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At least 937 records · Page 52Linked to original sources
PubMed2002

Pupillary response to four concentrations of pilocarpine in normal subjects: application to testing for Adie tonic pupil.

PURPOSE: To determine the amount of pupillary constriction to four different concentrations of pilocarpine in normal human subjects and to determine if pupillary constriction correlates with bioavailability of the instilled concentrations. The amount of pupillary constriction to dilute pilocarpine is utilized as a diagnostic test for Adie tonic pupil as distinguished from a normal pupil response. DESIGN: Twenty healthy volunteers had automated binocular infrared pupillography in the dark after instillation of four different concentrations of dilute pilocarpine. Ocular penetration of eye drops was also assessed using 2% fluorescein sodium as a tracer. METHODS: Prospective institutional double-masked study of both eyes of twenty healthy volunteers, ten with brown irides, ten with blue irides, between the ages of 20-40 years. RESULTS: A pilocarpine dose-dependent curve showed decreased pupil size within 15 minutes, peaking at 30-60 minutes. No difference was noted between right and left eyes, iris color, or corneal permeability. CONCLUSIONS: Normal pupils constrict to dilute concentrations of pilocarpine (0.25% or 0.125%), but constrict insignificantly to concentrations of 0.0313% or 0.0625%. Pupil constriction with 0.0625% pilocarpine should distinguish an Adie pupil from normal. This confirms the utility of this simple office diagnostic procedure.

Adult↗
PubMed1996

Surgical vs medical management of chronic open-angle glaucoma.

PURPOSE: We studied patients with chronic open-angle glaucoma who had similar intraocular pressures to determine whether surgical or medical therapy is more effective in preventing progressive, long-term, glaucomatous damage. METHODS: Included in this study were patients with chronic open-angle glaucoma who were followed for 3 years or longer and were treated, through either medical or surgical therapy, by adjusting intraocular pressure to 18 mm Hg or less as a therapeutic end point. We studied 31 matched pairs of patients in which one member was treated by surgery and one member had medical treatment. In every pair, we matched each patient individually by age, race, and intraocular pressure. RESULTS: For the matched pairs of patients in this study, the mean intraocular pressure following initiation of treatment was 13.5 and 13.1 mm Hg for the surgically and medically treated groups, respectively (P = .475). This study found no difference between groups in the incidence of glaucomatous progression following surgical (n = 3) or medical (n = 3) therapy (P > .99, McNemar's test) for an average follow-up of 40.0 +/- 10.0 and 43.4 +/- 8.4 months in the medical and surgical groups respectively. The glaucoma of three patients progressed on the basis of reduced visual acuity, two by visual field, and one by disk hemorrhage. Although the types of complications from therapy differed between groups, no vision loss or life-threatening events occurred directly from these treatments. CONCLUSIONS: When intraocular pressure is used as a therapeutic end point, both filtration surgery and medical therapy appear to be equally effective in maintaining long-term visual function and a stable optic disk in chronic open-angle glaucoma.

Adrenergic alpha-Agonists↗
PubMed1996

Accommodation in primate eyes after implantation of refilled endocapsular balloon.

PURPOSE: To restore accommodation after crystalline lens removal. METHODS: The crystalline lens of one eye of each of four primates was removed by phacoemulsification. Each operated-on eye underwent endocapsular silicone balloon implantation followed by filling with an organosilicone mixture. Seven months postoperatively, the anterior chamber depth and refractive power changes were measured before and after topical application of 4% pilocarpine. RESULTS: In the refilled eyes, the average anterior chamber depth reduction was 0.50 mm and the average maximal myopic change was 6.74 diopters. CONCLUSION: After lens removal, measurable accommodation was restored in the eyes with the endocapsular balloon filled with an organosilicone mixture.

Accommodation, Ocular↗
PubMed1997

Ultrasound biomicroscopic findings in humans with shallow anterior chamber and increased intraocular pressure after the prone provocation test.

