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| ARTICLES |
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| Year : 1982 | Volume
: 30
| Issue : 4 | Page : 229-231 |
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The role of beta blockers in open angle glaucoma
VJ Marmion
73, Pembroke Road, Clifton Bristol, United Kingdom
Correspondence Address:
V J Marmion
73 Pembroke Road Bristol
United Kingdom
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 6131867 
How to cite this article:
Marmion V J. The role of beta blockers in open angle glaucoma. Indian J Ophthalmol 1982;30:229-31 |
In 1957, a paper of Kaplan described the effect of Rauwolfia serpentina on the intra-ocular pressure. He noted, in a group of normal subjects, that the response to treatment was variable. It was more marked in the glaucomatous subjects and the intravenous administration was associated with a fall in intra-ocular pressure in some 100 per cent of the thirty seven patients which he examined. All are classical observations in relation to the effect of sympathetic blockade on intraocular pressure. It was, however, five years prior to this that the first observations had been made on the effect of chemical sympathetic blockade by Hexamethonium. It was known, prior to that again, that surgical sympathectomy produced a transient fall in intra-ocular pressure which was followed by a return to normal in a variable period of time and this left the patient in a state of super-sensitization to topically administered adrenelin.
The differentiation between alpha and betablockers by Alquist, 1947, had taken the work a stage further. Of the alpha blockers available, Dibenamine has not been suitable for topical application, Thymoxamine, which was investigated in 1968 and 1969, does produce a transient lowering of intra-ocular pressure. Subsequently, Mapstone has shown that thymoxamine is effective in lowering the intraocular pressure in patients with angle closure glaucoma. It has not been found to be effective in open angle glaucoma in long term studies.
The advent of guanethedine, 1962, which is both an alpha and a beta blocking agent, renewed the interest in the effect of sympathetic blockade and a lot of work has been done, particularly in the middle sixties, on the effect of guanethedine alone and, subsequently, using combinations of various strengths of guanethedine and adrenelin'. Various crossover studies have shown a greater percentage fall in pressure than with pilocarpine. Problems have arisen in relation to local side effects.
The advent of beta blockers was, perhaps, overshadowed, in part, by the adverse side effects locally to systemic practolol, which seems to be the most potent of that particular group in the lowering of the intraocular pressure[2]. Propranolol also has the effect of lowering the intraocular pressure when applied topically. (Bucci 1968), and this effect does not seem to be well sustained. Long term studies have shown a lack of local tolerance and side effects. The same has been true of atenolol. The most successful to date has been Timolol malleate, and this has been the subject of a substantial number of reports in the literature. It seems to be, broadly speaking, effective either alone, in 70 %, or in conjunction with other additional remedies, such as adrenelin or pilocarpine in a further twenty per cent of cases of open angle glaucoma. The studies, however, have not been on a long term basis and its future role is still somewhat in doubt. Some papers have also complicated the issue by discussing its role in a variety of forms of glaucoma, such asaphakic glaucoma of unspecified designation, secondary glaucoma also unspecified, and conditions such as buphthalmos, aniridia and Sturge-Weber disease.
There are two problems in relation to topical beta blockers which have yet to be fully evaluated. These are the local side effects and the long term tolerance. While it has been well documented that guanethidine has given rise to a dry-eye type syndrome, the same problem has arisen with local propranolol and atenolol. A number of patients on timolol have shown less marked reactions[3] and therefore, one has to be cautious about this in the long term.
The systemic absorption from guanethidine has not proved to be as marked as propranolol or with timolol. With absorbtion, both the bradycardia and the accentuation of bronchospasm need to be taken into account. There have been reports of bronchospasm after the application of timolol and also, at least one case of death during a severe bronchospasm, which has been atributed to Timolol. Some patients are aware of the bradycardia and this is of sufficient intensity for them to feel discomfort and a reduction of exercise tolerance. Although it is generally suggested that people do not have symptoms unless their pulse rate falls below forty, this is probably more relevant with patients who are on treatment for systemic hypertension and is not applicable, by and large, to people who are in a more elderly age group, and who do not suffer from an essential hypertension. These important complications amount to less than 10 per cent of the reported complications.
There are observations[2],[4], which indicate that beta blockers given systemically can control the intraocular pressure. It had been previously observed by Cotay and Drance that the absolute fall in intraocular pressure was proportional to the pre-treatment level. Further it was noted by Wettrell, that the maximum effect occurred three hours after treatment which corresponded with the known highest levels of serum propranolol. It could be anticipated that this would correspond with the highest receptor saturation although, according to Fitzgerald and O'Donnell,[5] serum levels may not entirely be consistent with receptor saturation. There is data also which indicates that atenolol has a similar effect to propranolol[6],[2] and our own observations would be consistant with this. It has also been shown that these two beta blockers, propronolol as atenolol, when given in combination with conventional treatment, do provide a synergistic effect. In this context, it would be interesting to quantify the overall suppressive effect of such combinations on the diurnal fluctuation of pressure.
Systemic beta blockers might also be of benefit in reducing the phenomenon of tachyphylaxis with adrenelin rendering the long term administration of topical adrenelin safar. While the reports on topical beta blockers indicate that they have little effect on outflow facility, it has been suggested in the work of Cotay and Drance, that oral propranolol does increase the outflow facility and this is also correlated by the work by Tickazay and Nanbur in 1976. There have also been reports indicating a similar effect from topical application[7]. The effect of beta blockers in relation to arterial blood pressure and ocular perfusion would need to be clarified in this context. Perhaps the overall suppression of the diurnal fluctuation of pressure could be the greatest benefit from the administration of beta blockers.
| References | |  |
| 1. | Nagasubrahmanian, R.C., Tripathi, R.C., Poinooswamy, D. and Gloster, J., 1976, Trans. Ophthalmol. Soc. U.K., 96 : 179.  |
| 2. | Phillips, C.I. Howitt, G. and Rowlands, D.J, 1967, Brit. J. Ophthalmol, 51 : 222 |
| 3. | Nielsen, N.V. and Eriksen, J.S., 1972, Acta Ophthalmol, 57 :418. |
| 4. | Wettrell, K., 1976, Acta. Ophthalmol. 1976-78 Supplementum 134. |
| 5. | Fitzgerald, J.D. and O'Donnel, S., 1971, Brit. J. Pharmacol. 43 : 222.235. |
| 6. | Macdonald, M.J., Cullen, P.M. and Phillips, C.I., 1976, Brit. J. Ophthalmol. 60: 789. |
| 7. | Krieglsteing, K., Sold-Darseff, J. and Leydhecker, W., 1977, Albrecht, von Graefes Arch. Klin. Ophthalmol. 202: 81. |
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