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PubMedDate not supplied

The effects of antiglaucomatous agents on conjunctiva used for various durations.

PURPOSE: The effect of antiglaucomatous agents on conjunctiva used for various durations evaluated histopathologically. METHODS: Conjunctiva biopsies were taken in 19 Mayis University Faculty of Medicine Ophthalmology Department from 31 eyes of 30 patients who underwent filtration surgery after a period of antiglaucomatous agent use and examined under light microscope. The results were compared with the results of conjunctival biopsies from 10 similar aged patients undergoing retinal detachment of cataract surgery and with no other ocular pathology. RESULTS: Five of the cases were using antiglaucomatous treatment for two months (Group A), four cases for two to 12 months (Group B) and 22 cases for more than 12 months (Group C) before the surgery. Four cases were using a beta blocker only, eight cases beta blocker + sympathomimetic or beta blocker + myotic and the remaining 19 cases were using a combination of beta blocker + sympathomimetic + myotic. Histopathologic evaluation with light microscope showed no pathologic change in group A, but, subepithelial increase of lymphocytes, mast cells, macrophages and fibroblasts in group C. CONCLUSIONS: It was detected that subconjunctival inflammatory reaction increases as the number of antiglaucomatous agents and the treatment duration increase. These changes might be considered as risk factors that decrease the success rate of filtration surgery.

Administration, Topical↗
PubMed1997

Ultrasound biomicroscopic analysis of the effect of pilocarpine on the anterior chamber angle.

BACKGROUND: This study was carried out to determine the effects of pilocarpine on the anterior chamber angle in healthy volunteers. METHODS: We measured changes in anterior chamber depth (ACD), trabecular-iris angle (TIA), angle opening distance at 250 and 500 microns from the scleral spur (AOD250 and AOD500), and iris thickness using ultrasound biomicroscopy in 48 eyes of 48 normal volunteers (ages 18-57 years, mean 34.8 years) before and 1 h after instillation of 2% pilocarpine. RESULTS: Pilocarpine altered the TIA by -18.6 degrees to +10.5 degrees (mean -4.16 degrees), and change in the TIA increased significantly and linearly in relation with decrease in the pretreatment TIA (r = 0.929). Pilocarpine altered AOD250 change by -136 to +94 microns (mean -38 microns) and AOD500 by -151 to +157 microns (mean -42 microns); changes in the AOD250 and AOD500 were significantly correlated to the pretreatment AOD250 and AOD500 values, respectively (r = 0.923 and r = 0.896, respectively). The pilocarpine-induced change in the ACD showed a linear relationship to the pretreatment ACD (r = 0.887). The changes in the TIA, AOD250 and AOD500 showed greater increases in association with lower pretreatment ACD (r = 0.848, r = 0.891, r = 0.842) and smaller change in the ACD (r = 0.834, r = 0.839, r = 0.812). CONCLUSIONS: The response of the anterior chamber angle to pilocarpine, narrowing or widening, depended on its pretreatment state. The ability to predict the pilocarpine-induced change in the angle before the instillation of pilocarpine would be helpful in treating patients with glaucoma.

Adolescent↗
PubMed2005

Effect of rilmakalim on detrusor contraction in the presence and absence of urothelium.

Openers of K(ATP) channels are known to inhibit KCl-, carbachol- and also electrically induced contractions in detrusor muscle strips from various species. Contractions of isolated strips of urinary bladder are usually of higher amplitude when the urothelium has been removed. This has been explained by the release of an urothelium-derived relaxing factor. In this study we examined whether intact urothelium may modulate the effect of the selective KATP channel opener rilmakalim. Contractile responses to 85 mM KCl and 10 microM carbachol were measured in detrusor strips from mouse, pig and man. In the presence of an intact urothelium, contractions were significantly reduced in strips from all three species investigated. In preparations with urothelium rilmakalim reduced KCl contractions with similar potency and efficacy [-logIC50 (M) 4.6 to 5.1; Effmax reduction to 14-30% of control]. However, in urothelium-denuded strips rilmakalim was more potent in pig (-logIC50 5.5) than in mouse and man (-logIC50 4.7 and 4.4, respectively). The order of potency for rilmakalim to suppress carbachol-induced contractions was pig (-logIC50 6.7)>man (5.8)>mouse (4.7); contractions were significantly more reduced in pig (Effmax reduction to 11+/-2%, n=10) and in mouse (21+/-2%, n=8) than in human detrusor (55+/-5%, n=5). The presence of urothelium did not affect the concentration-response curves for rilmakalim, with the exception of KCl-induced contractions in pig. Only the rilmakalim-induced relaxation of carbachol-mediated contractions in pig were prevented by the KATP channel blocker glibenclamide. We conclude that with this one exception, the responses to rilmakalim in detrusor contractions were not mediated by KATP channel opening.

