Ocular compression and noncorticosteroidal anti-inflammatory agents – docslide.com.br anoxia definicion

OCULAR COMPRESSION AND NONCORTICOSTEROIDAL

ANTI-INFLAMMATORY AGENTS

STEPHEN A. OBSTBAUM, M.D., AND STEVEN M. PODOS, M.D.

St. Louis, missouri

Ocular compression of the intact eye inâ­

Itially reduces intraocular pressure. The inâ­

Traocular pressure then rises to values greater

Than those recorded prior to compression.

Changes in vitreous volume accompany these

Pressure responses.1 mechanical irritation of

The eye also produces increased intraocular

Pressure, miosis, increased aqueous protein,

And hyperemia of the globe.;; this is presumâ­

Ably mediated by the production and release

Of prostaglandins.3 aspirin and indomethacin


Block the synthesis of prostaglandins and

Prevent the breakdown of the blood-aqueous

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Barrier.35 this study evaluates the effect of

The noncorticosteroid anti-inflammatory

Agents, aspirin, and indomethacin, on the inâ­

Traocular pressure responses after ocular

Compression in both rabbits and humans.

METHODS

Male albino rabbits weighing 2 to 3 kg

Were used. We measured intraocular presâ­

Sure in ten restrained, awake animals with

The mackay-marg electronic tonometer. Af­

Ter topical application of 0.5% proparacaine,

The right eye of each animal was digitally

Compressed for four minutes.1 intraocular

Pressure measurements were repeated imâ­

Mediately, three, five, ten, 30, and 60 minutes

After compression.

In a second group of six animals, after

Baseline measurements of intraocular presâ­

Sure, we injected 50 mg/kg of indomethacin

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Intraperitoneally. One hour later, the intra-

From the glaucoma center, department of

Ophthalmology, washington university school of

Medicine, st. Louis, missouri. This study was supâ­

Ported in part by special fellowship 1-F03-EY

54132 (dr. Obstbaum) and research grants EY

00036 and EY 00004 from the national eye instiâ­

Tute, bethesda, maryland.

Reprint requests to steven M. Podos, MD.,

Washington university school of medicine, deâ­

Partment of ophthalmology, 660 S. Euclid ave.,

St. Louis, MO 63110.

Ocular pressure was measured again, and the

Right eye compressed for four minutes. In­

Traocular pressure measurements were reâ­

Peated at similar time intervals, as indicated

For the control group. The same experiâ­

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Mental procedure was carried out in a third

Group of 11 animals pretreated with 10 mg/

Kg of indomethacin.

Ten ocular hypertensive patients without

Visual field loss and not using antiglaucoma-

Tous medications were included for both the

Control and the experimental portions of the

Study. Intraocular pressure was measured

With the goldmann applanation tonometer.

Baseline measurements were made after

Eight hours of fasting. Using the technique

Described by kirsch and steinman,6 we comâ­

Pressed the right eye of each patient for four

Minutes, and measured intraocular pressures

Immediately thereafter and at three, five, ten,

20, 30, and 60 minutes following compresâ­

Sion.

On another day, these patients returned,

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Having taken 600 mg of aspirin one hour

Prior to beginning the test. Baseline intraâ­

Ocular pressure was measured, and compresâ­

Sion of the right eye was performed for four

Minutes. Intraocular pressure was remea-

Sured at the same time intervals indicated for

The control portion of the experiment.

Slit-lamp evaluation for hyperemia of the

Conjunctiva and iris, and also for aqueous

Flare, was performed and recorded.

Statistical evaluation of animal data utiâ­

Lized the student i-test. Human results were

Evaluated by the paired r-test.

RESULTS

The control animals demonstrated an inâ­

Itial small fall in intraocular pressure with a

Rapid rise of 12.5 mm hg to peak levels at

Five minutes after the completion of comâ­

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Pression (table 1). A gradual reduction in

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VOL. 79, NO. 6 OCULAR COMPRESSION 1009

TABLE 1

OCULAR COMPRESSION AND INTRAOCULAR PRESSURE IN RABBITS

No

Treatment of

Animals

Control 10

Indomethacin (10 mg/kg IP) f 17

Indomethacin 6

(50 mg/kg IP)t

0

– 2 . 1 0

±1.66

-1 .09

±2.02

-3 .00

+ 1.26

Intraocular pressure change (mean ram hgâ±SD)

Time following compression,

3

+7.60

±4.90

0.00*

±2.28

-0 .67*

±2.16

5

+12.50

± 5.42

+ 1.00*

± 1.95

+ 0.33*

± 1.51

10

+11.30

±3.86

+ 1.73*

+ 1.74

– 0.50*

± 3.02

Min

30

+0.10

±1.79

0.00

+ 1.61

-0 .17

±3.49

60

-1 .00

±2.83

– 0 . 1 8

±1.47

-0 .33

±2.50

* significant difference between treated and control.

T IP denotes intraperitoneal injection.

