Correlation between intraocular pressure and biochemical changes in experimental glaucoma

MC Gupta; P Khosla; KN Garg

Home

Users Online: 3303

ARTICLES

Year : 1985 | Volume : 33 | Issue : 5 | Page : 309-312

Correlation between intraocular pressure and biochemical changes in experimental glaucoma

MC Gupta, P Khosla, KN Garg
Department of Pharmacology, Medical College, Rohtak, India

Correspondence Address:
P Khosla
18/8 F.M.. Medical Enclave, Medical College, Rohtak (Haryana)
India

Source of Support: None, Conflict of Interest: None

Check

PMID: 3843341

How to cite this article:
Gupta M C, Khosla P, Garg K N. Correlation between intraocular pressure and biochemical changes in experimental glaucoma. Indian J Ophthalmol 1985;33:309-12

How to cite this URL:
Gupta M C, Khosla P, Garg K N. Correlation between intraocular pressure and biochemical changes in experimental glaucoma. Indian J Ophthalmol [serial online] 1985 [cited 2021 Jan 26];33:309-12. Available from: https://www.ijo.in/text.asp?1985/33/5/309/30737

Several workers[1],[2] had paid attention to the role of biochemical changes in blood in the etiopathogenesis of glaucoma. Their investigations were not merely restricted to congestive form of glaucoma but also to the other manifestational forms of glaucoma.

Hanish[3] observed that in the origin of acute glaucoma attack, the neurovascular circulation plays an important role and that there is a rise in blood lipid concentration. Other workers have also pointed out an elevated lipid concentration in the blood and that the clinical improvement in the condition of the patient is closely accompanied by a reduction in different lipid fractions in the blood[4],[5]. However, Muselvic[6] observed that the blood cholesterin content of glaucoma patients corresponded to that of healthy in individuals. Nonay and Feldmann also observed that there was no correlation between cholesterin concentration and intra ocular pressure[7],[8].

An association of diabetes with rise in intraocular pressure had been observed by some workers[9],[10],[11],[12]. But according to Bouzas there was no difference in the mean intraocular pressure in diabetics and in the general population[13].

The present study of producing experimental glaucoma in rabbits for the purpose of establishing the relationship between intraocular pressure and the various biochemical changes in blood produced by glaucoma was under taken.

Material and methods

The study was carried out in a group of twenty rabbits of both the sexes and weighing from 1.5 to 2.0 kg. The diet was standardised balanced diet.

Experimental glaucoma was produced in one eye of the animal, the other eye serving as control. Glaucoma was produced by injecting 20% liquid paraffin into the anterior chamber of the eye after giving local surface anaesthesia with 2.0% xylocaine[14]

Intra-ocular pressure was recorded with the help of Sehiotz tonometer, before producing glaucoma and then after producing glaucoma for three hours at one hour interval and then on second and third day. Antibiotic drops were put into both eyes so as to prevent any possible infection. Blood samples were collected from the marginal ear vein with every intra ocular pressure recording.

The blood samples were subjected to the following biochemical investigations :

(i) Serum free fatty acids : estimated according to the method of Novak[15]. (ii) Serum cholesterol : It was estimated by the method of Chiamori and Hanry[16]. (iii) Serum triglycerides : Serum triglyceride levels were estimated accordingto Lowell[17]. (iv) Blood sugar : estimated by oxidation method of Folin and Wu[18].

The animals themselves served as controls for biochemical changes as the blood sample collected before producing glaucoma was subjected to the same biochemical investigations.

Observations

Intra-ocular Pressure

Intraocular pressure recordings were taken in both eyes before and then after producing glaucoma in left eye, while keeping the right eye as control. A marked rise in intra ocular pressure was observed on injection of 20% liquid paraffin into the anterior chamber. It started rising within an hour and reached the peak level by third hour. Average rise in intra ocular pressure was from a normal pressure of 23.0 ± 1.715 mm of Hg to 44.7 ± 2.10 mm of Hg in second hour (p <0.001) and 47.3 ± 1.96 mm of Hg in third hour (p <0.00i). Intraocular pressure started 'declining on second day and returned almost completely to normal on third day.

There was a marked congestion along with dilatation of pupil in the eye with experimental glaucoma. There was also oedema and bazziness of the cornea.

Biochemical Changes [Figure - 1]

1. Serum Free Fatty Acids (FFA) : There was a marked rise in the concentration of serum free fatty acids following production of experimental glaucoma. The rise in the concentration was corresponding to the rise in intaocular pressure. Peak levels were shen by third hour and these levels went on declining till third day when they were almost normal.

Average levels of serum FFA concentration was 1199±56.8 uEq/litre in the 2nd hour (P <0.001) and 1447±53.2 uEq/litre in the 3rd hour (P <0.001) as compared to the normal values of 607.5±33.5 uEq/litre.

2. Serum Triglycerides (STG)-The levels of STG also increased following experimental glaucoma. The rise started with the rise in intraocular pressure. Peak rise was in the 3rd hour then the levels started decreasing and reached normal by third day.

Average level of the concentration of serum triglycerides was 208±11.38 mg% in the 2nd hour (P <0.001) and 226.7±9.17 mg% in 3rd hour (P <0 001) as compared to normal levels of 133.5±4.49 mg%,

3. Serum Cholesterol -With increase in the intraocular pressure, there was a simultaneous increase in the serum cholesterol concentration following production of the experimental glaucoma.

The peak values were seen in the 3rd hour usually. Then the levels started declining on 2nd day and values came to normal on 3rd day. The mean value of serum cholesterol concentration before glaucoma was found to be 102.4±1.01 mg/100 ml. These values increased to 154.9±12.78 mg/100 ml in 2nd hour (P <0.01) and 161.8±11.29 mg/ 100 ml in 3rd hour (P <0 01).