PURPOSE: To investigate ultrasound biomicroscopic findings in human eyes with shallow anterior chamber and risk of anterior chamber angle-closure glaucoma after the prone provocation test. METHODS: A total of 32 consecutive patients (64 eyes) with bilateral shallow anterior chamber who were at risk for primary angle-closure glaucoma underwent the prone provocation test in a lit room. Before and immediately after measurement of intraocular pressure in this test, high-frequency ultrasound biomicroscopy was performed in the horizontal and vertical directions, and the chamber angle views were recorded at the 3-, 6-, 9-, and 12-o'clock positions. RESULTS: Ten eyes of six patients exhibited an increase in intraocular pressure of 8 mm Hg or more, a positive response, with the remainder showing a negative response to the test. In the eyes with a positive response to the test, the profile of the iris showed a markedly convex shape with a large space behind the posterior iris. However, the anterior chamber angle of each eye remained open, even during the high level of intraocular pressure caused by the provocation. CONCLUSIONS: The present results suggest that no angle closure occurs during the initial increase of intraocular pressure after the prone provocation test. Such an initial increase of intraocular pressure was associated with high pressure in the posterior chamber because of the relative pupillary block. A time lag was observed between the high intraocular pressure caused by the pupillary block and the occurrence of angle closure.

Acetazolamide↗
PubMed1995

Short-term efficacy of apraclonidine hydrochloride added to maximum-tolerated medical therapy for glaucoma. Apraclonidine Maximum-Tolerated Medical Therapy Study Group.

PURPOSE: We determined whether the addition of topical apraclonidine hydrochloride to eyes that are receiving maximal medical therapy but still have inadequate intraocular pressure control and that are scheduled to undergo surgery could adequately decrease intraocular pressure, postponing the need for further intervention. METHODS: We performed a prospective, 90-day, multicentered, placebo-controlled, double-masked parallel study. We enrolled one eye each of 174 glaucoma patients with inadequate intraocular pressure control who were on maximally tolerated medical therapy. We continued to administer maximum medical therapy for glaucoma. Study medications were either apraclonidine hydrochloride 0.5% or placebo (apraclonidine's vehicle). Patients were instructed to take the study medication every eight hours. We measured intraocular pressure, change in intraocular pressure from baseline, and the number of eyes requiring surgery after the addition of study medication. RESULTS: Fifty-two (60%) of 86 patients treated with apraclonidine maintained adequate intraocular pressure control throughout the study and avoided surgery, compared with 28 (32%) of 88 patients treated with placebo (P < .001). Apraclonidine treatment resulted in significantly more patients attaining an additional 20% reduction or more in intraocular pressure from baseline and an intraocular pressure less than or equal to 20 mm Hg (P < .05). The most common ocular complication was conjunctival hyperemia (11 of 86 patients, 12.8%). The most frequent nonocular problem was dry mouth (four patients, 4.7%). CONCLUSION: Apraclonidine appeared to be safe in all eyes and efficacious in some eyes. It significantly lowered intraocular pressure when used in combination with maximally tolerated medical therapy, which delayed or prevented further glaucoma surgery for at least 90 days in 52 (60%) of 86 treated patients.

Adrenergic alpha-Agonists↗
PubMed1995

Lichen planus associated with topical beta-blocker therapy.

PURPOSE: We studied two clinical cases that demonstrated an association between topical beta-blocker therapy and lichen planus. METHODS: Two patients developed skin lesions while on topical beta-blocker therapy for open-angle glaucoma. They underwent skin biopsies to determine the origin of the lesions. They were subsequently treated and followed up clinically. RESULTS: Skin biopsy specimens from each patient demonstrated infiltrates consistent with a lichenoid drug reaction. The symptoms resolved after discontinuation of the topical beta-blocker therapy. Neither patient developed a recurrence. CONCLUSION: We suggest that lichen planus is a possible side effect of topical beta-blocker therapy.

Administration, Topical↗
PubMed1999

Plateau iris syndrome: changes in angle opening associated with dark, light, and pilocarpine administration.