Animals↗
PubMed2005

BIBN4096BS and CGRP(8-37) antagonize the relaxant effects of alpha-CGRP more than those of beta-CGRP in human extracranial arteries.

We hypothesize that dilatation of extracranial arteries during migraine could be caused by CGRP. We compared the relaxant effects of alpha-calcitonin gene-related peptide (alpha-CGRP) and beta-calcitonin gene-related peptide (beta-CGRP) and the antagonism by BIBN4096BS and CGRP(8-37) on rings of human temporal and occipital arteries precontracted with KCl. beta-CGRP relaxed temporal (-logEC50M = 8.1) and occipital arteries (-logEC50M = 7.6) with 19-fold and 29-fold lower potencies respectively than alpha-CGRP. Nearly maximal effective concentrations of alpha-CGRP (4 nM) and beta-CGRP (50 nM) caused stable relaxations of the temporal artery for 4 h without fading. BIBN4094BS antagonized the effects of alpha-CGRP (pK(B) = 10.1 and 9.9, respectively) more than beta-CGRP (pK(B) = 9.3 and 9.2 respectively) on both temporal and occipital arteries. CGRP(8-37) antagonized the effects of alpha-CGRP (pK(B) = 6.6 and 6.4 respectively) more than beta-CGRP (pK(B) = 5.7 and 5.5 respectively) on both temporal and occipital arteries. Antagonism of the relaxant effects of alpha-CGRP (4 nM) and beta-CGRP (50 nM) by BIBN4096BS (10 and 100 nM) was reversible for beta-CGRP, but irreversible for alpha-CGRP, 1 h after BIBN4096BS washout. We conclude that alpha-CGRP and beta-CGRP interact either at different binding sites of the same CGRP receptor system or all together with different receptor systems in human extracranial arteries. BIBN4096BS binds more firmly to the receptor activated by alpha-CGRP than to the receptor activated by beta-CGRP.

Adult↗
PubMed2002

[Validity of anterior chamber depth measurements for the evaluation of accommodation after implantation of an accommodative Humanoptics 1CU intraocular lens].

BACKGROUND: Changes in the anterior chamber depth (ACD) after pilocarpin application are generally regarded as reflecting an accommodative effect of accommodative intraocular lenses (IOLs) METHODS: We implanted Humanoptics 1CU accommodative IOLs into 25 eyes of 20 patients aged 53.2+/-14.7 years (range: 30-83 years). In seven of these patients, we were able to measure anterior chamber depth changes after the application of pilocarpine (2%) eye drops 3 months postoperatively using a Zeiss IOLMaster, an Orbscan II topography system, as well as by ultrasound biomicroscopy (20 MHz-US-head). RESULTS: Uncorrected near acuity was on average 0.4+/-0.23 (0.1-0.8) and uncorrected distance acuity was 0.76+/-0.23 (0.3-1). Before pilocarpine, ACD was 3.19+/-2.11 mm (IOL-Master), 3.35+/-2.22 mm (Orbscan II) and 3.35+/-2.21 mm (US-biomicroscopy) ( P=0.96). After pilocarpine, ACD was 2.61+/-1.71 mm (IOL-Master), 2.63+/-1.78 mm (Orbscan II) and 3.15+/-2.08 mm (US-biomicroscopy) ( P=0.002). The average individual ACD change before/after pilocarpine was 0.83+/-0.25 mm with the IOL-Master, 1.04+/-0.39 mm with the Orbscan II System and 0.28+/-0.14 with US-biomicroscopy ( P=0.0004). DISCUSSION: The 1CU Humanoptics accommodative IOL presented with potential accommodative capabilities in clinical evaluation. Drug induced accommodation by pilocarpine does not reflect real accommodative effects. The differences in ACD measurements between three different methods were statistically significant. Evaluation methods for accommodative IOLs should be carefully analysed and further development of objective means for evaluation is needed.

