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PubMed1999

Pilocarpine treatments differentially affect alpha2-adrenoceptors which modulate the firing rate of locus coeruleus neurones and the synthesis and release of noradrenaline in rat brain.

We have investigated the effect of treatments with the muscarinic acetylcholine receptor agonist, pilocarpine, on the sensitivity of central alpha2-adrenoceptors that regulate the firing activity of rat locus coeruleus, the tyrosine hydroxylase activity in the rat cortex, hippocampus and hypothalamus, and the K(+)-evoked release of [3H]noradrenaline from rat cortical and hippocampal synaptosomes. Short-term (4 days), but not acute, treatment with pilocarpine caused a small but statistically significant increase in the inhibitory effect of the alpha2-adrenoceptor agonist clonidine on the firing rate of locus coeruleus neurones, with a decrease in the ED50 of 290% (P<0.001). However, no change in the effect of clonidine on the locus coeruleus was observed after longer pilocarpine (11 days) treatment. In the rat cerebral cortex, but not in hippocampus or hypothalamus, chronic (19 days) treatment with pilocarpine caused a decrease in the inhibitory effect of clonidine on tyrosine hydroxylase activity (55%, P<0.05), but did not change the stimulatory effect of the alpha2-adrenoceptor antagonist idazoxan. Moreover, treatments (4, 11 and 19 days) with pilocarpine did not alter the inhibitory effect of clonidine [10(-8)-10(-5) M] on the K(+)-evoked release of [3H]noradrenaline from rat cortical and hippocampal synaptosomes. These results indicate that administration of pilocarpine slightly potentiates some but not all the functional responses mediated by brain presynaptic alpha2-adrenoceptors. In conclusion, these results do not support the hypothesis that chronic treatments with pilocarpine lead to a suitable model of alpha2-adrenoceptor supersensitivity.

Animals↗
PubMed1978

Effect of vehicle on pilocarpine-induced ocular hypotension.

The effect of 1.4% polyvinyl alcohol and castor oil vehicles on pilocarpine-induced hypotension was studied in 50 patients with open-angle glaucoma. Diurnal tension curves showed that the mean intraocular pressure was lower and the maximum diurnal variation smaller during the treatment with oily drops of 2% and 4% pilocarpine instilled 2-3 times daily than when 2% and 4% pilocarpine in polyvinyl alcohol was instilled 3-4 times daily. The differences were statistically significant. In long-term treatment no marked pilocarpine tolerance developed in cases treated with oily drops of pilocarpine. It is concluded that in the treatment of patients with open-angle glaucoma, the hypotensive effect of pilocarpine in an oily vehicle instilled 2-3 times daily is greater and more even than that of pilocarpine of corresponding strength in polyvinyl alcohol administered 3-4 times daily.

Adult↗
PubMed1978

Effect of vehicle on pilocarpine-induced miosis.

To determine the effect of 1.4% polyvinyl alcohol (PVA) and castor oil vehicles on the pilocarpine-induced miosis, we studied the miotic effect of 2% pilocarpine-PVA and oily drops on 4 young and 10 elderly people and the miotic effect of 4% pilocarpine-PVA and oily drops on 13 elderly people. The miosis developed fast within 15 min, and maximum miosis was rached within 1 h. Oily drops of pilocarpine induced stronger maximum miosis than corresponding PVA-drops. The pupil remained contracted to less than 50% of its starting diameter after pilocarpine-PVA drops for 3-4 h and after oily drops for 9 h and returned to its starting diameter after pilocarpine-PVA drops 9-10 h and after oily drops 20-24 h following administration. The difference in the effect between pilocarpine-PVA and oily drops was independent of the subjects' age.

Adult↗
PubMed1988

Effects of pilocarpine on breathing movements in normal, chemodenervated and brain stem-transected fetal sheep.

