The Contribution Of Intraocular Pressure To The Eye Biology Essay

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The objectives of this experiment were to study the contribution of intraocular pressure to the eye and discovered the measurement of intraocular pressure by using a calibrated Schoitz tonometer with combination of manometer.

Aqueous humour produced by ciliary body and it is the fluid with an ionic composition that very similar to blood plasma, it filled the anterior chamber of the eye, nourishes the cornea, provide shape to the eye and maintain intraocular pressure (IOP) within normal range of 10mmHg to 21mmHg. Normal eye produces about 4 c.c. of aqueous humour a day and its equilibrium is preserve by homeostatic mechanisms but it may blocked at various sites along the pathway due to deposits of pigment or debris on the trabecular sheets. Small variations in either the production or outflow of aqueous may lead to significant changes in IOP.

Canal of schlemm contain a sieve like structure called trabecular meshwork, it serves as the main drainage channels for aqueous humour. The cells in trabecular meshwork deplete gradually as age increased and lead to a greater loss of trabecular meshwork function. The loss of trabecular capacity normally compensated by the concomitant natural where aqueous humour production may also decrease. However, when the loss of trabecular meshwork function cannot be compensated, this may leads to rise of IOP.

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Primary blockage of trabecular sheets commonly caused by the malfunctioning of the endothelial lining of the canal due to enzymatic, nutritional, or immunological factors. Perhaps it may be related to gentle, genetic defect, ageing process or abiotrophy and results to gradual increase in the resistance and gradual loss of cell activity. Physical activity like stress, rapid fluid intake, and caffeine may also affect the intraocular pressure reading.

IOP that consistently above 21mmHg indicates an ocular hypertension. An individual that has ocular hypertension should be observed more closely because onset of glaucoma will be higher. Glaucoma causes damage to the optic nerve and these may lead to blindness, early detection is very important in order to prevent serious loss of vision. Intraocular pressure slowly rises with increase of age; glaucoma is prevalent with aged.

Tonometry is a procedure used in optometry to produce a clinical measurement of intraocular pressure by using a tonometer to measure the tone or firmness from the eye surface. Tonometry is important in the diagnosis of glaucoma and in monitoring the effectiveness of medication used to control it. There are two categories of tonometer, either a contact tonometer or a non-contact tonometer. Thru contact tonometer, intraocular pressure can be measure by direct touching the eye with the instrument. While non-contact tonometer, as the name suggests, the intraocular pressure can be measure without touching the eye but with small puff of air onto the eye.

In this experiment, a contact tonometer shown in figure 1 was used. The Schiotz tonometer in figure 1 was invented in year 1905 by Prof. Schiotz, of Christiania (Bernard C. 1917). Schiotz tonometer is a classic tonometer that works with the principle of indentation where certain amounts of indentation were placed on the cornea and it was proportional to the intraocular pressure (David 1983). The reading of the intraocular pressure was estimated by the degree of indentation (Bernard C. 1917). Higher the Schiotz reading indicates lower

intraocular pressure in millimetre mercury (mmHg).

METHODS:

In this experiment, Schiotz tonometer was connected to a manometer and used to measure the intraocular pressure of bovine eyes. The tube leaded to the needle was filled with water as the experimental set-up shown in fig. 2 and the pressure was raised by pumped the bulb.

The needle was inserted to the anterior chamber through the limbus area but not too deep into the lens and left at the centre of the anterior chamber with supported to prevent distortion of the globe by the needle. The pressure within the chamber was lowered to 5mmHg before the needle was passed into the anterior chamber of the eye. The pressure was then raised to 20mmHg and the eye was left for a moment to assume its normal shape. A retort stand and clamp were used to position the Schiotz tonometer on the cornea. The clamp was attached to the handle of the tonometer. The tonometer was supported by the eye with the footplate rested directly on the cornea. The pressure was then lowered to 10mmHg and then the Schiotz reading started to taken. The pressure was rose in 5mmHg steps by pumping the bulb, each reading were recorded up to pressure of 45mmHg and then declined in 5mmHg step to back to 10mmHg. The whole procedure, 3 readings are taken and averaged. Average values were calculated and referred from the calibration table for the standard deviation pressure in 5.5gms undisturbed eye. The procedures above were then repeated for the second bovine eye. Data collected from eye 1 was recorded in table 1 and eye 2 was recorded in table 2.

