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PubMed1980

Effects of timolol on corneal sensitivity and tear production.

A double-masked study was carried out to assess the effect of timolol ophthalmic-solution on corneal sensitivity in seven normal volunteers. No significant change in corneal sensitivity was demonstrated during four weeks of timolol administration. Corneal sensitivity was determined in two age-matched groups, one comprising 27 glaucomatous patients on timolol therapy for at least three months and the other consisting of 24 normal individuals who had never been on any beta-blocking agents. No significant difference in corneal sensitivity was noted between the two groups. The tear production was determined by means of the Schirmer test I in 15 patients with primary open-angle glaucoma or ocular hypertension prior to and during timolol therapy of 13 months duration. No significant change in tear production was noted.

Adult↗
PubMedDate not supplied

Prevention of IOP-rise following Nd-YAG laser capsulotomy with topical timolol and indomethacin.

Short term observation following Nd-YAG laser capsulotomy indicates that serious elevation of intra-ocular pressure may occur, unrelated to the amount of incident energy used. In this study we evaluated the effect of pre-treatment with anti-prostaglandin eyedrops on the rise in IOP. The IOP in forty pseudophakic patients, undergoing Nd-YAG laser posterior capsulotomy, was measured before capsulotomy and 2 and 4 hours afterwards. The fellow-eye was used as a control. Thirty minutes pre-operatively the patients were given one of the four following combinations of eyedrops: 1 drop timolol 0.5% and 1 drop placebo, 1 drop indomethacin 1% and 1 drop placebo, 1 drop timolol 0.5% and 1 drop indomethacin 1%, 1 drop placebo and 1 drop placebo. Statistical analysis of the results showed that indomethacin alone has little influence on the IOP-rise, whereas timolol has. When indomethacin is added to timolol there is no significant enhancement.

Administration, Topical↗
PubMed1991

Reduced severity of oxygen-induced retinopathy in the newborn rat after topical administration of timolol maleate. A preliminary study.

The effects of timolol maleate on intraocular pressure (IOP) and the severity of retinopathy induced by exposure to 80% oxygen were studied in newborn Wistar rats. One drop of timolol maleate (0.25%) instilled in each eye twice a day for the first ten days of life substantially reduced intraocular pressure without significantly modifying arterial pressure. Forty percent of the ratlings treated in this way failed to develop oxygen-induced retinopathy (OIR) after exposure to 80% oxygen for the first five days of life; in the other 60% OIR was less severe than that seen in an identically oxygenated group that did not receive timolol. The authors hypothesize that the pharmacologically induced reduction in IOP may have attenuated the effects of the high concentrations of oxygen on the immature retinal vessels by improving the ocular perfusion pressure. The possibility that timolol maleate also exerts a direct action on the caliber of these vessels cannot be excluded.

Administration, Topical↗
PubMed1984

Short-term and long-term timolol maleate effects on corneal sensitivity.

The authors present data concerning the effect of timolol maleate on corneal sensitivity investigated with the Cochet-Bonnet aesthesiometer and with cotton wool wisps. Among 30 subjects with open-angle glaucoma, 15 subjects underwent a short-term trial with timolol maleate 0.50% in one eye, while 15 served in a long-term trial with timolol maleate 0.50% or 0.25% in both eyes. A light reduction in corneal sensitivity, which did not reach statistical significance, was found during timolol treatment. After discussing the possible explanations of this side effect, the authors advise monitoring this parameter during the therapy.

Adult↗
PubMed1991

Concentration of timolol in aqueous humour.

Two groups of twenty patients who were to undergo a routine e.c.c.e. applied eye-drops containing timolol 0.1% or 0.5% twice daily during the week preceding their operation. A third group of twenty patients, using placebo drops, served as control. During the cataract surgery a sample of aqueous was collected. The samples from the timolol 0.1% patient group contained a significantly lower concentration of timolol than those from the timolol 0.5% patient group, but there was considerable overlap.

Administration, Topical↗
PubMed1986

Prevention of IOP-rise following Nd-YAG laser capsulotomy with pre-operative timolol eye-drops and 1 tablet acetazolamide 250 mg systematically.