1. We examined the effects on fetal breathing movements (FBM) and electrocortical activity (ECoG) of the administration of pilocarpine to three groups of fetal sheep in utero: one group had peripheral chemodenervation; one group had peripheral chemodenervation and transection of the brain stem at the level of the colliculi; a third group of sham-operated animals acted as a control. 2. Pilocarpine induced a period of FBM characterized by their high amplitude (ca. 24 mmHg) and low frequency (ca. 0.65 Hz). It also produced low-voltage ECoG. These effects were seen both in normoxia and in hypoxia. They were independent of the ECoG state in which the drug was given. 3. In normoxia, pilocarpine-induced FBM were blocked by cholinergic antagonists which enter the central nervous system, atropine sulphate and scopolamine hydrobromide, but were either unaffected or were reduced in amplitude by antagonists with restricted access to the central nervous system, atropine methylnitrate and scopolamine methylbromide. In hypoxia, atropine sulphate and scopolamine hydrobromide again blocked FBM but now scopolamine methylbromide and atropine methylnitrate blocked the FBM in 42% of trials. In the remaining trials FBM remained virtually unchanged. 4. No differences were observed in the effects of pilocarpine on FBM or ECoG between chemodenervated fetuses and those which had been sham-operated. 5. In fetuses with transection of the brain stem, breathing was continuous irrespective of the ECoG. Pilocarpine increased the amplitude of FBM but did not alter the frequency of these FBM. These effects occurred both in normoxia and in hypoxia. 6. We conclude that pilocarpine produces effects on fetal behaviour via at least two sites in the central nervous system. One site lies in the pons or medulla and is responsible for the stimulation of FBM. The other site is above the level of the colliculi and is responsible for producing sustained low-voltage ECoG. These effects do not require the integrity of the peripheral chemoreceptors and we find no evidence to support the previous suggestion that the action of pilocarpine is via stimulation of these receptors.

Animals↗
PubMed2003

Oral pilocarpine for the treatment of ocular symptoms in patients with Sjögren's syndrome: a randomised 12 week controlled study.

OBJECTIVE: To evaluate the efficacy and side effects of oral pilocarpine for the treatment of ocular symptoms in patients with primary Sjögren's syndrome (SS). METHODS: A 12 week, single centre, randomised controlled study was performed. Twenty nine patients were randomly assigned to receive oral pilocarpine (5 mg twice a day), 28 only artificial tears, and 28 inferior puncta occlusion. Patients receiving oral pilocarpine and those with inferior puncta occlusion also received artificial tears. Patients were evaluated at baseline and throughout the study for their subjective global assessment of dry eyes and for their objective assessment of dry eyes (Schirmer's-I test, rose bengal test, and imprint test). RESULTS: Patients taking oral pilocarpine had significant improvement in subjective global assessment of dry eyes, as was evaluated by improvement of >55 mm on a visual analogue scale (VAS) for responses to the eye questionnaire, compared with patients treated with artificial tears (p<0.001) and those with inferior puncta occlusion (p<0.05). Furthermore, patients receiving oral pilocarpine also showed greater objective improvement, as measured by the rose bengal test (p<0.05), while Schirmer's-I test showed no differences between the treated groups. Commonly reported adverse events were headache, increased sweating, nausea, and vomiting in the pilocarpine group, while one patient in the inferior puncta occlusion group had blepharitis and was withdrawn from the study. CONCLUSION: 10 mg of pilocarpine daily given to patients with SS for 12 weeks had a beneficial effect on subjective eye symptoms, as evaluated by improvement >55 mm on a VAS. Additionally, an improvement of rose bengal staining was noted, but an increase in tear production, as measured by the Schirmer-I test, was not substantiated.

Administration, Oral↗
PubMed1976

Reduced surface tension in lungs of fetal rabbits injected with pilocarpine.