Pressure to below baseline values occurred by

30 minutes, indomethacin, 10 mg/kg, adminâ­

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Istered intraperitoneally one hour prior to

Compression, significantly reduced ( P

.001) the intraocular pressure rise at three,

Five, and ten minutes. A rise of less than 2

Mm hg above baseline values occurred at

Five and ten minutes postcompression. Intra­

Peritoneal administration of 50 mg/kg of

Indomethacin one hour prior to compression

Completely prevented the rebound of intraâ­

Ocular pressure at three (P .005), five

(P .001), and ten (P .001) minutes.

Compression produced a reduction of apâ­

Proximately 7 mm hg of intraocular presâ­

Sure in the patients studied before and after

Aspirin (ASA) pretreatment (table 2) . A

Rise of less than 2 mm hg in intraocular presâ­

Sure above initial value occurred with a peak

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Approximately 30 minutes after comâ­

Pression in untreated patients with a return

To baseline by one hour. When 600 mg of

Aspirin was administered to the same paâ­

Tients one hour prior to compression of the

Right eye, there was a complete inhibition of

The rebound elevation of intraocular presâ­

Sure. At 30 minutes after compression of the

Same eye, the change in intraocular pressure

Was significantly less (P .001) when the

Patient was pretreated with aspirin ( â2.6 ±

2.4 mm hg) , as compared to the control

Value ( + 1.7 ± 2.1 mm hg) .

Hyperemia of the iris and conjunctiva ocâ­

Curred in animal and human control groups

To a greater extent than after indomethacin

Or aspirin administration. With aspirin adâ­

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Ministration prior to compression, none of

The patients showed aqueous flare, although

We frequently observed conjunct!Val hyperâ­

Emia.

TABLE 2

OCULAR COMPRESSION AND INTRAOCULAR PRESSURE IN HUMANS

Treatment no. Of

Patients

Intraocular pressure change (mean mm hgâ±SD)

Time following compression, min

0 10 20 30 60

Control 10

Aspirin (600 mg p.O.)t 10

-6 .80 -6 .00 -5 .50 – 3 . 9 0 -1 .50

±1.75 ±2.11 ±1.78 ±2.73 ±2.76

– 6 . 7 0 – 6 . 6 0 – 6 . 0 0 – 5 . 2 0 – 3 . 5 0

±1.70 ±1.65 ±1.76 ±2.35 ±1.90

+1.70 +0.50

±2.11 ±1.58

-2 .60* -1 .80*

±2.41 ±2.35

* significant difference between treated and control.

T p.O. Denotes oral administration.

1010 AMERICAN JOURNAL OF OPHTHALMOLOGY JUNE, 1975

DISCUSSION

Intraocular pressure rebound after ocular

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Compression was reported previously.1 our

Animal investigations showed a definite presâ­

Sure response, while the human data were

Not as dramatic. In the previous studies, both

Digital massage and baillart ophthalmo-

Dynamometric compression were used and

Provided qualitatively similar reductions in

Intraocular pressure. The intragroup reducâ­

Tion in pressure using each method of comâ­

Pression fell within a similar range. Since

Digital massage is the simpler of the two

Methods and is also the technique clinically

Employed prior to intraocular surgery, we

Chose this means of compression in the presâ­

Ent study.

Reduction in intraocular pressure immediâ­

Ately after compression was quantitatively

Different in the animal and human segments

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Of this study. In human subjects, there was a

Pronounced reduction in pressure after digiâ­

Tal massage, with a gradual rise to peak levels

At 30 minutes. In an earlier work intraocular

Pressures approximated precompression

Values at the 20-minute interval.1 rabbits

Demonstrated a more modest decrease in

Intraocular pressure after massage, with an

Elevation of pressure in the subsequent time

Periods occurring earlier and with greater

Magnitude than in humans. The reasons for

These species differences were not evident.

Conceivably, variations in the structure of the

Vitreous and anatomic differences in the cilâ­

Iary body and iris were implicated. As the

Human volunteers were ocular hypertensives

With elevated baseline intraocular pressures, a

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Small reduction in intraocular volume could

Result in a greater decrease in intraocular

Pressure than with normal baseline pressures.

Despite these species differences in initial

Pressure reductions, the course following

Completion of compression was qualitatively

Similar and demonstrated an increase in intraâ­

Ocular pressure after ocular compression.

Postcompression elevation of intraocular

Pressure is associated with increased aqueous

Flare and hyperemia of the conjunctiva and

Iris. The sequence of events observed folâ­

Lowing ocular compression appears to be a

Consequence of disruption of the blood-aqueâ­

Ous barrier.3·5 identical findings are observed

Following topical or intracameral administraâ­

Tion of prostaglandins, and also with a topâ­

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Ical preparation of arachidonic acid, a PGE2

Precursor.710 it appears that the breakdown

Of the blood-ocular barrier is prostaglandin-

Mediated.