Short-term observation following Nd-YAG laser capsulotomy indicates that serious elevation of intra-ocular pressure may occur, unrelated to the amount of energy used. In this study the IOP in 3 groups of 10 pseudophakic patients undergoing Nd-YAG laser posterior capsulotomy was measured before capsulotomy and 2 and 4 hours afterwards, using the fellow-eye as control. The first group received no medication, the second received timolol 1/2% eyedrops preoperatively, the third group a combination of timolol 1/2% and 1 tablet of acetazolamide 250 mg systemically. Pretreatment with timolol 0.5% minimizes IOP-rise but does not give complete protection. The combination of timolol 0.5% with 1 tablet of acetazolamide 250 mg proves to be a safe procedure for the prevention of IOP-rise after YAG laser capsulotomy. To prevent other complications it is advisable to make a small capsulotomy of 2-3 mm diameter using as little energy as possible. Also a defocussing system in the laser is a great advantage. Indomethacin drops during a period of 6 weeks after Nd-YAG laser capsulotomy should prevent cystoid macular edema.

Acetazolamide↗
PubMed1979

[The effect of timolol and parasympathicomimetica in the treatment of the elevated intraocular pressure (author's transl)].

45 patients with ocular hypertension or open-angle glaucoma were tested to see if, and to what extent timolol and three other different parasympathicomimetics (pilocarpine 2%, carbachol 1.5%, aceclydine 2%) produced an supplementary reduction of the intraocular pressure. An equally marked, additional drop in eye pressure was achieved when patients who had been given timolol over an extended period of time, were additionally treated with one dose of pilocarpine 2% or carbachol 1.5%. Aceclydine 2% produced no statistically significant additional effect. Patients who had only been treated with pilocarpine 2% over an extended period of time and then were given one dose of timolol 0.25% produced a drop in eye presure more than double that of those patients who had been primarily treated with timolol and then received pilocarpine or carbachol. These results will be discussed on the basis of the mode of action of the applied medications.

Carbachol↗
PubMed1988

Differential effects of timolol and metoprolol on platelet function at rest and during exercise.

Ten male patients suffering from stable angina pectoris were studied at rest and immediately after exercise during treatment either with timolol (a non-selective beta-blocker) or with metoprolol (a beta 1-selective blocker). Timolol induced a significant increase in platelet aggregation and a reduction in platelet cyclic AMP, and it also raised the plasma adrenaline at rest and during exercise as compared to the pre-treatment level. Metoprolol had none of these effects. Prior to medication and during metoprolol treatment, exercise led to an increase in the peripheral platelet count, whereas timolol was associated with a reduction of platelets during physical effort. Neither drug affected platelet thromboxane B2 at rest. During exercise, its level was not affected in the pre-treatment period or during metoprolol treatment but it was sharply increased by timolol therapy.

Adrenergic beta-Antagonists↗
PubMed1977

Long term effect of timolol and hydrochlorothiazide, or hydrochlorothiazide and amiloride, in essential hypertension.

Twenty-four patients with mild to moderate hypertension were treated for up to 60 weeks with hydrochlorothiazide and either placebo, timolol, or timolol and amiloride. The effect of adding timolol and amiloride to hydrochlorothiazide was evaluated in a double blind trial. In 22 of the 24 patients a supine diastolic blood pressure below or equal to 95 mm Hg was produced by hydrochlorothiazide and timolol. Replacing a potassium supplement with amiloride increased the antihypertensive effect.

Adult↗
PubMed1992

Long-term drift and timolol therapy: possible role for pulsed therapy.

Eyes treated with a topical betablocker may exhibit the phenomenon of longterm drift, leading to loss of intraocular pressure control. It has been suggested that discontinuation of the betablocker may restore sensitivity to betablocker therapy, and that this phenomenon might be enhanced by the administration of an adrenergic agonist during this holiday period. This study was set up to examine further this hypothesis. Nine patients with ocular hypertension receiving treatment with timolol were entered into the study. Timolol was discontinued then re-started after four weeks of treatment with dipivefrin. This treatment cycle was repeated after a further four weeks. IOP was measured every two weeks. Re-introduction of timolol was associated with a significant lowering of IOP at two weeks (3.2 mmHg in the first cycle, p < 0.01, 3.4 mmHg in the second cycle, p < 0.01). Discontinuation of timolol and treatment with dipivefrin was not associated with a significant change in IOP.

Aged↗
PubMed1997

The effect of latanoprost 0.005% once daily versus 0.0015% twice daily on intraocular pressure and aqueous humour protein concentration in glaucoma patients. A randomized, double-masked comparison with timolol 0.5%.

