a phenomenological equation for strain-dependent permeability due to Lai and Mow [11]. The analysis considers the trabecular meshwork to be cylindrical annular ring (Fig. 1) with thickness H containing a uid inside it at pressure Pm. The polar coordinates of the cross section are taken as r and h while z is the axial coordinate. The external pressure Po is set at zero for reference. To develop a mathematically tractable model of the meshwork, the following assumptions are introduced. 2.1. Assumptions (i) The trabecular meshwork is an isotropic, homogenous, porous, deformable matrix swollen with continuously owing aqueous humor. (ii) The permeability of the meshwork is a function of the dilatation.

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Fig. 1. Schematic diagram of the proposed model of the trabecular meshwork.

(iii) (iv) (v) (vi) (vii) (viii) (ix)

Only the uid mechanical aspects of aqueous ow phenomenon are considered. Both the constituents of the system are isothermal. The aqueous uid and solid matrix are intrinsically incompressible. Inertial and body forces are neglected and diusional couples do not exist. The displacement of the tissue depends only on radial position. Aqueous ow is steady, slow, laminar, Newtonian, viscous and incompressible. The protein accumulation, the muscular contraction, the nervous control and the ciliary muscle traction are neglected. (x) Due to uid ow in the lumen, the axial wall shear stress is negligible in comparison to other stresses acting on the wall.

Using the symbols S ij Eij for the components of the extra stress (strain) tensor in the tissue matrix, P for the interstitial uid pressure, Ur for the radial displacement of the tissue, W for the ltration velocity, k and G for the Lame constants of the tissue, l for the uid viscosity and k for the permeability, the governing equations are as follows: dP 1 d 1 rS rr S hh ; dr r dr r dP l W; dr j d rW 0: dr 1 2 3

Eq. (1) represents the force balance describing equilibrium in the bulk material; Eq. (2) is Darcys law which relates the interstitial uid ow to the uid pressure gradient; and Eq. (3) is the continuity equation assuming a stationary solid phase. The trabecular meshwork tissue is assumed to be isotropic and linearly elastic so that S ij kEij dij 2GEij ; where dij is the Kronecker Delta Function. The only non-vanishing components of the strain tensor are Err dU r dr and Ehh Ur : r 5a; b 4

Substituting Eqs. (4) and (5) into Eq. (1) and replacing Ur (only non-vanishing displacement) by U, we nd   dP d 1 d k 2G rU ; 6 dr dr r dr where the term (k 2G) is referred to as the aggregate elastic modulus.

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Lai and Mow [11] proposed the following non-linear relationship between permeability and strain for cartilage; k k 0 expM !; 7 where k0 and M are material constants and is the dilatation ( = Ekk). Although Eq. (7) was determined for cartilage, it is reasonable to expect k = k() for the trabecular meshwork tissue since the meshwork and cartilage are both porous, uid lled solids, consisting largely of collagens bres. The change in the water content per unit volume of the porous sample is equal to the dilatation (), if the density of the solid is assumed to be constant. Since the deformation of the solid matrix of the soft meshwork induces a change in its microstructure, the permeability of the material is, in general a function of deformation. Lai and Mow [11] have demonstrated the validity of the following two- parameter model in their study of small strains of articular cartilage: 1 1 1 M !: k k0 8a

This was later used by Klanchar and Tarball [14] while studying water transport through arterial walls for which for small M is equivalent to k k 0 1 M !: 8b Eq. (8b) is, of course, the small strain expansion of Eq. (7) and is a general approximation to any k() for sufciently small . The dilatation in cylindrical coordinates is represented by ! dU U : dr r 9

Substitution of Eqs. (8a) and (9) in Eq. (2) yields    dP l dU U 1M W: dr j0 dr r

10

Eqs. (3), (6) and (10) constitute a system of equations governing the aqueous ow in the trabecular meshwork. 3. Boundary conditions The tissue is assumed to be homogenous and the pressure continuous in the radial direction. The pressures are specied at the inner and outer walls P r R P m S rr r R 0; P r R H 0: S rr r R H 0: 11i 11ii But at these boundaries the extra stresses are zero

4. Dimensionless scheme We non-dimensionalize the governing Eqs. (3),(6) and (10) with respect to the radius of anterior chamber R and the Lame constant (2G + k) and the following non-dimensional variables are introduced:  p P ; 2G k  r r ; R  u U ; R  w W ; U0 H  h ; R  sij S ij : 2G k

Introducing these variables, Eqs. (6), (10) and (3), respectively, are converted into the following normalized forms (Dropping the bars for convenience): dp d2 u 1 du u ; dr dr2 r dr r2 12

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    dp lRU 0 du u 1 w; M dr 2G kj0 dr r d rw 0: dr Boundary conditions (11i) and (11ii) in dimensionless forms become as follows: pr 1 Pm p r 1 h 0; 2G k srr r 1 0 srr r 1 h 0:

13 14

15i 15ii

Eqs. (8a), (9), (12), (13) and (14) must be solved subject to appropriate boundary condition which will be discussed subsequently. Integrating of Eq. (14) gives w A1 : r 16

where A1 is a constant to be determined. Substituting the above value of w in Eq. (13), and using the resulting equation in, Eq. (12) we have:     lRU 0 A1 du u d2 u 1 du u ; M 1 2 dr r dr r dr r 2 2G krk 0 which is linear equation for u(r), Eq. (17) can be cast in the form of an Euler equation: r2 d2 u du A1 BCr ; 1 A1 BC r A1 BC 1u dr2 dr M lM ; k 0 2G k 18 17

where dimensionless parameters are B C RU 0 :

The solution of Eq. (18) is A2 r ; 19 A3 rA1 BC1 2M r where A2 and A3 are new integration constants. The pressure distribution is obtained by substituting Eq. (19) into Eq. (12) and integrating the resulting equation. u p A3 A1 BC 2rA1 BC A4 ; du k u dr 2G k r 20

where A4 is the nal integration constant. The extra stress component, srr given in non-dimensional form: srr 21

is calculated by substitution of Eq. (19) into Eq. (21) with the result:     k A2 k 1 A1 BC 1 : srr A3 A1 BC 1 r k 2G M r k 2G

22

Solving for the integration constants in Eqs. (20) and (22) using above boundary conditions, we nd the following approximate relationship for w in terms of pressure and radial position: Pm 2G kh2 2hG khwrBC : MhwrBC 2G k 2G k 23

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Now the ltration velocity can be expressed as w 2G kP m k 0 : rlh 2hG k MP m C

2

24

Notice that the hydraulic conductivity (w/Pm) now depends on the hydrostatics pressure Pm and the new material parameter M must be a negative quantity. At r = 1, it can be expressed as Lp 2 G k k 0 : lh 2hG k MP m C
2

25

An expression for the permeability variation within the tissue can be derived by substituting Eq. (9) and (19), into Eq. (8a), in the form: k rA1 BC : k 0 MA3 A1 BC 2 26

The deviation of the ratio k/k0 from unity is an indication of the extent of strain induced permeability variation within the material. An expression for the dilatation variation in the meshwork can be obtained by substituting Eq. (19) into Eq. (9). ! A3 A1 BC 2rA1 BC 1 : M 27

On Comparison Eq. (24) with Eq. (16), we nd A1 2 G k P m k 0 : lh 2hG k MP m C

2

Using the boundary conditions, we nd the following integration constants: A2 A3 P m A1 BC 2G k 2G k G k 2G kA1 BC 21 1 h Pm P m 1 hA1 BC 2G k1 1 h
A1 BC A1 BC

2G ;

2G kA1 BC 21 1 hA1 BC :

A4

5. Results and discussion Computational results for a representative human eye have been obtained from the above solutions by introducing appropriate values of the physiological parameters listed in Table 1. The elastic properties of

Table 1 Typical values of the parameters used in the model computations Parameter Po Pm E R H U0 k0 M m Description Pressure at the outer wall of the meshwork Pressure at the inner wall of the meshwork Elastic modulus of the meshwork Radius of the anterior chamber Thickness of the trabecular meshwork Characteristic velocity of aqueous uid Permeability of the meshwork Material constant Poissons ratio Typical value 0 5 mm Hg 4.5 Nm2 5.62 103 m .01 103 m 3.03 106 m s1 1.99 1012 m2 4.5 .35