Accommodation, Ocular↗
PubMed2003

[Atypical tonic pupil as a complication of chickenpox infection].

BACKGROUND: Pupillary disorders following varicella infections are rare and few cases have been reported which were only partially pharmacologically tested. MATERIALS AND METHODS: A 5-year-old boy presented with a left-sided dilated and unreactive pupil, 3 months before he had suffered from chickenpox and in the course of the acute disease developed anterior uveitis which was treated with local prednisone and mydriatics. The pupil remained dilated despite discontinued medication, light reaction was absent and accommodation was impaired. Pilocarpine supersensitivity was an indication against a lesion of the sphincter muscle and reduced response to cholinesterase inhibitors (physostigmine) pointed towards a postganglionic lesion. CONCLUSIONS: It is probable that a varicella virus infection of the short ciliary nerves and the ciliary ganglion caused anterior uveitis and a postganglionic parasympathetic nerve lesion, clinically presenting as a tonic pupil. According to cases previously reported an irreversible nerve lesion has to be assumed.

Anti-Inflammatory Agents↗
PubMed1997

[Reduction of endothelial cell number by cataract operation with intraocular thymoxamine administration. A randomized, double-blind study].

BACKGROUND: Thymoxamine, an alpha-1-receptor blocker, considerably enhances miosis when given intraocularly in combination with acetylcholine. We investigated whether intraocular use of thymoxamine 0.02% reduced the number of endothelial cells. PATIENTS AND METHODS: After phacoemulsification of 59 eyes, either thymoxamine 0.02%, acetylcholine 1.0% or buffered saline solution was given intraocularly. With a contact specular microscope, corneal endothelial cell photographs were taken on the day before treatment and 3 days and 6 weeks after surgery. RESULTS: There were no statistically significant differences between endothelial cell counts of eyes treated with thymoxamine (-7.2%), acetylcholine (-10.2%) or BSS (-9.4%). CONCLUSION: This study shows for the first time that thymoxamine, when given in the anterior chamber after phacoemulsification, does not cause a greater loss of endothelial cells than acetylcholine or buffered saline solution.

Acetylcholine↗
PubMed1999

Effects of dipivefrin and pilocarpine on pupil diameter, automated perimetry and LogMAR acuity.

BACKGROUND: A study was carried out to ascertain, in ophthalmologically normal subjects, the short-term effects of dipivefrin hydrochloride 0.1% on visual performance and make comparisons with pilocarpine. METHODS: Twelve normal volunteers aged 20-26 years attended on three occasions. One eye, randomly selected, received one drop of either pilocarpine 2%, dipivefrin or saline 0.9%. High- and low-contrast LogMAR acuity at 6 m and pupil diameter (measured by infra-red pupillometry) were recorded at baseline (T0) and at intervals up to 90 min following instillation of drops. Program 30-2 of the Humphrey Visual Field Analyzer (HFA) was run at T0 and at 60 min after treatment instillation (T60). Saline was always instilled at visit 1, to allow for learning effects. On visits 2 and 3 either pilocarpine or dipivefrin was randomly instilled into the treated eye. RESULTS: Pilocarpine significantly worsened the field global indices mean deviation (P < 0.001) and pattern standard deviation (P < 0.01) compared with T0. There was no significant change with dipivefrin. A significant (P = 0.01) pupil dilation from 5.44 mm (SD 0.79) at T0 to 6.19 mm (SD 1.09) at T90 occurred with dipivefrin. Pilocarpine caused significant miosis. No significant changes in LogMAR values were found with dipivefrin. Pilocarpine significantly (P < 0.01) increased LogMAR values (i.e. reduced acuity) compared with dipivefrin. At T30 the mean increase in LogMAR was 0.76 (SD 0.30) for high and 0.83 (SD 0.11) for low contrast. By T90 recovery of acuity was virtually complete. CONCLUSIONS: In normals dipivefrin causes mydriasis but does not affect the central visual field global indices (as assessed by STATPAC), or high- and low-contrast LogMAR acuity. Pilocarpine adversely affects the visual field and both measures of acuity. Knowledge of these effects is of value in glaucoma therapy and when monitoring the progression of visual loss.