After opening the maternal abdomen under methoxyflurane anesthesia, fetal rabbits 25.5-28.5 days gestation were given an intraperitoneal injection of pilocarpine (150 mg/kg) or saline through the intact uterine wall. They were delivered by hysterotomy and sacrificed without breathing 2.5 h later. Newborn rabbits 29.5 days gestation received an injection of pilocarpine or saline at birth and breathed 30-120 min. Other newborn rabbits 29.5 days gestation were alternately sacrificed at birth or after breathing 30 min. Static pressure-volume curves with air showed decreased recoil and improved air retention on deflation in fetal rabbits 25.5-27.5 days injected with pilocarpine. There was no change in the static pressure-volume curve of lungs filled with saline. The data suggest that pilocarpine reduced surface tension by producing secretion of surfactant into air spaces. No change in lung recoil occurred with pilocarpine at 28.5 days, or with pilocarpine or breathing at 29.5 days. This may mean that air spaces at 28.5-29.5 days contained optimal surfactant, so further secretion of surfactant stimulated by pilocarpine or breathing failed to reduce surface tension.

Animals↗
PubMed2005

A comparative study on the protection profile of lidocaine, amifostine, and pilocarpin on the parotid gland during radiotherapy.

The aim of this study was to evaluate the individual and the synergetic radioprotective effect of lidocaine, amifostine, and pilocarpin on the parotid gland. Forty-nine rabbits were randomized into seven groups (n = 7)--control, irradiated sham-treated, irradiated/lidocaine-pretreated, irradiated/amifostine-pretreated, irradiated/pilocarpin-pretreated, irradiated/lidocaine + pilocarpin-pretreated, and irradiated/amifostine + pilocarpin-pretreated groups. One week before irradiation (15 Gy) and 72 hours as well as 1 month afterward, the parotid gland was investigated morphologically, sialoscintigraphically, and immunohistochemically with the use of tenascin-C and alpha smooth muscle actin. Compared with control animals, there was a significant reduction of the salivary ejection fraction in the irradiated untreated group 72 hours following radiation. Only animals pretreated with lidocaine or amifostine (alone or combined with pilocarpin) showed a slight nonsignificant reduction of salivary ejection fraction. Immunohistochemically, we observed a significant loss of alpha smooth muscle actin and an up-regulation of tenascin-C expression in irradiated/untreated glands. These changes were less evident in animals pretreated with lidocaine or lidocaine + pilocarpin. Amifostine and pilocarpin did not show any influence on tenascin-C or alpha smooth muscle actin expression. Ultrastructural damage was observed in irradiated untreated and pilocarpin-pretreated glands. In contrast, lidocaine and amifostine could largely preserve the glandular ultrastructure. One month postradiation, all changes were regressive regardless of treatment protocol. Potential radioprotective agents show different effects on both morphology and function of the parotid gland. Associated immunohistochemical and ultrastructural findings could prove the prevailed protection profile of lidocaine. This may provide a prophylactic approach in the field of radioprotection of salivary glands.

Actins↗
PubMed1992

Salivary flow induction by buccal permucosal pilocarpine in anesthetized beagle dogs.

We tested whether permucosal delivery of pilocarpine nitrate could be used to elicit significant salivary secretion. Pilocarpine (pKa 6.6 at 37 degrees C) was applied as solutions (pHs 5.6, 6.6, 7.6; 15 mg/mL) to the buccal mucosa (2.8 cm2) of 6 anesthetized dogs. Saliva was collected continuously from cannulated submandibular and parotid ducts and blood sampled during and after drug administration. Plasma pilocarpine levels were determined by reversed-phase HPLC. Absorption rates were determined by use of data from separate zero-order intravenous infusions to the same dogs. Pilocarpine was buccally absorbed at a constant rate of 72.9 +/- 38.5 micrograms/kg/h following its application at pH 7.6. At this pH of the drug solution, the time to appearance of pilocarpine in blood plasma was 0.31 +/- 0.08 h, and the time to appearance of salivary flow was 0.86 +/- 0.32 h. A threshold dose of 32.9 +/- 7.5 micrograms/kg was required to induce secretion with the pH 7.6 drug, the steady-state submandibular flow rate was 0.14 +/- 0.11 mL/min/gland pair. Salivary flow induction was symmetrical and reached levels as high as 0.35 mL/min/submandibular gland pair without apparent tachyphylaxis. Results at pHs 5.6, 6.6, and 7.6 were consistent with the hypothesis that pilocarpine is primarily absorbed as un-ionized drug. The data indicate that transmucosal delivery of pilocarpine, avoiding "first pass" hepatic loss, may hold promise for the treatment of xerostomia.

