A C T A O P H T H A L M O L O G I C A V O L . 4 9 1 9 7 1

From the Dtflartment o f Ophthalmology, Ncw Y o r k Medical College,

Cenler for Chroiaie Disease, Bird S. Coler Hospital, W e l f a r e Island, New Y o r k , New Y o r k 10017

VOLUMETRIC STUDIES OF OPHTHALMIC ARTERY PERFUSION PRESSURE

AND OCULAR RIGIDITY

BY

MICHAEL BLUMENTHAL, MILTON BEST, MILES A. GALIN

& NORMAN WALD

Although Friedenwald postulated a constant ocular pressure-volume relation- ship over a wide range of intraocular pressures (1937), a number of studies have indicated the variability of this relationship (Perkins & Gloster 1957, Macri et al. 1957, Ytteborg 1960, Eisenlohr & Langham 1962). One component of this variable relationship may be due to alterations that occur in scleral elasticity as the tension in the ocular coats is changed with alterations in intraocular pressure (Gloster, Perkins & Pommier 1957). In addition, changes in intraocular blood volume a t different intraocular pressures may play an important role in the pressure-volume relationship (Ytteborg 1960). Attempts to study the effect of ocular blood volume on this relationship, however, have yielded inconsistent results, perhaps because inadequate attention was paid to the measurements of perfusion pressure in the ocular vascular bed (Ytteborg 1960, Eisenlohr & Lang- ham 1962, Pollack & Becker 1961, Best, Pola & Galin 1969).

Previous studies from this laboratory using manometric techniques indicated that there is an inverse relationship between ocular rigidity and ophthalmic artery perfusion pressures between 40 and 100 mm Hg (Blumental, Best & Galin 1970). Although ocular volume changes in this study were induced with a to-

Aided by USPHS Grant No. NS 07162-04 and Grant No. 69-869 from the American Heart Association. Received July 20, 1971.

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nometer and were subject to the errors involved in applying human calibration tables to the cat eye, the relative changes in ocular rigidity were significant. In order to avoid calibration errors the present study was undertaken to evaluate the effect of ophthalmic artery perfusion pressure on the ocular pressure-volume relationship using volumetric techniques.

Material and Methods

Adult cats weighing 3 to 5 kg were sacrificed with intravenous pentobarbital sodium after anticoagulation had ben effected with 2,000 units of intravenous heparin sodium. The eyes were enucleated and the ophthalmic artery cannulated with PE-50 polyethylene tubing as described previously (Rest et al. 1969). The eye was positioned in a Styrofoam socket and the anterior chamber was cannu- lated at the limbus both with a 23 gauge needle connected to a saline reservoir and with a 25 gauge needle attached to a 50 ,ul graduated microsyringe (Fig. 1 ) . Intraocular pressure was controlled with the saline reservoir and was monitored with a transducer and recorder. OphthaImic artery perfusion pressure was con- trolled with a reservoir of lactated Ringer’s solution and was monitored with a

II MICROSYRINGE II

Fig . I . Schematic diagram of apparatus used to perfuse the ophthalmic artery and measure

ocular prcssurc-volume relationship.

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s" F F

W (z 3 v, U, W (z a

a (z

-I I> 0

? a

z [L I-

100 1

0 ' I I I I I I

10 15 20 25 30 35

Volurrc in jec ted -A/ F i g 2.

Intraocular pressure changcs after anterior chamber injection at ophthalmic artery perfusion pressures of zero (lower trace) and 90 mm Hg (upper trace).

pressure transducer placed between the ophthalmic artery cannula and the per- fusing reservoir.

Pressure-volume curves for each eye were constructed from data obtained by rapidly injecting 5 to 50 1 4 1 of lactated Ringer's solution into the anterior chamber in increments of 5 pl. Each injection was performed at a baseline intra- ocular pressure (Po) of 20 mm Hg, and the resulting intraocular pressure (P,) was recorded on the dynograph. Just prior to injecting the lactated Ringer's solution, the open system was converted to a closed one by turning the stopcock. The linear and semi-logarithmic pressure-volume relationships for each eye were plotted a t ophthalmic artery perfusion pressures of 0, 20, 30, 40, 50, 70 and 90 mm Hg. Ocular rigidity was determined a t each ophthalmic artery perfusion pressure from the slope of the semi-logarithmic plot.