PURPOSE: To report changes in angle configuration associated with dark, light, and pilocarpine administration in plateau iris syndrome. METHOD: In 10 eyes of 10 patients with plateau iris syndrome and persistent narrow angles after patent peripheral Nd:YAG laser iridotomy, ultrasound biomicroscopy was used to image variations in angle opening, iris thickness, and trabecular-ciliary process distance. Measurements were taken in the dark, in full room light, and after administration of pilocarpine 2%. RESULTS: Average angle opening distance increased in the light compared with the dark (113+/-34 microm vs. 22+/-34 microm, P = .0001) and increased further after pilocarpine administration (171+/-52 microm vs. 113+/-34 microm, P = .0034). Average iris thickness decreased in the light compared with the dark (338+/-34 microm vs. 436+/-58 microm, P = .0009) and decreased further after pilocarpine administration (253+/-48 microm vs. 338+/-34 microm, P = .0002). Average trabecular meshwork-ciliary process distance measurements were smaller than normal and did not change significantly in the light compared with the dark (481+/-42 microm vs. 464+/-44 microm, P = .4001) or after pilocarpine administration compared with light (451+/-67 microm vs. 481+/-42 microm, P = .1304). CONCLUSIONS: In plateau iris syndrome, anteriorly located ciliary processes support the peripheral iris. Changes in angle opening in dark and light are solely related to changes in iris thickness. Pilocarpine produces iris thinning and is an effective method of opening the angle. Ultrasound biomicroscopy can be used to perform a darkroom provocative test, which provides information on whether the angle anatomically closes in the dark.

Anterior Eye Segment↗
PubMed1998

Intraoperative intracameral carbachol in phacoemulsification and posterior chamber lens implantation.

PURPOSE: To evaluate the use of intraoperative intracameral carbachol in association with phacoemulsification and posterior lens implantation. METHODS: We prospectively randomly assigned 41 eyes (41 patients) to receive either placebo or a 50:50 dilution of carbachol 0.01% after intraocular lens insertion and phacoemulsification. RESULTS: Twenty-one eyes of 21 patients treated with intracameral carbachol showed a statistically significant (P = .0373) reduction in intraocular pressure (15.9 mm Hg) at 6 hours postoperatively compared with 20 eyes of 20 patients who had received placebo (20.4 mm Hg). At day 1, the carbachol group measured 15.0 mm Hg vs 17.6 mm Hg for placebo (P = .0376), and a 1.5-line improvement in visual acuity in the carbachol vs the placebo group was noted (P = .0263), which was maintained on glare testing. On quality of life testing using a modified SF-36 test, carbachol-treated patients within the first postoperative week more often attempted to descent stairs in both bright (P = .007) and dim (P = .037) light than did patients treated with placebo. At month 2, no difference was observed between groups except that depth of focus was statistically greater in the carbachol group (P = .025). Safety was similar between the two groups in terms of ocular and systemic adverse events. CONCLUSIONS: Patients treated with carbachol intracamerally after phacoemulsification and posterior chamber lens implantation demonstrate lower intraocular pressure within the first day postoperatively. These findings are associated with improved visual acuity and potentially greater ambulation in bright light within the first postoperative week.

Aged↗
PubMed2001

Involvement of CGRP and CGRP1 receptor in nociception in the nucleus accumbens of rats.

The present study was performed to investigate the role of calcitonin gene-related peptide (CGRP) and its antagonist CGRP8-37 on nociception in the nucleus accumbens of rats. Hindpaw withdrawal latencies (HWLs) to noxious stimulation induced by hot plate and Randall Selitto tests were measured. The HWL to both thermal and mechanical stimulation increased significantly after intra-nucleus accumbens administration of 0.5 or 1 nmol of CGRP, but not 0.1 nmol, indicating that CGRP plays an anti-nociceptive effect in the nucleus accumbens of rats. The anti-nociceptive effect induced by intra-nucleus accumbens administration of 1 nmol of CGRP was blocked significantly by following intra-nucleus accumbens administration of 1 nmol of CGRP8-37, a selective antagonist of CGRP1 receptor. Furthermore, the HWLs to both thermal and mechanical stimulation decreased significantly after intra-nucleus accumbens administration of 0.02, 0.1 and 0.5 nmol of CGRP8-37 alone. The hyperalgesic effect of intra-nucleus accumbens administration of CGRP8-37 lasted for more than 60 min after the injection, suggesting that CGRP1 receptor is involved in anti-nociception in the nucleus accumbens of rats. The results indicate that CGRP and CGRP1 receptor have important roles in nociceptive modulation in the nucleus accumbens of rats.