Administration, Buccal↗
PubMed1993

A multicenter, randomized, double-blind, placebo-controlled, dose-titration study of oral pilocarpine for treatment of radiation-induced xerostomia in head and neck cancer patients.

PURPOSE: To determine the efficacy and safety of pilocarpine hydrochloride for symptomatic relief of postradiation xerostomia symptoms and for saliva production in patients with head and neck cancer. PATIENTS AND METHODS: One hundred sixty-two head and neck cancer patients who had received at least 40 Gy of radiation (117 patients had received > 60 Gy) with clinically significant xerostomia were enrolled onto a randomized, double-blind, placebo-controlled, multi-center clinical investigation. Patients received 2.5-mg tablets for the first 4 weeks, 5.0-mg tablets for the second 4 weeks, and 10.0-mg tablets for the last 4 weeks of the 12-week study. Patients were allowed to titrate pilocarpine or placebo for improvement in symptoms or to reduce side effects. Patients were evaluated for symptomatic relief by questionnaires and visual analog scales (VAS), and for saliva production by sialometry. RESULTS: Pilocarpine produced a significant improvement (P = .035) in overall global assessments compared with placebo. There was a statistically significant (P = .020) decreased use of oral comfort agents such as artificial saliva, hard candy, and water. Values for symptomatic improvement in dryness approached significance (P = .057). There were statistically significant postdose improvements in whole and parotid salivary flow in pilocarpine treatment groups versus placebo. All pilocarpine dosages tested were judged to be safe. Adverse experiences were primarily sweating, rhinitis, headache, nausea, and urinary frequency, with the most common side effect being mild to moderate sweating. There were no serious drug-related adverse experiences in any of the pilocarpine treatment groups. CONCLUSION: It is concluded that pilocarpine produces clinically significant benefits for the symptomatic treatment of postradiation xerostomia. Best results were obtained with continuous treatment for 8 to 12 weeks with doses greater than 2.5 mg three times per day.

Administration, Oral↗
PubMed2006

Characterization of pilocarpine-loaded chitosan/Carbopol nanoparticles.

Patients using ophthalmic drops are faced with frequent dosing schedules and difficult drop instillation. Therefore, a long-lasting pilocarpine-loaded chitosan (CS)/Carbopol nanoparticle ophthalmic formulation was developed. The physicochemical properties of the prepared nanoparticles were investigated using dynamic light scattering, zeta-potential, transmission electron microscopy, Fourier transform infrared ray spectroscopy (FT-IR) and differential scanning calorimetry (DSC). The sustained-release effects of pilocarpine-loaded nanoparticles were evaluated using in-vitro release and in-vivo miotic tests, and compared with pilocarpine in solution, gel and liposomes. We found that the prepared nanoparticles were about 294 nm in size. DSC and FT-IR studies suggested that an electrostatic interaction between CS and Carbopol contributes at least in part to the stabilization of pilocarpine/CS/Carbopol nanoparticles. When compared with pilocarpine in solution, gel or liposomes, the best slow-release profile of pilocarpine from the prepared nanoparticles occurred in a dissolution test. In the in-vivo miotic study, pilocarpine-loaded CS/Carbopol nanoparticles showed the most significant long-lasting decrease in the pupil diameter of rabbits. The advantages of CS and Carbopol are good biocompatibility, biodegradability and low toxicity. CS is also a mucoadhesive polymer. Thus, pilocarpine/CS/Carbopol nanoparticles may provide an excellent potential alternative ophthalmic sustained-release formulation of pilocarpine for clinical use. CS/Carbopol nanoparticles may also be useful for a variety of other therapeutic delivery systems.