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the material are specied by the Youngs modulus, E, and Poissons ratio, m. The Lame constants G and k, dening the elastic properties of the meshwork, are related to parameters by G E=21 m k Em=1 m1 2m: The curves depicted in Figs. 2ac and 3ac represent the characteristic proles of the normalized solid phase displacement and the uid pressure, respectively, in the trabecular meshwork for dierent values of intraocular pressure dierential (Pm). These proles demonstrate that there is a continuous decrease in the displacement along the radial direction. Evidently, the displacement is the maximum at the inner wall and approaches to zero at the outer wall of the meshwork. The characteristic graphs also show the eect of intraocular pressure dierential across the meshwork on the dimensionless displacement. It is evident from the Fig. 2ac that an increase in the pressure dierential increases the displacement. These observations provide support to the fact that raised pressure differential causes greater compression in the meshwork, reducing interstitial space available for the aqueous passage. Increased pressure dierential causes larger local displacement in the meshwork with greater compression. Fig. 3ac displays the eect of pressure dierential on the pressure distribution in the meshwork. The curve demonstrates that increasing pressure dierential induces an increase in the uid pressure in the meshwork. The curves depicted in Fig. 4 show the eect of intraocular pressure dierential on the normalized permeability of the meshwork. As the pressure dierential increases, the permeability of the meshwork decreases. This result provides support to the fact that the decreased interstitial space of aqueous outow pathways due to raised pressure dierential-induced compression oers greater resistance to aqueous outow and so the permeability decreases. Decreased permeability retards aqueous ow in the meshwork with concomitant increase in the uid accumulation in the anterior chamber leading to further rise in IOP. This result is supported by a observations [21]. Fig. 5, shows the distribution of the dilatation of the solid matrix in trabecular meshwork as a function of thickness of the meshwork and the eect of the pressure dierential (IOP) across the meshwork on the dilatation. Increased pressure dierential enhances the dilatation. The change in volume of the meshwork material and change in aqueous content in the meshwork increases with a rise in the pressure dierential. A raised IOP forces more aqueous to percolate into the meshwork enhancing the aqueous content and volume of the material in the meshwork. The curve in Fig. 6 depicts the variation in ltration velocity of aqueous humor in response to the changes in the pressure dierential. Evidently, the ltration velocity or volume ux of the aqueous humor in the meshwork at its inner wall increases with a rise in the pressure dierential. The curve depicted in Fig. 7 shows variation in the hydraulic conductivity (aqueous outow facility) as a function of the pressure dierential. The curve shows the signicant reduction of aqueous outow facility with an increasing pressure dierential. Elevated, IOP causes greater compaction between the intratrabecular sheets and lamellae with reduced intratrabecular uid space which decreases the aqueous outow facility of the meshwork. This result is supported by a number of experimental observations [15,21]. 6. Concluding remarks The prime objective of the present work was to construct a simple mathematical model for describing the outow of aqueous humor in the trabecular meshwork of eye, to provide an estimate of eect of intraocular pressure on the ow characteristics of the aqueous and a simple framework for interpreting ophthalmologists experiments on the aqueous outow through the meshwork. The results presented above that a rise in the intraocular pressure causes an increases in the uid pressure, the displacement, the dilatation and aqueous ltration (percolation) velocity in the meshwork whereas it decreases the permeability as well as the hydraulic conductivity of the porous trabecular meshwork. Thus, intraocular pressure has a outow facility decreasing eect which is well established by experimental observation [12]. The eect occurs through the compression in the trabecular meshwork matrix. From a clinical point of view, glaucoma therapy should be evolved which attempts to minimize these secondary eects. A therapy which tends to counteract the compression by neutralizing the intraocular pressure rise may be operative in treatment of glaucoma. It may be more appropriate

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1.316

1.314

1.312 Pm=3mmHg

u x 10-11 (displacement)
0.998

1.31

1.308

1.306

1.304

1.302

1.3 1 1.002 1.004 1.006 1.008 1.01 1.012

r
2.07

2.065

u x 10-11 (displacement)

2.06

Pm=5mmHg

2.055

2.05

2.045

2.04 0.998 1 1.002 1.004 1.006 1.008 1.01 1.012

r
2.82 2.815

u x 10-11 (displacement)

2.81 2.805 2.8 2.795 2.79 2.785

Pm=7mmHg

0.998

1.002

1.004

1.006

1.008

1.01

1.012

Fig. 2. (a)(c) Eect of intraocular pressure on the normalized displacement distribution.

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0.69 0.68 0.67

743

p x 104 (pressure)

0.66 0.65 0.64 0.63 0.62 0.61 0.6 0.59 Pm=3mm Hg

0.998

1.002

1.004

1.006

1.008

1.011

1.012

r
1.68 1.67 1.66 1.65

p x 104 (pressure)

Pm=5mmHg 1.64 1.63 1.62 1.61 1.6 1.59 1.58

0.998

1.002

1.004

1.006

1.008

1.01

1.012

r
5.68 5.67 5.66

p x 104 (pressure)

5.65 5.64 5.63 5.62 5.61 5.6 5.59 5.58 5.57

Pm=7mmHg

0.998

1.002

1.004

1.006

1.008

1.01

1.012

Fig. 3. (a)(c) Eect of intraocular pressure on the normalized pressure distribution.

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0.9885

0.988 Pm=3mmHg 0.9875 Pm=5mmHg Pm=7mmHg 0.987

k/ko (permeability)
0.998

0.9865

0.986

0.9855 1 1.002 1.004 1.006 1.008 1.0 1.012

Fig. 4. Eect of intraocular pressure on permeability distribution.

0.0033 0.0032 0.0031

Pm=3mmHg Pm=5mmHg Pm=7mmHg

dilatation
0.998

0.003 0.0029 0.0028 0.0027 0.0026 1 1.002 1.004 1.006 1.008 1.01

1.012

Fig. 5. Eect of intraocular pressure on dilatation distribution.

16 14 12

W (filtration velocity)

10 8 6 4 2 0 0 1 2 3 4 5 6 7 8 9 10

pm

Fig. 6. Variation of ltration velocity with intraocular pressure.

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1.55 1.549 1.548

745

Lp (outflow facility)

1.547 1.546 1.545 1.544 1.543 1.542 1.541 0 1 2 3 4 5 6 7 8 9 10

pm

Fig. 7. Variation of hydraulic conductivity (outow facility) with intraocular pressure.

and realistic for future researchers to conduct and unsteady state analysis of the aqueous ow through the biphasic meshwork, by incorporating more generalized stressstrain relationship into the theoretical frame work of the present study. References
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