Animals↗
PubMed1999

CGRP microinjection into the ventromedial or dorsomedial hypothalamic nucleus activates heat production.

Unilateral microinjection of calcitonin gene-related peptide (CGRP, 1.6 pmol; 0.2 microl) into the ventromedial hypothalamus (VMH) and dorsomedial hypothalamus (DMH) immediately increased oxygen consumption (VO2), heart rate (HR), colonic temperature (Tco), and temperature of interscapular brown adipose tissue (TIBAT) in urethane-anesthetized rats, whereas vehicle saline injection into the VMH and CGRP injection into other hypothalamic regions such as the preoptic area, lateral hypothalamic area, paraventricular nucleus, and bed nucleus of the stria terminalis had no effect. The effects of CGRP injection into the VMH were dose-dependent over the range of 0.016-1.6 pmol. CGRP administration to the lateral ventricle (LV) required 16-320 pmol to elicit similar degrees of responses that were observed after the injection into the VMH. The increase in TIBAT was always higher than that in Tco after CGRP injection. Injection of [Cys(ACM)2,7]hCGRPalpha, a selective CGRP2 receptor agonist, did not induce any thermogenic effects. Human CGRP8-37, a proposed CGRP1 receptor antagonist, by itself induced heat production responses with no signs of inhibition of CGRP-induced responses. Thus, the receptor subtype of the thermogenic effect of CGRP could not be determined by the available pharmacological tools. The present results show that centrally administrated CGRP induces heat production in the BAT specifically through the VMH or DMH.

Adipose Tissue, Brown↗
PubMed1999

Neurogenic calcitonin gene-related peptide: a neurotrophic factor in the maintenance of acetylcholinesterase molecular forms in adult skeletal muscles.

This work addresses the role of calcitonin gene-related peptide (CGRP) in the physiological maintenance of acetylcholinesterase (AChE) molecular forms in motor endplate regions of adult Sprague-Dawley rat fast-twitch anterior gracilis muscles. Results show that: (a) CGRP is present in obturator nerve motor neurons which supply the gracilis muscle, as well as in the corresponding motor endplate regions where high levels of both AChE activity and acetylcholine receptors (AChRs) are detected; (b) endplate-associated CGRP declines with muscle denervation several hours before any changes in AChE forms are detected; (c) a single subcutaneous injection of CGRP reversibly reduces the activities of all AChE forms in endplate regions of normally innervated and otherwise untreated gracilis muscles; and (d) similar treatment with hCGRP(8-37), a potent and selective CGRP antagonist, produces the opposite effects, i.e., it reversibly elevates the activities of all AChE forms. These and other findings indicate that CGRP and hCGRP(8-37) influence the mechanism(s) by which AChE forms are maintained in intact adult gracilis muscles. Indeed, the findings lend strong support to the hypothesis that nerve-derived CGRP plays a key role in the trophic regulation of AChE forms at the neuromuscular junction.

Acetylcholinesterase↗
PubMed1998

Calcitonin gene-related peptide in myocardial ischaemia and reperfusion in the pig.

OBJECTIVE: In myocardial ischaemia, slow conducting capsaicin-sensitive C-fibres are activated. Apart from the mediation of pain, activation of these fibres causes release of various peptides, such as calcitonin gene-related peptide (CGRP), which is a potent vasodilator. The aim of this study was to investigate the role of CGRP in the context of myocardial ischaemia in vivo. METHODS: The left anterior descending coronary artery (LAD) was occluded during 45 min in 27 anaesthetised open-chest pigs. LAD flow, mean arterial pressure (MAP), heart rate, peak dP/dt, arterial and coronary venous concentration of CGRP was measured prior to ischaemia, and during 4 h of reperfusion. The extent of myocardial infarction was measured using staining with triphenyl tetrazolium chloride. RESULTS: Retroinfusion of CGRP (100 micrograms) into the ischaemic myocardium was associated with a more pronounced hyperaemia, and systemic hypotension, during early reperfusion. The infarct size in relation to the area at risk was not affected by CGRP or the CGRP antagonist CGRP(8-37), and averaged 67 +/- 3%. There were no changes in plasma CGRP levels during ischaemia or reperfusion. CONCLUSION: Exogenously administered CGRP can cause systemic hypotension and augments postischaemic coronary flow. In this model, no cardioprotective effect of CGRP could be proven.