Acrylic Resins↗
PubMed2005

Lovastatin reduces neuronal cell death in hippocampal CA1 subfield after pilocarpine-induced status epilepticus: preliminary results.

OBJECTIVE: To further characterize the capacity of lovastatin to prevent hippocampal neuronal loss after pilocarpine-induced status epilepticus (SE) METHOD: Adult male Wistar rats were divided into four groups: (A) control rats, received neither pilocarpine nor lovastatin (n=5); (B) control rats, received just lovastatin (n=5); (C) rats that received just pilocarpine (n=5); (D) rats that received pilocarpine and lovastatin (n=5). After pilocarpine injection (350 mg/kg, i.p.), only rats that displayed continuous, convulsive seizure activity were included in our study. Seizure activity was monitored behaviorally and terminated with an injection of diazepam (10 mg/kg, i.p.) after 4 h of convulsive SE. The rats treated with lovastatin received two doses of 20 mg/kg via an oesophagic probe immediately and 24 hours after SE induction. Seven days after pilocarpine-induced SE, all the animals were perfused and their brains were processed for histological analysis through Nissl method. RESULTS: The cell counts in the Nissl-stained sections performed within the hippocampal formation showed a significant cell loss in rats that received pilocarpine and presented SE (CA1=26.8 +/- 13.67; CA3=38.1 +/- 7.2; hilus=43.8 +/- 3.95) when compared with control group animals (Group A: CA1=53.2 +/- 9.63; CA3=63.5 +/- 13.35; hilus=59.08 +/- 10.24; Group B: CA1=74.3 +/- 8.16; CA3=70.1 +/- 3.83; hilus=70.6 +/- 5.10). The average neuronal cell number of CA1 subfield of rats that present SE and received lovastatin (44.4 +/- 17.88) was statically significant increased when compared with animals that just presented SE. CONCLUSION: Lovastatin exert a neuroprotective role in the attenuation of brain damage after SE.

Animals↗
PubMed2005

Decreased salivary flow rate as a dipsogenic factor in hemodialysis patients: evidence from an observational study and a pilocarpine clinical trial.

Decreased salivary flow rate causes xerostomia (symptoms of oral dryness) in patients who undergo hemodialysis (HD); however, whether it thus contributes to thirst and excess interdialytic weight gain (IDWG) remains undetermined. In the observational study, 3 mo of data of 90 stable HD patients were collected, and sensations of thirst and xerostomia were assessed by 100-mm visual analog scales (VAS). Multivariate analyses revealed that the VAS oral dryness score was an independent determinant for thirst, daily IDWG, and IDWG%. Unstimulated whole salivary flow rate (UWS) was measured in 45 participants and was negatively correlated with VAS oral dryness score (r = -0.690, P 2%/d) were randomly assigned to either the sequence pilocarpine (2 wk)-washout (3 wk)-placebo (2 wk)-washout (2 mo)-placebo (3 mo) or placebo (2 wk)-washout (3 wk)-pilocarpine (2 wk)-washout (2 mo)-pilocarpine (3 mo) with 35 participants completing the trial. During the 2-wk crossover period (the first to seventh weeks), pilocarpine increased UWS and decreased xerostomia and thirst. The IDWG(2d) decreased (by approximately 0.2 kg; P = 0.013) but not IDWG(3d). During the 3-mo interventional period, pilocarpine increased UWS but decreased both IDWG(2d) (by 0.76 kg; P = 0.021) and IDWG(3d) (by 1.07 kg; P = 0.007). It also modestly increased serum albumin and decreased mean BP. Pilocarpine-related adverse effects were generally mild. In conclusion, decreased salivary flow is a dipsogenic factor in HD patients, and pilocarpine can alleviate it.