RESULTS:

Table 1: Manometer values in mmHg, Schiotz tonometer values in arbitrary unit and conversion figures to standard deviation in mmHg for eye 1.

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Manometer Value

(mmHg)

Schiotz Tonometer Reading In Arbitrary Unit (AU)

Standard Deviations,Pressure In (5.5gm) Undisturbed Eye (mmHg)

Reading 1

Reading 2

Reading 3

Mean

Average

10

6.0

3.0

2.0

3.7

35.4

15

4.0

3.0

2.0

3.0

37.1

20

3.0

2.5

2.0

2.5

38.9

25

2.8

2.0

1.5

2.1

40.9

30

2.2

1.5

1.0

1.6

43.1

35

2.0

1.0

1.0

1.3

43.1

40

1.0

0.8

0.8

0.9

45.5

45

0.5

0.5

0.5

0.5

48.3

40

0.5

0.5

0.5

0.5

48.3

35

0.5

0.5

0.5

0.5

48.3

30

0.8

0.5

0.5

0.6

48.3

25

0.8

0.5

0.5

0.6

48.3

20

0.8

0.8

0.5

0.7

48.3

15

1.0

1.0

1.0

1.0

45.5

10

1.0

1.2

1.0

1.1

45.5

Table 1 shows the 1st, 2nd, 3rd values taken from the Schiotz tonometer as a result of a changed in pressure created by the manometer for eye one, the mean averages of these 3 results and the standard deviations of the pressure in an undisturbed eye. The standard deviation values are the values converted from the mean value by referred to Friedenwald's 1955 calibration table. Table 1 indicated that the pressure created by the manometer increased; the Schiotz tonometer readings of the eye decreased and the standard deviation increased. The results of manometer values and the standard deviation values were presented in the form of a scatter graph with smooth line shown in fig. 3.

Table 2: Manometer value in mmHg, Schiotz tonometer value in arbitrary unit and conversion figures to standard deviation in mmHg for eye 2.

Manometer Value (mmHg)

Schiotz Tonometer Reading In Arbitrary Unit (AU)

Standard Deviations, Pressure In (5.5gm) Undisturbed Eye (mmHg)

Reading 1

Reading 2

Reading 3

Average Reading

10

2.2

2.2

2.8

2.4

38.9

15

2.0

1.8

2.4

2.1

40.9

20

1.8

1.8

2.0

1.9

40.9

25

1.6

1.4

1.8

1.6

43.1

30

1.2

1.2

1.2

1.2

45.5

35

1.0

1.0

1.0

1.0

45.5

40

0.8

1.0

1.0

0.9

45.5

45

0.8

0.8

0.6

0.7

48.3

40

0.8

0.8

0.8

0.8

45.5

35

0.8

0.8

0.6

0.7

48.3

30

0.8

0.8

0.6

0.7

48.3

25

1.0

1.0

0.8

0.9

45.5

20

1.0

1.0

1.0

1.0

45.5

15

1.2

1.2

1.2

1.2

45.5

10

1.4

1.8

2.0

1.7

43.1

Table 2 shows the 1st, 2nd, 3rd values taken from the Schiotz tonometer as a result of a changed in pressure created by the manometer for eye two, the mean averages of these 3 results and the standard deviations of the pressure in an undisturbed eye. The standard deviation values are the values converted from the mean value by referred to Friedenwald's 1955 calibration table. Table 2 indicated that the pressure created by the manometer increased; the Schiotz tonometer readings of the eye decreased and the standard deviation increased. The results of manometer values and the standard deviation values were presented in the form of a scatter graph with smooth line shown in fig. 4.

Figure 3: The Schiotz intraocular pressure versus manometer pressure of eye one.

In both figure 3 and figure 4, the crosses indicated the standard deviation values converted from the Friedenwald's calibration table and the smooth lines were the polynomial lines of the standard deviation values. Bell curve line in figure 3 was mostly goes through all the points on the ascending and descending line with R2 value of 0.9821. The polynomial line that added to the graph had shown how accurate the results are. The accuracy of the results is backed up by the R2 values calculated where the closer the R2 value is to 1, the greater the accuracy is.