Animals↗
PubMed1999

An autocrine or a paracrine role of adrenomedullin in modulating cardiac fibroblast growth.

OBJECTIVE: The aim of the present study was to determine the role of adrenomedullin (AM) in cardiac fibroblasts. METHODS: The production and secretion of AM were examined in cultured neonatal rat cardiac fibroblasts, and the effects of AM on proliferation and protein synthesis of these cells were assessed by [3H]thymidine and [3H]phenylalanine incorporation, respectively. RESULTS: Cultured cardiac fibroblasts secreted AM into the medium time-dependently at a rate of 20.3 +/- 3.0 fmol/5 x 10(4) cells/48 h, mean +/- S.D. Northern blot analysis showed expression of preproAM mRNA of 1.6 kb in these cells. In addition, 10(-6) mol/l of angiotensin II (Ang II) and endothelin-1 (ET-1) significantly increased the AM secretion by 55 and 48%, respectively. Synthetic AM significantly reduced 10(-6) mol/l Ang II- or 10(-7) mol/l ET-1-stimulated [3H]thymidine and [3H]phenylalanine incorporation in a dose-dependent manner, and these effects were attenuated by a calcitonin gene-related peptide (CGRP) type 1 receptor antagonist, CGRP(8-37). Synthetic AM also had a dose-dependent stimulatory effect on cAMP accumulation in these cells, which was significantly attenuated by CGRP(8-37). A cAMP analogue, 8-bromo-cAMP, mimicked the AM effects, inhibiting the Ang II-stimulated [3H]thymidine and [3H]phenylalanine incorporation. Blockage of the effect of endogenous AM by anti-AM monoclonal antibody not only significantly reduced the basal level of intracellular cAMP, but also enhanced the [3H]thymidine and [3H]phenylalanine incorporation into the cells. CONCLUSIONS: Cultured neonatal rat cardiac fibroblasts produce and secrete AM, and the secreted AM may inhibit proliferation and protein synthesis of these cells. AM may exert these inhibitory effects partly by elevating intracellular cAMP. It is suggested that AM has an important role in modulating the growth of cardiac fibroblasts in an autocrine or a paracrine manner.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2000

Mitogen-activated protein kinase inhibitors suppress prostaglandin F(2alpha)-induced myosin-light chain phosphorylation and contraction in iris sphincter smooth muscle.

The purpose of this study was to investigate the potential role of mitogen-activated protein (MAP) kinase in contraction by monitoring MAP kinase phosphorylation (activation) and contraction during agonist stimulation of cat iris sphincter smooth muscle. Changes in tension in response to prostaglandin F(2alpha), latanoprost, a prostaglandin F(2alpha) analog used as an anti-glaucoma drug, and carbachol were recorded isometrically, and MAP kinase activation was monitored by Western blot using a phosphospecific p42/p44 MAP kinase antibody. We found that treatment of the muscle with 2'-Amino-3'-methoxyflavone (PD98059) (10 microM), a specific inhibitor of MAP kinase kinase (MEK), inhibited significantly prostaglandin F(2alpha)- and latanoprost-induced phosphorylation and contraction, but had little effect on those evoked by carbachol. Prostaglandin F(2alpha) increased MAP kinase phosphorylation in a concentration-dependent manner with EC(50) value of 1.1 x 10(-8) M and increased contraction with EC(50) of 0.92 x 10(-9) M. The MAP kinase inhibitors PD98059, Apigenin and 1,4-Diamino-2,3-dicyano-1, 4bis(2-aminophenylthio)butadiene (UO126) inhibited prostaglandin F(2alpha)-induced contraction in a concentration-dependent manner with IC(50) values of 2.4, 3.0 and 4.8 microM, respectively. PD98059 had no effect on prostaglandin F(2alpha)- or on carbachol-stimulated inositol-1,4,5-trisphosphate (IP(3)) production. In contrast, the MAP kinase inhibitor inhibited prostaglandin F(2alpha)-induced myosin-light chain (MLC) phosphorylation, but had no effect on that of carbachol. N-[2-(N-(4-Chloro-cinnamyl)-N-methylaminomethyl)phenyl]-N-[2- hydroxyethyl]-4-methoxybenzenesulfonamide (KN-93) (10 microM), a Ca(2+)-calmodulin-dependent protein kinase inhibitor, and Wortmannin (10 microM), an MLC kinase inhibitor, inhibited significantly (by 80%) prostaglandin F(2alpha)- and carbachol-induced contraction. It can be concluded that in this smooth muscle p42/p44 MAP kinases are involved in the mechanism of prostaglandin F(2alpha)-, but not in that of carbachol, induced contraction. In addition, these data clearly indicate that the stimulation of the iris sphincter with prostaglandin F(2alpha) and carbachol activate two distinct pathways, the MAP kinase pathway and the Ca(2+) mobilization pathway.