Body Weight↗
PubMed1999

Pilocarpine toxicity in retinal ganglion cells.

PURPOSE: Muscarinic agents reduce intraocular pressure by enhancing aqueous outflow, probably by stimulating ciliary muscle contraction. However, pilocarpine is a well characterized neurotoxin and is widely used to generate animal seizure models. It was therefore investigated whether pilocarpine was also toxic to retinal ganglion cells. METHODS: Dissociated whole retinal preparations were prepared from postnatal day 16 to 19 rats. Retinal ganglion cells had been previously back-labeled with a fluorescent tracer. Retinal cells were incubated with pilocarpine, lithium, and inositol derivatives, and viability of the retrogradely labeled retinal ganglion cells was assayed after 24 hours. RESULTS: Pilocarpine was toxic to retinal ganglion cells in a dose-dependent fashion. This toxicity was potentiated by lithium and blocked by epi- and myo-inositol. CONCLUSIONS: Pilocarpine is toxic to retinal ganglion cells in a mixed culture assay. This toxicity appears to depend on the inositol pathway and is similar to its mode of action in other neurons. However, 0.4 mM pilocarpine (the lowest concentration that did not affect ganglion cell survival) is roughly 1000-fold higher than the vitreal concentration and 20-fold higher than the scleral concentration that can be obtained with topical administration of 2% pilocarpine in the rabbit eye.

Animals↗
PubMed2000

Intracameral pilocarpine in topical phacoemulsification.

PURPOSE: To evaluate the efficacy and corneal toxicity of intracameral pilocarpine. METHOD: A randomized, control trial using contralateral eye as control was designed to evaluate the effect of intracameral pilocarpine during phacoemulsification in 30 patients. 0.13 mg/ml pilocarpine in BSS was used as an irrigating solution to remove viscoelastic agents at the end of the operation while BSS was used in the control group. The outcome measurements composed of intraoperative pre and post irrigation pupil diameter, pre and post operative endothelial cell count and corneal thickness. SETTING: Priests Hospital. RESULTS: The pre-irrigation pupil size in the pilocarpine group and the control group was 7.62 +/- 0.75 mm and 7.60 +/- 0.77 mm respectively. The post-irrigation pupil size in the pilocarpine group and the control group was 5.40 +/- 0.79 mm and 7.18 +/- 0.79 mm. There were no statistically differences in pre and post-operative endothelial cell density, central corneal thickness, and the average corneal thickness between the pilocarpine group and the control group during six months follow-up. CONCLUSION: Intracameral pilocarpine in a low concentration (0.13 mg/ml) effectively constricts the pupil without significant changes of corneal endothelium compared to the control group.

Aged↗
PubMed1990

[Electroanalytical chemistry study of pilocarpine].

The electrochemical behaviour of pilocarpine was investigated by differential pulse polarography and cyclic voltammetry. The optimum conditions for the determination of pilocarpine were as follows: The electrolyte was 0.4 mol/L HAc-NaAc(pH 4.0) buffer solution, Zn (II) 1.0 x 10(-3) mol/L; initial potential -0.80 V (vs Ag-AgCl), final potential -1.30 V (vs Ag-AgCl), and voltage sweep rate 5 mV/s. A fair reproducibility in the above procedure and a good relationship between peak current and pilocarpine concentration (4.0 x 10(-6)-4.0 x 10(-5) mol/L) were achieved. The detection limit was 8.0 x 10(-7) mol/L. This paper also reports that the application of cyclic voltammetry to study electrode process behavior has been established. The PVC membrane ion-selective electrode for pilocarpine also was studied. It is based on the use of tetraphenylborate pilocarpine ion pair complex as the active material. The PVC membrane electrode showed Nernstian response over the pilocarpine concentration range from 1.0 x 10(-2) to 3.0 x 10(-5) mol/L, with a slope of 36 mV/decade, the detection limit being 3.0 x 10(-6) mol/L. The electrode gave fast response and good reproducibility. This method provides a rapid and simple way to the determination of pilocarpine in pharmaceutical preparations.