4. Blood Sugar -There was a rise in the levels of blood sugar with a rise in intraocular pressure. The maximum concentration was observed by 3rd hour and then the concentration started declining so as to return to normal levels, usually by 3rd day.

The average values of blood sugar concentration in 2nd hour and 3rd hour were 85.6±6.54 mg/100 ml (P <0.05) and 89.6± 6.78 mg/100 ml (P <0.05) respectively as compared to the normal values of 67.5±4.2 mg/100 ml.

Discussion

In the present study, a marked increase in the concentration of free fatty acids was observed following production of experimental glaucoma. The levels of serum free fatty acids started rising with the rise in intra-ocular pressure. Their maximum concentration accompanied peak rise in intraocular pressure and started declining simultaneously with fall in intra-ocular pressure. So the changes in serum free fatty acid concentration almost ran parallel with changes in intra ocular pressure.

This is in correlation with the observations of Hanisch, et al who showed a parallel relationship between the rise of serum free fatty acids and the rise in intra ocular pressure[2],[3],[19].

Mayer and Connell[20] found an increased viscosity and increased lipid content in glaucoma patients as compared to their levels after the intra ocular pressure returned to normal. In patients affected by glaucoma higher concentration and after the passage of emergency, lower concentration of FFA was found[3]. It was shown that changes in serum FFA and blood viscosity run parallel with changes in intra-ocular pressure.

As regards the other lipid fractions like serum triglycerides and serum cholesterol, similar observations have been made. This has been corroborated by our experiments. Their levels increased with the rise in intraocular pressure and declined when intra ocular pressure came down so pointing out an inter-relationship between the two changes, however, were not as marked as in serum FFA but still they were statistically significant. The correlation between intraocular pressure and blood sugar has been shown by various authors[9],[12],[21],[23]. On the other hand no specific association between diabetes and glaucoma was found by Bougas[13]. In our study, only slightly higher levels of blood sugar were registered after producing glaucoma.

Orban observed that disease conditions which are accompanied by changes in the composition of blood could give rise to an elevation or depression of the intra ocular pressure[2] Hanisch found that in the origin of acute attack of glaucoma, neuro vascular circulation may play a part[3]. An elevation of blood lipid concentration is generally known in other vascular crises. The similar association of the rise in blood lipid concentration has been made' in glaucoma in the present study and by other workers[2],[3],[24],[25].

On the basis of these various biochemical changes occurring in blood in glaucoma, it may be concluded that the rise in various lipid fractions especially serum FFA may be associated with acute attack of glaucoma since the rise and fall of the biochemical fractions closely corresponded with the rise and fall in intraocular pressure in the present study.

This brings us to the surmise that blood lipids play an important role in the pathomechanism of glaucoma and that if by some mechanism, the rise in blood lipid concentration could be prevented, it may help to prevent an acute attack of glaucoma and may also provide some therapeutic benefit in the treatment of glaucoma.

Summary

In an experimental model, endeaver has been made to correlate high IOP to levels of blood lipids concentrations.

References

1.	Dule Elder, S. 1969, Glaucoma, System of Ophthalmology. Vol. Xl.
2.	Orban T., Hanish, J., Vereb K. 1966, Klin. Monat. Fur. Augenheilk, 149:847.
3.	Hanisch, J , Blumenfeld, G., Hegedus A., 1966, Klin. Monat. Fur. Augenheilk. 148;850
4.	Goth E. and Blumenfeld G., 1964., Orv. Hetil. 105:1786.
5.	Kahan, A. and Mitarb, U., 1965 , Orv. Hetil. 106:871.
6.	Muselvic, A„ 1930. Arch. Oftal. 7:529.
7.	Noray, T. 1930. Oiv. Hetil, 74:315.
8.	Feldmann, J.B., 1939., A.M.A. Arch. Ophtbalmole 22:595,
9.	Lieb W.A., Stark N., Jelinek, C.M.B. and Malzi R., 1967., Berlin. Deutsb, ophth. Gest. 68:437.
10.	christiansson, J., 1961., Acta Ophthalmole 37:155.
11.	Sugar, H.S,, 1564., Modern Ophthalmology. 4, 554.
12.	Becker, B., 1971.. Amer. J. Ophthalmol. 71:1.
13.	Bouzas, A.G., 1971, Arch. Ophthalmole., 85: 423.
14.	Garg, K.N. and Sangha, S.S., 1964, Orient. A. Ophtbalmole 2:121.
15.	Novak, M.,1965, J. Lipid Res, 6:431.
16.	Chiamori N. end Henry, RJ., 1959, Amer J Clin. Path. 37:365.
17.	Lowell, B., Foster, P. and Ralph. T.D., 1973, Acta Clin. Chem. 19:338.
18.	Follin, O. and Wu, H.J., 1926, J. Bioli Chem 67:357.
19.	Shafrir, E., 19(5, Diabetes, 14:77.
20.	Mayer, G.A. and Conell, W.P., 1961. Circulation, 24:1098.
21.	Armstrong, J.R., Daily, R.K. and Dobson, H.L, 1960. Am. J. Ophthalmole., 50:55.
22.	Larsen, H.W. and Poulsen, J.F. 1962, Acta Opbthalmole 40:580.
23.	Bankes, J,L.K., 1967, Erit. J. Ophthalmole 51:557.
24.	Dienstbeer, E., Balik, J. and Fischer, 0 , 1961, CSL. Oftal.17:205.
25.	Miller, S,J.H., 1972, Trans. Ophthalmole Soc. U.K. 92:5638.