Animals↗
PubMed1997

Effect of amylin in various experimental models of gastric ulcer.

Subcutaneous administration of amylin (20-40 micrograms/kg) prevented, in a dose-dependent manner, reserpine- and serotonin-induced gastric damage, but the anti-ulcer effect was not present when lesions were induced by pylorus ligation. The protective effect of amylin was inhibited by pretreatment with capsicin as well as CGRP-(8-37), a calcitonin gene-related peptide (CGRP) and amylin receptor antagonist, and was significantly reduced by domperidone, a dopamine D2 receptor antagonist, or neostigmine, an inhibitor of acetylcholinesterase. Our data suggest that the gastroprotective activity of amylin in some experimental models of gastric ulcers involves capsaicin-sensitive fibers and CGRP receptors. Moreover, the peptide interferes, at least in part, with the dopaminergic and parasympathetic systems.

Amyloid↗
PubMed1995

PGF2 alpha/pilocarpine interactions on IOP and accommodation in monkeys.

We investigated whether (i) single or repeated topical treatment with either the tromethamine salt or the isopropyl ester of prostaglandin F2 alpha (PGF2 alpha-TS or PGF2 alpha-IE) inhibits the accommodative response to pilocarpine; (ii) pilocarpine given after PGF2 alpha inhibits the latter's ocular hypotensive effect, as occurs with the reverse order of administration. PGF2 alpha-IE (2 micrograms) or PGF2 alpha-TS (50 micrograms) was applied topically to the right eye of five cynomolgus monkeys twice daily for 4 days. Before initial dosing, and 1 hr after the initial and final dose the animals were anesthetized with ketamine, and intraocular pressure (IOP) and refraction determined bilaterally. Following post-PG IOP and refraction determinations, pilocarpine HCl was given topically (bilaterally) or infused i.m. over 10 min, after which refraction was determined periodically for 50 min. IOP was then again determined. After a single unilateral dose of PGF2 alpha-TS or PGF2 alpha-IE, IOP was unchanged. Both eyes accommodated markedly and equally in response to pilocarpine, and IOP fell bilaterally by a statistically significant 3 mmHg in response to pilocarpine. Repeated doses of PGF2 alpha-TS or PGF2 alpha-IE did not significantly affect the accommodative response to pilocarpine, while pilocarpine did not alter the approximately 10 mmHg ipsilateral IOP fall induced by repeated dosing of PGF2 alpha-TS or PGF2 alpha-IE. It is concluded that repeated unilateral topical application of PGF2 alpha-TS or PGF2 alpha-IE to the cynomolgus monkey eye markedly reduces ipsilateral IOP, but has no effect on the ipsilateral or contralateral eye accommodative response to pilocarpine. Pilocarpine reverses the PGF2 alpha-TS or PGF2 alpha-IE-induced fall in IOP when given before the PGF2 alpha, but does not prevent it when given after, within the parameters of this study.

Accommodation, Ocular↗