Pretreatment with the anti-inflammatory

Agents, indomethacin and aspirin, interferes

With the synthesis or release of prostaglandin

By inhibiting the enzymes which generate

Prostaglandin. Pretreatment with indomeâ­

Thacin blocks the intraocular pressure rise

After topical administration of arachidonic

Acid, but has little effect on the pressure inâ­

Crease due to topical administration of

PGEZ.10 other workers showed that aspirin

Prevented the disruption of the blood-aqueâ­

Ous barrier in rabbits, presumably by inhibitâ­

Ing prostaglandin synthesis.3

The elevation of intraocular pressure folâ­

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Lowing ocular compression could occur as a

Consequence of several possible mechanisms :

A reduction in outflow facility, an increase in

Ocular volume as a consequence of the breakâ­

Down of the blood-ocular barrier, or an inâ­

Crease in aqueous production. Studies showed

That intracamerally or topically administered

Prostaglandin did not reduce outflow facility,

And an enhanced outflow facility may have

Occurred.11·12 it does not appear that reducâ­

Tion in outflow facility is responsible for the

Elevation of intraocular pressure. PGEj may

Stimulate an active transport mechanism, proâ­

Mote increased aqueous production, and eleâ­

Vate intraocular pressure.11

Finally, disruption of the blood-ocular barâ­

Rier may permit easier access for flow of

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Materials from the vascular system to the

Eye. Greater permeability through the tight

Junctions of the retinal pigment epithelium

May allow passage of fluid from the choroid

To the vitreous body. Similarly, movement of

VOL. 79, NO. 6 OCULAR COMPRESSION 1011

Fluid through the ciliary processes, as a conâ­

Sequence of increased permeability, also may

Contribute to increased vitreous volume. The

Effect of indomethacin and aspirin on the reâ­

Duction of the intraocular pressure response

And on vascular permeability in our animal

And human studies confirms the observation

Of previous workers that aspirin stabilizes

The blood-aqueous barrier in irritated

Eyes.8·10 fur ther studies are needed to evalâ­

Uate the state of the vitreous body after

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Treatment with anti-inflammatory drugs unâ­

Der conditions which might influence disrupâ­

Tion of the blood-aqueous barrier. As digital

Compression is commonly employed prior to

Intraocular surgery, the results of such

Studies may have important clinical implicaâ­

Tions.

S U M M A R Y

Pretreatment with indomethacin, 10 m g /

Kg given intraperitoneally to rabbits, and asâ­

Pirin, 600 mg given orally to humans, sigâ­

Nificantly reduced the rebound alteration of

Intraocular pressure after ocular compresâ­

Sion as compared to untreated controls.

REFERENCES

1. Obstbaum, S. A., robbins, R., best, M., and

Galin, M. A. : recovery of intraocular pressure and

Vitreous weight after ocular compression. Am. J.

Ophthalmol. 71:1059, 1971.Anoxia definicion

2. Duke-elder, P. M., and duke-elder, W. S.:

The vascular responses of the eye. Proc. R. Soc.

Biol. 109:19, 1931.

3. Neufeld, A. H., jampol, L. M., and sears,

M. L. : aspirin prevents the disruption of the

Blood-aqueous barrier in the rabbit eye. Nature

238:158, 1972.

4. Vane, J. R. : inhibition of prostaglandin synâ­

Thesis as a mechanism of action of aspirin-like

Drugs. Nature new biol. 231:232, 1971.

5. Cole, D. F., and unger, W. G. : prostaâ­

Glandins as mediators for the responses of the eye

To trauma. Exp. Eye res. 17:357, 1973.

6. Kirsch, R. E., and steinman, W. : digital presâ­

Sure an important safeguard in cataract surgery.

Arch. Ophthalmol. 54:697, 1955.

7. Beitch, B. R., and eakins, K. E. : the effect

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Of prostaglandins on the intraocular pressure of the

Rabbit. Br. J. Pharmacol. 37:158, 1969.

8. Eakins, K. E. : increased intraocular pressure

Produced by prostaglandins ei and es in the cat

Eye. Exp. Eye res. 10:87, 1970.

9. Kelly, R. G. M., and starr, M. S. : effects of

Prostaglandins and a prostaglandin antagonist on

The intraocular pressure and protein in the monkey.

Can. J. Ophthalmol. 6:205, 1971.

10. Podos, S. M., becker, B., and kass, M. A.:

Indomethacin blocks arachidonic acid-induced eleâ­

Vation of intraocular pressure. Prostaglandins

3 :7, 1973.

11. Kass, M. A., podos, S. M., moses, R. A., and

Becker, B. : prostaglandin ei and aqueous humor

Dynamics. Invest. Ophthalmol. 11:1022, 1972.

12. Waitzman, M.Anoxia definicion B., and king, C. D. : prostaâ­

Glandin influences on intraocular pressure and pupil

Size. Am. J. Physiol. 212:329, 1967.