Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PILOCARPINE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources

Modification of apomorphine-, physostigmine- and pilocarpine-induced yawning after long-term treatment with neuroleptic or cholinergic agents.

Chronic treatment with haloperidol, physostigmine and scopolamine exerted different effects on the frequency of yawning induced by apomorphine (0.25 mg/kg, i.p.), physostigmine (0.2 mg/kg, i.p.) and pilocarpine (4 mg/kg, i.p.) as compared with chronic treatment with saline. Haloperidol decreased the apomorphine- and physostigmine-induced yawning but not the pilocarpine-induced yawning. Physostigmine reduced only the pilocarpine-induced yawning without affecting the apomorphine- and physostigmine-induced yawning. However, physostigmine showed the most rapid onset- and peak-time of yawning induced by a high dose of physostigmine (0.75 mg/kg, i.p.) as well as that of pilocarpine (8 mg/kg, i.p.), and potentiated apomorphine (1 mg/kg, i.p.)-induced stereotypy, as compared with that observed in the saline group. Scopolamine potentiated the physostigmine- and pilocarpine-induced yawning but not the apomorphine-induced yawning. A single pretreatment with scopolamine (0.5 mg/kg, i.p.), however, depressed these yawning responses. The results suggest that yawning induced by physostigmine, but not by pilocarpine, may be modified by long-term treatment with haloperidol. The stereotypy mediated by the postsynaptic dopaminergic system, but not the yawning mediated by the presynaptic system, may be altered by chronic treatment with physostigmine, while long-term treatment with scopolamine seems to produce a supersensitivity to cholinergic receptors.

Animals↗

Flux of topical pilocarpine to the human aqueous.

Aqueous fluid was withdrawn from eyes of patients undergoing cataract extraction at various intervals after administration of two drops 2% pilocarpine-HCl in a standard manner. Determination of aqueous pilocarpine concentration was made both by spectroscopy of a ferric hydroxylamine complex and by gas-liquid chromatography. These methods were consistent in indicating that concentration does not rise beyond 5 micrograms/ml at any time following topical instillation. The mean of 71 GLC determinations of aqueous tapped between 2 and 32 minutes after drops was 1.67 micrograms/ml. With assumption of a total chamber volume of 400 microliter, the average total pilocarpine in aqueous in these circumstances is less than 1 microgram. These findings correlate well with investigations of transcorneal flux of pilocarpine for the rabbit in a partial in vitro transport chamber system, with which comparable low flux efficiency was found after simulated drop administration. This serves to validate in some measure in extrapolation of other findings in chamber experiments to the living human eye. The combined in vitro and in vivo experimental results suggest that two distinct mechanisms govern the flux of pilocarpine across the cornea. High doses, comparable to those in standard clinical use, whether administered in drops or in constant flow, are transported inefficiently with kinetics indicating a diffusional mechanism and are associated with intracorneal retention or degradation of a substantial moiety. Low doses, if continuously applied, are much more efficiently transported. Hydrogel polymer vehicles appear to mobilize this low-dose mechanism by retaining drug against mechanical dissipation and elution by tear flow, but also by retaining drug against the capability of the cornea to take up more pilocarpine than can be transported to produce an intracorneal drug "depot." Although the exact nature of the "depot" is not clear, it is not elutable as pharmacologically active drug. It is consistently associated with the relatively poor flux efficiency found with high doses, and thus may act in some manner to disable a more efficient mechanism. The flux efficiency found with hydrogel mediation is more than double the best found in constant flow determinations. Vehicular mediated flux is rate limited by the cornea, independent of dose, linear with time despite exponentially secreasing available drug, and not associated with an intracorneal drug "depot." These features are consistent with carrier mediation of some type.

Animals↗

Clinical comparison of pilocarpine preparations in heavily pigmented eyes: an evaluation of the influence of polymer vehicles on corneal penetration, drug availability, and duration of hypotensive activity.