BACKGROUND: Latanoprost is a PGF2 alpha analogue which reduces the intraocular pressure (IOP) by increasing the uveoscleral outflow. The objective of this study was to investigate the effect of two different regimens of latanoprost on the diurnal IOP and also the effect of latanoprost on the blood-aqueous barrier measured with a laser flare cell meter (Kowa FM-500). Moreover, the safety aspects of the two regimens regarding hyperemia were studied. METHODS: A double-masked, randomized study was performed in 30 patients (9 males, 21 females; mean age 61.9 years) with primary open-angle glaucoma or pseudoexfoliation glaucoma. Twenty patients were treated with latanoprost 0.0015% twice daily or 0.005% once daily for 3 weeks in a cross-over design. Ten patients received timolol 0.5% twice daily as control. RESULTS: Latanoprost 0.005% once daily reduced IOP (+/- SEM) more effectively than latanoprost 0.0015% twice daily (9.8 +/- 0.9 mm Hg and 6.7 +/- 0.9 mm Hg, respectively). There was a statistically significant increase in the aqueous humour protein concentration within the timolol group (P = 0.004), but not within the latanoprost group (P = 0.97). There was no statistically significant difference in the change in aqueous humour protein concentration from baseline between latanoprost and timolol groups (P = 0.08). No statistically significant difference in conjunctival hyperemia between the two latanoprost regimens was found (P = 0.37). CONCLUSION: Latanoprost 0.005% once daily reduced IOP more effectively than latanoprost 0.0015% twice daily (P < 0.001). Latanoprost had no statistically or clinically significant effect on the blood-aqueous barrier. There was no difference in hyperemia between the two regimens. Both concentrations of latanoprost reduced IOP at least as well as timolol 0.5% eye drops.

Adrenergic beta-Antagonists↗
PubMed1984

R-enantiomer of timolol: a potential selective ocular antihypertensive agent.

Various studies were conducted to evaluate the effects of timolol, an S-enantiomer, relative to its R-enantiomer upon intraocular pressure and related ocular systems in the rabbit. The R-enantiomer was about one-third as potent as timolol in displacing 3H-dihydroalprenolol binding to iris-ciliary body tissue, reducing aqueous humor formation, and lowering intraocular pressure of alpha-chymotrypsin hypertensive eyes. In contrast, the R-enantiomer was 50 to 90 times less potent than timolol in antagonizing the effects of isoproterenol on pulmonary and atrial beta-adrenergic receptors. The data indicate that the R-enantiomer may lower intraocular pressure in man at concentrations less likely than timolol to block extraocular beta-adrenergic receptors. Finally, to account for the differential effect of the R-enantiomer upon ocular as opposed to extraocular beta-adrenergic receptors, it is tentatively suggested that this agent may also act upon a population of ocular beta-adrenergic receptors showing relatively poor stereoselectively.

Animals↗
PubMed2000

Long-term effects of timolol therapy in ocular hypertension: a double-masked, randomised trial.

BACKGROUND: Increased intraocular pressure (IOP) has been shown to be one of the most important risk factors for developing glaucoma. Yet it has not been clearly demonstrated that IOP-lowering treatment can reduce the incidence of glaucoma damage in patients with ocular hypertension. The aim of the current paper was to report the results of a long-term study addressing this very problem. METHODS: We conducted a randomised, double-masked study comparing timolol and placebo treatment in 90 patients with ocular hypertension plus some additional risk factor. Patients were followed at 3-month intervals prospectively for 10 years or until glaucomatous field loss could be demonstrated with computerised perimetry. A post-study analysis was performed including all available data, thus extending maximum follow-up to 17 years. RESULTS: After 5 years of follow-up eight patients in the placebo group and five patients in the timolol group had developed glaucomatous field loss (NS); the corresponding figures after 10 years were 15 patients in the placebo group and seven patients in the timolol group. Survival analysis showed a tendency but no statistically significant difference between treatment groups (P = 0.07). Study attrition was large. Eighteen patients in each group had developed glaucomatous field loss when also post-study data were included. IOP reduction was greater in eyes passing the 10-year visit without field loss (5.7 mmHg), than in those that reached an end-point (2.3 mmHg; P = 0.0002). CONCLUSION: In this long-term study we found a tendency but failed to prove a beneficial effect of topical timolol treatment in patients with elevated IOP, normal visual fields and some additional risk factor. The intent-to-treat analysis showed no difference between treatment groups. The high attrition shows the difficulties associated with very long follow-up.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Binding affinity of bunazosin, dorzolamide, and timolol to synthetic melanin.