Adult↗
PubMed2000

The additive intraocular pressure-lowering effect of latanoprost 0.005% daily once and pilocarpine 2% t.i.d. in patients with open-angle glaucoma or ocular hypertension. a 6-month, randomized, multicenter study. German Latanoprost Study Group.

PURPOSE: To compare the additional intraocular pressure-lowering effect of latanoprost 0.005% administered once daily with that of pilocarpine 2% administered three times daily in patients with primary open-angle glaucoma or ocular hypertension currently on monotherapy with timolol 0.5% twice daily. METHODS: In a 6-month, multicenter, randomized, open-label study 242 patients with POAG or OH whose IOP was not controlled with timolol 0.5% b.i.d. were enrolled. Eyes had not been treated with pilocarpine and latanoprost for at least 2 years. An analysis of covariance with diurnal IOP change from baseline to month 6 for study eyes was performed. RESULTS: Four patients on latanoprost 0.005% and 35 on pilocarpine 2% did not complete the study (P<0.001). Two hundred and forty patients were included in the intent-to-treat analysis. For both treatments the diurnal IOP reduction after 6 months was statistically significant (P<0.001). IOP (mean+/-SD) was reduced from 23.3+/-2.8 to 17.8+/-2.8 (-5.6) mmHg in the latanoprost 0.005% group and from 23.0+/-3.2 to 18.5+/-2.4 (-4.8) mmHg in pilocarpine 2% t.i.d.-treated eyes. The mean difference of -0.8 mmHg (per protocol, PP) and -1.6 mmHg (intend-to-treat, ITT) was statistically significant (P<0.04, PP; P<0.001, ITT) in favor of latanoprost 0.005%. Two eyes treated with latanoprost showed an iris color change. Thirty-six patients in the latanoprost group and 106 in the pilocarpine 2% group reported ocular adverse events (P<0.001). CONCLUSION: From the data we conclude that the additivity of latanoprost 0.005% is at least as effective as pilocarpine 2% t.i.d. in reducing IOP when added to eyes currently on monotherapy with timolol 0.5% b.i.d. Latanoprost was better tolerated than pilocarpine 2% eye drops in this study. The increase in iris pigmentation requires further investigation.

Adrenergic beta-Antagonists↗
PubMed1996

Secretagogue-induced apocrine secretion in the Harderian gland of the rat.

Harderian glands of male albino rats were stimulated with secretagogues and examined by transmission and scanning electron microscopy for the purpose of studying the apocrine secretory mechanism. Rats in the control group were perfused with standard HEPES-buffered Ringer's solution. Their glandular endpieces showed wide lumina that contained few secretory materials; spontaneous exocytosis was sometimes observed. However, there were no features suggestive of an apocrine secretory mechanism or myoepithelial cell contractions. After stimulation with NaF+AlCl3 or carbachol in HEPES-buffered Ringer's solution, the rats shed "bloody tears" and the glandular lumina were jammed with apical protrusions, cytoplasmic material and secretory products. The basal surface of the glandular cells showed bulging caused by myoepithelial cell contraction. Perfusion with HEPES-buffered Ringer's solution containing papaverine inhibited secretagogue-induced myoepithelial cell contraction but not the enhanced secretory activities of the glandular cells. The present results demonstrate that the Harderian gland of the rat can release secretory material not only by exocytosis, but also by an apocrine mechanism under stimulating conditions, and that myoepithelial cell contraction may not be involved in causing apical protrusion in the glandular cells.

Aluminum Chloride↗