Electrodes↗
PubMed1977

Pilocarpine administration by contact lens.

A previous investigation had indicated that pilocarpine delivered to the eye by means of a hydrophilic contact lens provided better control of the intraocular pressure over a longer period and with a smaller concentration of pilocarpine. To clarify the situation further, an animal experiment was undertaken with radioactive labelled pilocarpine. Three situations were compared: pilocarpine administered by a contact lens, by drops, and by subconjunctival injection. The results indicated that the contact lens gave a greater concentration of the pilocarpine in the iris and ciliary body than either the drops or the subconjunctival pilocarpine. A high concentration of pilocarpine was achieved in the conjunctiva with drop administration and was comparable to that of subconjunctival administration.

Animals↗
PubMed1996

Ocular hypotensive efficacy and safety of a combined formulation of betaxolol and pilocarpine.

PURPOSE: To evaluate the ocular hypotensive efficacy and safety of a fixed combination of betaxolol (0.25%) and pilocarpine (1.75%). METHODS: Three multicenter, double-masked, parallel trials were completed in patients with primary open-angle glaucoma or ocular hypertension of 3 months' treatment duration. Studies 1 and 2 were three-arm comparisons of betaxolol, pilocarpine, and a fixed combination, each used 3 times daily. Study 3 was a two-arm study of the fixed combination with and without a surfactant, used twice daily. In all studies, there was a 1-month runin period with betaxolol 0.25% suspension given twice daily. There were 182 patients in Study 1, 186 patients in Study 2, and 166 patients in Study 3. RESULTS: In all 3 studies, approximately 10% to 15% of patients treated with pilocarpine or the combination therapy were terminated from further participation because of typical pilocarpine side effects (eg, blurred vision, headache). In studies 1 and 2, there was a mean reduction in intraocular pressure from a betaxolol baseline of approximately 3 to 4 mmHg. Patients continuing on betaxolol alone or randomly assigned to pilocarpine alone experienced a mean reduction of 1 to 2 mm Hg. Overall, the combination was approximately 2 mmHg more effective than either betaxolol or pilocarpine alone. In Study 3, the two betaxolol combinations had equivalent efficacy. CONCLUSION: In patients requiring more than one ocular hypotensive agent, the combination of betaxolol and pilocarpine in a single formulation appears to be an effective and relatively safe agent. The use of this combination agent promises the potential for enhanced patient convenience.

Adrenergic beta-Antagonists↗
PubMed1996

[An experimental study on corneal collagen shield vehicle for delivery of pilocarpine].

OBJECTIVE: The study was designed to clarify the role of corneal collagen shield made in China as a drug vehicle for the delivery of pilocarpine in different ways. METHODS: 80 eyes of New Zealand white rabbits were randomly divided into three groups, corneal collagen shield immersed with pilocarpine, corneal collagen shield with topical application of pilocarpine and synthetic collagen pilocarpine shield. At 0.5, 1, 3 and 6 hours after the delivery, the aqueous concentrations of pilocarpine and the pupillary sizes of all the eyes were measured. RESULTS: This study showed that shortly after the delivery of pilocarpine in the 3 groups, in spite of difference in ways of its delivery, its aqueous concentrations reached a relatively high level and maintained for more than six hours, the shield acting as a temporary "drug source". The aqueous pharmacokinetics of corneal collagen shield for pilocarpine delivery was consistent with the first-order kinetics and it was confirmed by the observations of miotic response. CONCLUSIONS: The corneal collagen shield made in China is a fine vehicle for drug delivery.

Animals↗