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Year : 1985  |  Volume : 33  |  Issue : 5  |  Page : 313-315

Evaluation of effects of clofibrate, an antilipaemic agent on intraocular pressure in experimental glaucoma

Department of Pharmacology, Medical College, Rohtak, India

Correspondence Address:
P Khosla
18/8 FM, Medical Enclave Medical College, Rohtak (Haryana)
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Source of Support: None, Conflict of Interest: None

PMID: 3843342

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How to cite this article:
Gupta M C, Khosla P, Garg K N. Evaluation of effects of clofibrate, an antilipaemic agent on intraocular pressure in experimental glaucoma. Indian J Ophthalmol 1985;33:313-5

How to cite this URL:
Gupta M C, Khosla P, Garg K N. Evaluation of effects of clofibrate, an antilipaemic agent on intraocular pressure in experimental glaucoma. Indian J Ophthalmol [serial online] 1985 [cited 2021 Jan 24];33:313-5. Available from: https://www.ijo.in/text.asp?1985/33/5/313/30738

In the origin of acute glaucoma attack the neurovascular circulation plays an important role[1]. In other vascular crises an elevation of blood lipid concentration is generally known. Higher concentrations of free fatty acids were found during acute attack of glaucoma which were lowered after the passage of the emergency[1].

In the vascular crises there is an increased viscosity of blood and the serum lipid content is higher[2]. Shafrir also found increased concentration of nonesterified fatty acids in cases of glaucoma[3]. Miller[4] studied fasting plasma lipoprotein levels and showed an elevation of plasma cholesterol in low tension glaucoma.

Dienstbier showed that serum lipoprotein contents of glaucoma patients agree with those of arteriosclerotic patients[5].

Clofibrate, an antilipaemic agent, was introduced for the reduction of serum chole­sterol and serum triglycerides levels in pati­ents with ischaemic heart disease[6]. It redu­ces serum lipids and interferes with blocd clotting.

The idea of using clofibrate in glaucoma patients seems to have arisen from investiga­tions by Hanisch of the blood chemistry during attacks of acute congestive glaucoma, which suggested an increase in the concen­tration of unesterified fatty acids[1].

Orban used clofibrate in the treatment of acute closed angle glaucoma and it was clai­med that single dose of clofibrate relieved the attack in eight out of ten cases[9],[10] Cullen tried effect of clofibrate in patients with chronic simple and secondary glaucoma, who had not responded to other treatment and in whom operation was envisaged. In half of the patients intra-ocular pressure fell signi­ficantly[11].

Gloster studied effects of clofibrate on the intraocular pressure in rabbits. No signifi­cant difference was found in the level of tension between treated and untreated animals[12]. Ramsell and Roth in a trial of clofibrate treatment of chronic simple glau­coma found no significant difference in intra­ocular pressure before and after treatment[13]

In the present study, experimental glaucoma was produced in rabbits to evaluate the effects of clofibrate, an antilipaemic agent, on the intra-ocular pressure.

  Material and methods Top

This study was carried out in a group of thirty albino rabbits of both sexes and weigh­ing from 1.5-2.0 kg. These were kept on a controlled standard diet. Water was provi­ded ad. lib. These were further divided into three sub groups of ten animals each.

Sub-group I; control; No drug was given. Glaucoma was produced in one eye[14] the other eye serving as control.

Sub-group II: In this subgroup of animals clofibrate was given before producing glaucoma in daily dose of 625 mg I/M for four days. On the fifth day glaucoma was produced.

Sub-group III : In these animals clofibrate was given 625 mg I/M after producing Glaucoma.

Intra ocular pressure was recorded in both the eyes with the help of Schiotz's tonometer, before producing glaucoma and after pro­ducing glaucoma for three hours, at one hour interval and then on second and third day. Antibiotic drops were put into both the eyes so as to prevent any possibility of infection.

  Observations Top

Sub-group I :

In these animals a marked rise in intra­ocular pressure occurred. It started rising within an hour and reached the peak levels by third hour. Average normal intraocular pressure of 23.0±0.54 mm of Hg increased to 47.3±1.96 mm of Hg in 3rd hour (P<0.001)­ [Figure - 1]. Intraocular pressure started declin­ing by second day and returned almost to normal levels by third day. There was marked congestion along with dilatation of the pupil. There was also oedema and hazi­ness of cornea.