Heavily pigmented eyes have been shown to be relatively resistant to pilocarpine, and present special problems in management of open-angle glaucoma. Studies have suggested that the hypotensive effect of pilocarpine may be influenced by the vehicle; therefore, 13 relatively resistant black patients (26 eyes) were selected for a clinical comparison of pilocarpine as delivered in two different polymer vehicles. One vehicle was composed of 1.67% polyvinylpyrrolidone and BP water-soluble polymers (Adsorbobase); the other of hydroxypropyl methylcellulose 0.5%. All patients had been under treatment with the pilocarpine/methylcellulose preparation; 20 of the 26 eyes were judged to be uncontrolled (IOP above 21 mm Hg). Control of intraocular pressure was promptly obtained with the pilocarpine/Adsorbobase solution, and maintained at lower pilocarpine concentrations than with the previous therapy. Often, frequency of instillation could be decreased. This clinical comparison suggests that the Adsorbobase vehicle appreciably enhances corneal penetration and availability of pilocarpine. Three cases are discussed demonstrating the need for titration when instituting a new therapy with as little as one fourth the concentration of the previous pilocarpine therapy.

Aged↗

Inhibition of pilocarpine-induced aqueous humor flare, hypotony, and miosis by topical administration of anti-inflammatory and anesthetic drugs to dogs.

OBJECTIVE: To investigate the mechanism by which pilocarpine causes increased aqueous humor (AH) flare, hypotony, and miosis in dogs. ANIMALS: 6 dogs with normal eyes. PROCEDURE: Both eyes of each dog were treated topically with a 2% solution of pilocarpine, and 1 eye of each dog was additionally treated with commercially available ophthamic solutions. Breakdown of the blood-aqueous barrier (BAB) was quantitated in each eye, using laser flaremetry to measure AH flare. Intraocular pressure and pupil size were also measured. RESULTS: Pilocarpine caused increased flare from BAB breakdown that was inhibited by the drugs tested. Inhibition (most to least) of BAB breakdown was flurbiprofen more than diclofenac, proparacaine, or suprofen, which were more than 0.125 or 1.0% prednisolone. Inhibition appeared dose-dependent and caused consensual inhibition in the contralateral eye. Intraocular pressure was decreased only in proparacaine-treated eyes and increased in eyes treated with nonsteroidal anti-inflammatory drugs (NSAID). Flurbiprofen and proparacaine were the most effective at blocking miosis. CONCLUSIONS: Pilocarpine produced a predictable, reproducible BAB breakdown in dogs. Miosis and increased AH flare were inhibited equally by proparacaine or NSAID, suggesting that these signs were caused by neuropeptide release into the AH from antidromic stimulation, which subsequently triggers prostaglandin production. Hypotony was inhibited only by anti-inflammatory drugs. CLINICAL RELEVANCE: Proparacaine in combination with pilocarpine would be the best choice for treating dogs with acute glaucoma. Topical administration of NSAID should not be used to treat dogs with acute glaucoma, because they increase intraocular pressure and negate the effects of pilocarpine.

Administration, Topical↗

Successful Treatment of Dry Mouth and Dry Eye Symptoms in Sjögren's Syndrome Patients With Oral Pilocarpine: A Randomized, Placebo-Controlled, Dose-Adjustment Study.

BACKGROUND: : Sjögren's syndrome is characterized by the presence of xerostomia and/or xerophthalmia. Pilocarpine, a muscarinic cholinergic agonist, has been proven to be efficacious in treating radiation-induced xerostomia (up to 30 mg/day) and symptoms of dry mouth in Sjögren's patients (up to 20 mg/day). OBJECTIVE: : To compare the safety and efficacy of oral pilocarpine (dose-adjusted) versus placebo in the treatment of dry eye and dry mouth symptoms in Sjögren's syndrome at 6 and 12 weeks. METHODS: : In this 11-center, 256-patient placebo-controlled study, the safety and efficacy of oral pilocarpine (20 mg to 30 mg daily) for relief of Sjögren's-related dry mouth and dry eye symptoms was assessed. Changes in symptoms and salivary flow were measured over 12 weeks. RESULTS: : Compared with placebo, salivary flow was significantly increased in the pilocarpine group (P</= 0.0001) after the first dose and throughout the study. Significant improvement in patients' global assessment of dry mouth (P</= 0.0001) with relief in 5 of 7 separate oral symptoms (P</= 0.02) was reported by the treated patients throughout study. Minimal differences in 3 of 8 ocular symptoms were noted at 6 weeks (5-mg dose), but at 12 weeks (5- to 7.5-mg dose), the pilocarpine group demonstrated both significant improvement in global assessment of dry eyes (P</= 0.0001) and relief in 6 of 8 related symptoms (P</= 0.04). The drug was well tolerated at both doses. The most common pilocarpine-related side effects were sweating, urinary frequency, flushing, and chills. CONCLUSIONS: : Significant relief in dry mouth symptoms was noted at 20 mg/day, and significant relief in ocular symptoms, including lower artificial tear requirement, was noted after the dose was increased to 30 mg/day.

