OUTFLOW
III
The Aqueous Circulation
The review and analysis of the retinal and choroidal
circulations in previous issues serve as background for our
consideration of the aqueous circulation.
We describe the dynamics of aqueous drainage from the
eye in terms of pressure, flow and resistance. The
algebraic formula states that pressure is the product of
resistance times flow. Although on the face of it, this
formula would seem to articulate a fundamental natural
principle, it is, in fact, somewhat tautologous, inasmuch as
resistance is ascertained by determining the rate at which
fluid under a known pressure will flow through a given
aperture. The question immediately arises whether sustained
elevations of intraocular pressure must invaryably be
attributed to increases in outflow resistance, hether they
might not also sometimes be attributable to sustained
increases in the rate at which fluid is secreted into the
eye. One must beware not to presume to offer a dogmatic
answer to this question. It is likely however, that even in
the normal eye, the rate of aqueous secretion is far from
constant, but varies diurnally as a function of blood
osmolarity and possibly of undefined hormonal influences.
Yet whatever fluctuation of aqueous secretion the eye might
sustain, there appears, in the healthy eye, to be relatively
little associated diurnal variation of the intraocular
pressure. This relative constancy of intraocular pressure
is atributable in large partt to the circumstance that the
episcleral venous bed constitutes a sink that is able to
accommodate with pressure elevation whatever flow the
emissary veins pour into it. To the extent that the
resistance to outflow is offered not by the episcleral
venous pressure but by resistance withing the outflow tract
of the globe, it is apparent that given normal intraocular
pressures this resistance may constitute as little as 10%
and is never more than 600 percent of the total resistance,
so that in the absence of disease autoregulation of the
intraocular pressure by one of the available control
mechanisms, is probably not of great importance.
The question "Where is the sidte of resistance in
glaucoma is oversimplified." It implies that there is only
one site of resistance; it implies also that the site of
resistance in glaucoma corresponds to the site of resistance
in the normal eye. This presupposition has guided research
efforts in the field.
There are three areas that require review. The
assumption that significant resistance to outflow might
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occur in the aqueous veins within the sclera has been
controverted both by experimental and by analytic studies.
There remain the possibilities that resistance might occur
from collapse and subsequently dynamic occlusion of the
canal of Schlemm, and finally the possibilit that the site
of outflow resistance is within the trabecular meshwork,
specifically it juxtacanalicular portion. It is the last of
these possibilities that has received the most attention.
A clue to the solution of this puzzle is the effect of
pilocarpine on the outflow system. The only known
pharmacologic action of pilocarpine in the eye is its
stimulation of parasympathetically innervated smooth muscle
within the eye, specifically, the iris sphincter and the
musculature of the ciliary body. Inasmuch as the ciliary
muscle is attached at the scleral spur, the assumption has
been firmly established that contraction of the ciliary
muscle, as from pilocarpine by traction on the scleral spur.
Subject to the caveat that this assumption still requires
laboratory confirmation, If we rely on this assumption
subject to the caveat that it still awaits laboratory
confirmation and demonstration, we may take another look at
the angle structures as wee see them as they are
demonstrable with gonioscopy, light and electron microscopy.
The trabecular meshwork brighes the trabecular sulcus like a
sagging clothesline. Traction on the scleral spur, as from
pilocarpine, would stretch the meshwork. It is not
immediately apparaent that such stretching would widen any
pores in the meshwork. It would however tend to pull inward
the inner wall of the canal of Schlemm. If that inner wall
were flaccid, it would open up and widen the canal of
Schlemm. If that inner wall were rigid, tension on the
scleral spur would tend to separate the trabecular lamellae
one from another. Given the (improbable) hypothesis of a
rigid inner wall, the greatest separation would occur in
those lamellae which were bound together least tightly,
while those lamellae which were bound together most tightly
would be susceptible to the least separation. Thus, in
order to postulate that traction on the scleral spur
decreased resistance to outflow by widening spaces between
the lamellae of the trabecular meshwork, one would have to
accept two improbable hypotheses. One would have to assume,
in the first place, that the inner wall of schlemms canal
was rigid to the point of being able to offer the counter-
force to the inward traction on the meshwork. This
possibility appears precluded by experiments in which the
Canal of Schlemm was found to dilate widely when the
intraocular pressure descreaed from normal values to zero.
An inner wall so demonstrably flaccid could not possibly
oppose traction of 10 or 15 mm Hg, such as that experted by
pilocarpine when it countered the intraocular pressure.
Then there is the further consideration that those layers of
the meshwork most affected by tangential strains would be
the ones least tightly bound one to another, and conversely
- 3 -
those most tightly bound one to another would be least
affected by tangential strains, hence such strains, if they
were effective at all, would clearly be overtly inefficient
in decreasing the meshwork resistance.
These considerations lead to the conclusion that the
effect of pilocarpine is inward traction on the inner wall
of the canal of Schlemm tensing to open that structure.
This mechanical and anatomic consideration also immediately
suggests a mechanism for the autoregulation of the
intraocular pressure as simple and direct in its way as the
mechanism for the autoregulation of the retinal venous
pressure that we have already described. When one looks at
the trabecular meshwork with the miscroscope one gets the
impression that it's structure is looser, more cellular and
less firbous, and consequenly more elastic than that of
sclera. Dissection of the enucleated eye appears to confirm
this hypothesis. To the extent that it is true, an increase
of intraocular pressure will tend to cause the scleral spur
to retract, will tend to make the trabecular sulcus to gape,
just as does pilocarpine, thus providing a mechanism for
autocontrol of the intraocular pressure.
* * * * *
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Copyright 2006, Ernst Jochen Meyer