PURPOSE: The purpose of this study was to compare the binding affinity of bunazosin and dorzolamide to synthetic melanin relative to that of timolol. METHODS: Synthetic melanin was prepared from dopa by the action of tyrosinase. Timolol, dorzolamide, and bunazosin were incubated separately at a concentration of 10(-4) M in 2 ml of 0.066 M phosphate buffer containing 5 mg of synthetic melanin. After centrifugation, the absorbance of each free drug in the supernatant was measured at its optimum wavelength. The percentage of each drug bound to melanin was calculated directly from the change in absorbance relative to the initial value. RESULTS: The increase in the binding rates of all three drugs seemed to reach a plateau after 30 min. After incubating for 60 min, the binding rate of timolol was 22.2% +/- 4.9%, bunazosin 36.3% +/- 2.5%, and dorzolamide 8.5% +/- 1.9%. There were statistically significant differences between the binding rates of each drug. CONCLUSIONS: Under our study conditions, the order of binding affinity of these ocular hypotensive agents to synthetic melanin seems to be as follows: bunazosin>timolol>dorzolamide.

Antihypertensive Agents↗
PubMed1985

Circulating catecholamine and potassium concentrations early in acute myocardial infarction: effect of intervention with timolol.

In a prospective study, 20 patients with a first acute myocardial infarction and no current treatment with diuretics or cardioactive drugs were randomized to treatment with intravenous timolol (10 patients) or placebo (10 patients). Plasma adrenaline, noradrenaline, and serum potassium were estimated at baseline (mean +/- SD 3.6 +/- 0.8 hours after the onset of the infarction) and 4 hours after the start of treatment. The patient selection criteria embraced a low-risk study population. Before treatment, the serum potassium concentrations correlated inversely with plasma adrenaline but not with plasma noradrenaline concentrations. A rise of serum potassium (mean +/- SD mmol/L) from 4.1 +/- 0.3 to 4.4 +/- 0.4 (p less than 0.05) in the placebo group and from 4.0 +/- 0.4 to 4.5 +/- 0.5 (p less than 0.05) in the timolol group was in multivariate analysis associated with infarct size, estimated as cumulative creatine kinase release, in the placebo group, and with the mean individual plasma adrenaline concentrations in the timolol group. By reversing the effect of adrenaline from a decrease to an increase in the serum potassium concentrations, timolol changes the relationships between circulating adrenaline, potassium, and infarct size.

Aged↗
PubMed1979

Corneal anesthesia after timolol maleate therapy.

Symptomatic superficial punctate keratitis associated with complete corneal anesthesia occurred in three patients after they had been taking timolol maleate for glaucoma. After discontinuation of the timolol maleate and substitution of conventional antiglaucomatous collyria, the keratitis gradually cleared with restoration of normal corneal sensitivity. Corneal sensitivity, measured in 25 additional patients taking timolol maleate, was markedly diminished in four patients, all of whom were elderly and had been using the drug for a minimum of three months. Timolol maleate does appear to have some local anesthetic properties in human cornea after chronic use by susceptible individuals.

Aged↗
PubMed1979

Apneic spells associated with timolol therapy in a neonate.

A 2-week-old premature child with congenital glaucoma secondary to anterior cleavage syndrome was treated with timolol maleate and cyclocryotherapy. The patient had apneic spells of up to 30 seconds that stopped soon after timolol maleate therapy was discontinued. No apnea was seen before timolol maleate administration, and no further spells were noted after subsequent cyclocryotherapy without timolol maleate treatment. Possible central nervous system toxicity of timol maleate or its metabolic by-products in neonates with immature blood-brain barriers was noted.

Acetazolamide↗
PubMed1982

The effects of timolol maleate and acetazolamide on the rate of aqueous formation in normal human subjects.

We used a double-masked, randomized, placebo-controlled study of the effect of acetazolamide alone and timolol maleate alone and of the two in combination on the rate of aqueous humor flow in 21 normal subjects. The rate of aqueous flow was measured by fluorophotometry over an eight-hour period. Timolol decreased the flow by 33%, acetazolamide by 27%, and the drug combination by 44%, compared to the placebo treated eye (P less than .01). Timolol produced a 26% decrease in intraocular pressure. Timolol decreased the intraocular pressure in the fellow eye by 16%, acetazolamide by 21%, and the two drugs together by 35% (P less than .01). Neither drug significantly affected the anterior chamber volume, the endothelium's permeability, or the estimated endothelial pump rate.

Acetazolamide↗