Figure 4: The Schiotz intraocular pressure versus manometer pressure of eye two.

Whereas in figure 4, the smooth polynomial line was mostly goes through all the points on the ascending and descending line with R2 value of 0.8899.

Figure 5: Comparison of the standard deviations of Schiotz Intraocular pressure versus manometer pressure for eye 1 and eye 2.

In figure 5, the blue line had shown the polynomial lines for eye 1 and red for eye 2. From both of the R2 values, the results taken for eye 1 were more accurate compared to eye 2, this may be due to the readings of the both eye are taken by different peoples and caused uncertainties error. The polynomial line of eye 1 was steeper compared to eye 2, this may be due to the different aged of the eye; older eye may have least sensitivity compared to a younger eye. Hence, the lines of both eyes shown a bell-shaped, these indicated that when the pressure of the manometer increased, the standard deviation values of Schiotz pressure increased. Vice versa, when the pressure of the manometer decreased, the standard deviation values of the Schiotz pressure decreased.

DISCUSSION: (3 pages maximum)

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From this experiment, it was recognized that the effect of a Schiotz tonometer may vary and the variability effects may related with the eye's scleral rigidity, corneal elasticity and corneal rigidity (Jackson 1965). When scleral rigidity is high, the intraocular pressure will over estimate and the tension recorded will be less, if the scleral rigidity is lower than the reading will be normal (Agrawal et al.1991). Not only the rigidity of the ocular coats but also the compressibility of the vascular contents of the eye, and with the ease of the fluid expressed through the drainage channels, both of aqueous and blood (Jackson 1965).

However, the conversion charts for Schiotz tonometer (the Friedenwald's 1955 scale) that based on an average scleral rigidity make Schiotz tonometer expected to give readings of intra-ocular pressure which are of an acceptable standard of accuracy. Schiotz tonometer and Goldmann tonometer that known as "gold-standard tonometer" which determine intraocular pressure by measuring forces exerted on a constantly-sized area, the contact tonometer still widely used as routine tonometry and glaucoma screening equipment because this method is more accurate than "the air puff test," known as non-contact tonometry (Bengtsson 1972).

Tonometry findings are not the only way used to diagnose glaucoma, but one of the several findings that may consider. When IOP run over normal range, it may affect the optic nerve head where the retinal ganglion cells start to damage and caused vision loss. But in certain cases there will have no optic nerve head or visual field changes. Hence, most but not all glaucoma with elevated of IOP. Glaucoma was categories into several types, the two main types of glaucoma are primary open-angle glaucoma, and closed-angle glaucoma. These are manifest by an increase of IOP. When optic nerve damage has occurred regardless IOP, this called normal tension glaucoma. Secondary glaucoma are usually caused by another disease and contributed to the increased of IOP resulting in optic nerve damage and vision loss.

There are many factors that increased the risk of onset of glaucoma, which are related with increased of IOP, genetic or family related, racial background, and age. Open-angle and closed-angle glaucoma are normally occurred when drainage canals within the eye are physically blocked. Closed-angle glaucoma can be sudden or chronic. While in acute closed-angle glaucoma, a sudden increase in IOP occurs due to the build-up of aqueous humour. Acute closed-angle glaucoma considered emergency because optic nerve damage and vision loss can occur within hours of the onset of the problem may cause vision damage without symptoms.

The investigation completed from Investigative Ophthalmology & Vision Science unit clarified that rise of IOP strongly affected retinal ganglion cell apoptosis with an experiment prepared by induced pressure to created changes in extracellular matrix in the retina and optic nerve head in model rats' eyes. In normal control eyes, the mean numbers of retinal ganglion cells are about 115,000, while the mean numbers of apoptotic retinal ganglion cells in control eyes were 324.50, and in surgical eyes were about 1516.22. These values showed a significant correlation of retinal ganglion cells apoptosis with integral of IOP (Li Guo et al. 2005).