Results

Fig. 2 is a typical record of intraocular pressure changes after injections of 5 to 50 ,ul of lactated Ringer's solution into the anterior chamber at ophthalmic artery perfusion pressures of zero (lower trace) and 90 mm H g (upper trace). P,, was 20 mm H g in all cases. For each volume of injection, the resulting P,

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s" F F W n 3 v)

v) W z a

n U _1 3 V 0

4 n c 5

loor

10 20 30 40 5 0

Volume I n j e c t e d - 1 1 1

Fig. 3. Pressure-volume relationship of a n eye at ophthalmic artery perfusion pressure of zero

(a), 40 (A) and 70 mm Hg (w) .

value was progressively less and the slope of intraocular pressure decline from the resulting Pt value progressively steeper as ophthalmic artery perfusion pres- sure was raised to 90 mm Hg.

From this type of data the pressure-volume relationship was plotted (Fig. 3) a t ophthalmic artery perfusion pressures of 0, 40 and 70 mm Hg. Although the shapes of the curves are similar, a shift to the right occurs as ophthalmic artery perfusion pressure is increased. Fig. 4 shows similar data plotted semi-loga- rithmically.

I- 1 0 1 , z 0 10 20 30 40 5 0

Volume injected - ~ l

Fig . 4 . Semilogarithmic plot of pressure-volume relationship of a n eye at ophthalmic artcry

perfusion pressures of zero (a), 50 (A) and 90 mm Hg (m).

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Table I .

Effective perfusion No. of 1 eyes I Ocular rigidity ?L S.D. pressure‘’ P:’

O0

10

20

30

70

23 0.0129 * 0.0012

17 0.0127 k 0.0012 0.05

11 0.0119 k 0.00133 0.001

18 0.0109 k 0.00142 0.001

17 0.0101 * 0.00129 0.001

” Perfusion pressure in ophthalmic artery minus intraocular pressure. t Paired “ t ” test comparing zero ophthalmic artery perfusion pressure to each effective

perfusion pressure. ’ Atmospheric pressure.

Ocular rigidities a t each ophthalmic artery perfusion pressure studied are shown in Table I, which includes a statistical analysis of the results. The results indicate that there is a gradual increase in ocular rigidity as perfusion pressure in the ophthalmic artery is reduced. The changes in ocular rigidity are statisti- cally significant using the paired “ t ” test.

Discussion

A previous study using the manometric method for determining ocular rigidity indicated that blood expulsion from the eye during tonometry is of importance in measuring intraocular pressure and ocular rigidity (Blumenthal, Best & Galin 1970). The present study, using a volumetric technique, confirms this finding and shows the volume of fluid expelled from the vascular compartment is di- rectly related to the ophthalmic artery perfusion pressure. The kinetics of fluid expulsion from the eye after injection of lactated Ringer’s solution into the anterior chamber is represented in Fig. 2 where intraocular pressure change is plotted for ophthalmic artery perfusion pressures of zero and 90 mm Hg. Injec- tions of fluid in the former case cause an intraocular pressure increase which is followed by a small, but rapid decline in intraocular pressure to a new level. This rapid decline in intraocular. pressure is more apparent with increasing in- jection volumes and is probably related to the viscoelastic properties of the sclera (McEwen 1967). The rapid decline is followed by a slower, continuous decline in intraocular pressure that is apparently due to outflow of fluid from

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the anterior chamber angle. After anterior chamber iiijection in the eye whose ophthalmic artery was perfused a t 90 mm Hg, however, the rapid decline in intraocular pressure from its new level was very much more marked and was most likely due to rapid expulsion of fluid from the intraocular vascular com- partment through the venous outflow channels as well as to scleral viscoelasticity.