Sub-group II :

In these animals there was a rise in intra­ocular pressure but the values were much less as compared to the values in subgroup I. Average intraocular pressure was only 37.8±0.91 mm of Hg in the third hour as compared to 47.3±1.96 mm of Hg in sub­group I (p<0.01).

Sub-group III :

In this subgroup in which treatment with clofibrate was given after producing glau­coma, the mean value of intraocular pressure was only 34.8±0.96 mm of Hg in the third hour as compared to a value of 47.3±1.96 mm of Hg in the untreated animals (p<0.01). There was a rise in intraocular pressure after injecting 20% liquid paraffin into the anterior chamber. But there was no further rise following injection of clofibrate.

  Discussion Top

On the basis of the biochemical changes occurring in the blood, it has been hypothe­sized that if in acute cases of glaucoma, the concentration of various lipid fractions and thereby viscosity of blood could be brought down by administration of certain drugs, then the intraocular pressure also must become lowered. If in cases of glaucoma, lipid concentration is brought down or nor­malised by clofibrate, then the manifestations of glaucoma attack should also cease. In the present study clofibrate by its antilipaemic action has been used for this purpose.

Clofibrate could be used in glaucoma patients also, was revealed by Hanisch[1] wh demonstrated an increased concentration of free fatty acids and other lipids during glaucoma attack. Many other workers used clofibrate in glaucoma patients and found it to be effective in the cases where there was no response to other drugs[10],[11],[15],[16].

In other studies, however, it was reported that clofibrate did not have any significant use in patients with glaucoma or in certain animal studies[12],[13].

In our study clofibrate was given both before and after producing glaucoma in rabbits. This was done so as to find out any effect of cloribrate to prevent glaucoma attack or its usefulness as a treatment.

In the animals where it was given prior to producing glaucoma, a much less significant rise in the intraocular pressure occurred as compared to the animals in which no drug was given. It means that the drug may have a prophylactic value which could be utilised to prevent an acute attack of glaucoma. The drug also prevented any further rise of the intraocular tension when it was given after production of glaucoma. The pressure rather started falling down.

It brings us to the conclusion that the administration of antilipaemic drugs like clofibrate by correcting disturbances in fat metabolism in patients in whom glaucoma is somewhat anticipated, may prevent its acute attack and may be useful to some extent as a therapeutic measure for its treatment.

  Summary Top

Experimental glaucoma was produced in rabbits. There was a marked rise in the intraocular pressure. Clofibrate, an antili­paemic agent given before producing glaucoma prevented a marked rise in the intra-ocular pressure and given after produ­cing glaucoma caused a decline in the intra­ocular pressure, thereby showing that the drug could be of significant prophylactic and also some therapeutic value.

  References Top

Hanisch, J , Blumenfeld G , Hegedus A., 1966, Klin. Monat. Fur. Augenheilk. 148: 850.  Back to cited text no. 1
Mayer, GA, and Conell W.P, 1961, Circulation 24: 1098.  Back to cited text no. 2
Shafrir, E,, 1965, Diabetes 14:77.  Back to cited text no. 3
Miller SJH, 1972, Trans, Ophthal. Soc. U K. 92 : 563.  Back to cited text no. 4
Dienstbier E.. Batik J., Fischer, O., 1961, CSL Oftal, 17 : 205.  Back to cited text no. 5
Oliver M.F., 1962, Lancet 1 : 1321.  Back to cited text no. 6
Thorp J.M., 1962, Lancet 1 : 1323  Back to cited text no. 7
Cullen J.F., 1964, Trans. Ophthal. Scc. U K. 84 : 281.  Back to cited text no. 8
Orban, T., 1967, Orv. Hetil, 118:873.   Back to cited text no. 9
Orban, T. 1968, Lancet 1:47.   Back to cited text no. 10
Cullen, J.F., 1967, Lancet 2 : 892.  Back to cited text no. 11
12, Gloster, J., 196F, Brit J. Ophthalmol, 52:793   Back to cited text no. 12
Ramsell, T.G. and Roth JA, 1960, Brit. J. Ophthalmol 53:230.  Back to cited text no. 13
Garg, K.N. and Sangha SS, 1964, Orient. A. Ophthalmol 2:121.  Back to cited text no. 14
Nolan, J., 1974, Trans. Ophthal Sec. U K. 94 : 563.  Back to cited text no. 15
Orban T. Hanisch, J , Vereb, K., 1966, Klin. Monat. Fur. Augenheilk. 149: 847.  Back to cited text no. 16


  [Figure - 1]


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