Beside the significant correlation of retinal ganglion cells, control eyes showed suggestive decreased in laminin deposition in the retinal ganglion cells layer in all IOP-elevated eyes and showed a significant negative correlation with IOP integral (Li Guo et al. 2005) then an increased in TIMP-1 immunolabeling in IOP-elevated eyes and showed a significant correlation with IOP exposure but no change in MMP-1. The studies demonstrated a significant increase in collagen I deposition in the retinal ganglion cell layer with elevated IOP, but not in collagen IV. In addition, TGF-β2 labelling showed a decrease in the retinal ganglion cell layer, and the change was significantly correlated with integral IOP. These proved that raised IOP was significantly positively related to expression of matrix metalloproteinase (MMP-9) a matrix-degrading enzymes that affect the pattern of matrix remodelling, TIMP-1 (a natural inhibitor for MMP), and collagen I in the retinal ganglion cell layer; in contrast, it correlated negatively with laminin and TGF-β2 (a secreted protein known as cytokine). MMP-9 activities suggest important mechanism mediating with glaucomatous retinal ganglion cells loss, where TGF-β2 and collagen I deposition associates significantly with raised IOP at the optic nerve head; these supports the theory of IOP elevation determines the extent of retinal ganglion cells loss. (Li Guo et al. 2005).

Apoptosis is a genetically controlled form of cell death that ganglion cells undergo during normal development of the retina and in diseases affecting the optic nerve, such as glaucoma. This mechanism of cell death is controlled by specific genes and their products that are activated in the dying cell. To date, the mechanism of ganglion cell apoptosis is poorly understood, but research on cell death in other areas has provided a blueprint for the study of dying ganglion cells in animal models. Extensive research of the genetic pathways of apoptosis of neurons, in general, has yielded new information about the principal genes that are involved in this process. This review is meant to survey the major genetic players that are active in neuronal cell death and discuss their possible roles in retinal ganglion cells. One of the primary regulatory steps is the activation of the tumor-suppressor protein, p53. This protein functions as a transcription factor that can up-regulate the expression of the proapoptotic gene bax and down-regulate the expression of the antiapoptotic gene brl-2. Changes in the concentrations of these gene products can further stimulate apoptotic events, including changes in mitochondria that ultimately lead to the activation of a family of cysteine proteases called caspases that digest the dying cell from within. An understanding of the genetic pathways of apoptosis may lead to the design of new treatments that could prevent its activation or arrest the process when started.

Visual fields and careful evaluation of the optic nerve heads and the retinal nerve fibers are extremely important in diagnosing glaucoma. If I had to pick one of the above as the most important finding in predicting the possibility of a patient having glaucoma I would have to say the appearance of optic nerve heads and retinal nerve fiber layer. One cannot be too dogmatic for a patient's visual fields, optic nerve heads, and nerve fiber layer are so very closely related.

Early reduction of nerve fibre in glaucoma eye caused slit gaps among the uniform striated retinal nerve fibre. The nerve fibre layer thins progressively, and its vessels become exposed as these defects grow together, the onset with advancing disease becomes deepen, and widen. These changes in the peripapillary retina are exemplified photographically and compared with perimetric findings. We believe that these fundoscopic signs provide the earliest objective evidence of nerve fiber wasting in eyes with chronically elevated intraocular pressure.

Recent data on people with ocular hypertension from the Ocular Hypertension Treatment Study have shown that they have an average estimated risk of 10% of developing glaucoma over 5 years. This risk may be decreased to 5% (a 50% decrease in risk) if eye pressure is lowered by medications or laser surgery. However, the risk may become even less than 1% per year because of significantly improved techniques for detecting glaucomatous damage. This could allow treatment to start much earlier, before vision loss occurs. Future studies will help to further assess this risk of glaucoma development. No one knows why certain ethnic groups, such as African Americans, have higher rates of glaucoma that lead to blindness. Primary open-angle glaucoma is the leading cause of blindness among African Americans and Alaska Natives, occurring 6-8 times more often than in whites, often in the earlier stages of life.

Differences in pressure readings between the two eyes of 3 mmHg or more must be questioned, this is not normal. There are several conditions which must be considered when this occurs.

(1) Glaucoma

(2) Retinal Detachment

(3) Uveitis-Iritis

(4) Poor Technique