At higher ophthalmic artery perfusion pressures, therefore, more fluid is available in the vascular bed for expulsion a t the increased intraocular pressure. resulting in the very prominent peaking of the biphasic intraocular pressure decay curve. Injections of the same amount of fluid into the anterior chamber at different ophthalmic artery perfusion pressures, consequently, are imme- diately buffered by discharge from the vascular bed, resulting in smaller in- creases in intraocular pressure at the higher ophthalmic artery perfusion pres- sures as compared to the lower ones. This explains the findings of a shift to the right of the pressure-volume curve as ophthalmic artery perfusion pressure is increased.

When the ophthalmic artery perfusion pressure was increased to only 10 mm H g above intraocular pressure, the shift in the pressure-volume relationship did not occur using zero ophthalmic artery perfusion pressure as the comparative baseline. This is probably due to the fact that an ophthalmic artery perfusion pressure of only 10 mm H g greater than intraocular pressure is unable to pre- vent critical closure of intraocular vessels from occurring (Best et al. 1969). The phenomenon of critical closure occurs in many vascular beds as transmural pressure approaches zero, and perhaps provides the explanation for several ob- served ocular vascular phenomena (Blumenthal et al. 1970). Under these cir- cumstances filling of the intraocular vascular bed does not occur. When oph- thalmic artery perfusion pressure exceeded intraocular pressure by 30 mm Hg or more, however, the anticipated alterations in the pressure-volume relationship were detected (Table I).

Summary

The pressure-volume relationship of enucleated cat eyes was studied by a volu- metric technique while the perfusion pressure of the intraocular vascular bed was controlled by cannulating the ophthalmic artery. The intraocular pressure changes induced by intracameral injection of lactated Ringer’s solution were significantly reduced as ophthalmic artery perfusion presure was increased. This probably results from the rapid reduction of the intraocular vascular compart- ment through the venous outflow channels at higher ophthalmic artery perfusion pressures. The results indicate an inverse relationship between ocular rigidity and ophthalmic artery perfusion pressure.

References

1. Best, M., Blumenthal, M., Futterman, H. & Galin, M. A. (1969) Critical closure of intraocular blood vesscls. Arch. Ophthnl. 82, 385-392.

2. Rest, M., Pola, R. & Galin, M. A. (1969) Ocular volume and common carotid occlu- sion in the rabbit. Invcst. Op/zlhnl. 8 , 365-372.

3. Blumenthal, M., Best, M. & Galin, M. A,: The effect of ophthalmic artery perlusion pressure on ocular rigidity. Ophthalmologito. Submitted for publication.

4. Blumenthal, M., Best, M., Gitter, K. A. & Ga!in, M. A. (1971) Studies in ocular cir- culation. An analysis of the effcct of induced ocular hypertension on retinal and choroidal blood flow in humans. Amcr. J . Ophthal. 71, 819-825.

5. Eisenlohr, J. E. & Langham, M. E. (1962) The relationship between pressure and volume changes in living and dead rabbit eyes. Invest. Ophthnl. 1, 65-77.

6. Fricdenwald, J. S. (1937) Contribution to the theory and practice of tonometry. Amer . J . Ophthnl. 20, 985-1024.

7. Gloster, J., Perkins, E. S. & Pommier, M. L. (1957) Extensibility of strips of sclera and cornea. Brit. /. Ophthal. 41, 103-110.

8. Macri, F. J., Wanco, T., Grimes, P. A. & von Salltnann, L. (1957) Thc elasticity of the eye. Arch. Ophthal. 58, 513-519.

9. McEwen, W. K. (1967) Difficulties in measuring intraocular pressurc and ocular rigidity. In: Glnucomrc Synzfiosirrrr~ Tzilzing casllc, pp 92-125. Karger, New York.

10. Perkins, E. A. & Gloster, J. (1957) Distensibility of thc cyc. Brit. /. Ofihthnl. 41, 93-102.

11. Pollack, I. P. & Becker, B. (1961) The effect of hypothcrtnia on aqueous humor dynamics. Amer . /. Ophthal. 51, 1039-1047.

12. Ytteborg, J. (1960) The role of intraocular blood volume in rigidity mcasurcmcnts on human eyes. Actn ophtknl. (Kbh. ) ,?8, 410.436.

Reprint request to Bird S. Colcr Hospital, Welfare Island, New York, New York l0Oli (Dr. Best).

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