Journal Article↗

Ocular penetration of pilocarpine in rabbits.

Aqueous humor pilocarpine hydrochloride concentration was measured at 15, 30, 60, and 120 minutes after instillation in the rabbit eye of a radioactively labeled 2% pilocarpine solution in various vehicles. Maximum concentrations were found with a vehicle containing 1.67% polyvinylpyrrolidone and other water-soluble polymers (Adsorbotears) and 1% hydroxypropyl methylcellulose. These produced pilocarpine concentrations during the first two hours after administration three times greater than those found with either saline, 1.4% polyvinyl alcohol, or 0.5% hydroxypropyl methylcellulose. Benzalkonium chloride, 0.01%, enhanced pilocarpine penetration into the aqueous by as much as 50% at all time intervals. The vehicle viscosity was unrelated to efficacy of pilocarpine penetration into the aqueous. The equally effective 1% hydroxypropyl methylcellulose and Adsorbotears have viscosities of 112 and 20 centistokes, respectively, while 0.5% hydroxypropyl methylcellulose (13 centistokes), 1.4% polyvinyl alcohol (3 centistokes), and sodium chloride solution (0.85 centistokes) are much less efficacious.

Animals↗

Ultrastructural stereologic analysis of fetal rabbit type II alveolar epithelial cells following maternal pilocarpine treatment or fasting.

We have previously reported that subcutaneous administration of 5 mg/kg pilocarpine HCl, a muscarinic agonist, to pregnant white rabbits on days 24 through 27 of gestation results in an acceleration of fetal lung maturation. In the present study the ultrastructural differences observed within alveolar type II cells of 28-day fetuses from the pilocarpine and control groups were quantified by stereologic analysis. In addition, maturational changes occurring within the lungs of 28-day fetuses obtained from pregnant rabbits which were fasted for 7 days (days 21-28) were similarly analyzed. Stereologic analysis revealed that the fetal type II cells in the pilocarpine-treated group possessed a significantly greater volume density of lamellar inclusion bodies and rough endoplasmic reticulum and a significantly smaller volume density of glycogen than did controls. The volume density values for fetal type II cells of the fasted group were, with the exception of the Golgi apparatus, found to be intermediate between those of control and the pilocarpine-treated groups. It was also noted that a high percentage of the lamellar inclusion bodies within type II cells of the fasted group appeared morphologically abnormal, being characterized by a highly irregular outline and tightly packed lipid membranes. The results of this study substantiate and quantify our previously reported observation of accelerated maturation in pilocarpine-treated fetuses. In addition, they suggest a similar, though not as pronounced, effect of maternal fasting prior to delivery. However, the abnormal morphology of the lamellar inclusion bodies in the fasted group may reflect a qualitative change in the pulmonary surfactant produced by these fetuses.

Animals↗

Cellular and network properties of the subiculum in the pilocarpine model of temporal lobe epilepsy.

The subiculum was recently shown to be crucially involved in the generation of interictal activity in human temporal lobe epilepsy. Using the pilocarpine model of epilepsy, this study examines the anatomical substrates for network hyperexcitability recorded in the subiculum. Regular- and burst-spiking subicular pyramidal cells were stained with fluorescence dyes and reconstructed to analyze seizure-induced alterations of the dendritic and axonal system. In control animals burst-spiking cells outnumbered regular-spiking cells by about two to one. Regular- and burst-spiking cells were characterized by extensive axonal branching and autapse-like contacts, suggesting a high intrinsic connectivity. In addition, subicular axons projecting to CA1 indicate a CA1-subiculum-CA1 circuit. In the subiculum of pilocarpine-treated rats we found an enhanced network excitability characterized by spontaneous rhythmic activity, polysynaptic responses, and all-or-none evoked bursts of action potentials. In pilocarpine-treated rats the subiculum showed cell loss of about 30%. The ratio of regular- and burst-spiking cells was practically inverse as compared to control preparations. A reduced arborization and spine density in the proximal part of the apical dendrites suggests a partial deafferentiation from CA1. In pilocarpine-treated rats no increased axonal outgrowth of pyramidal cells was observed. Hence, axonal sprouting of subicular pyramidal cells is not mandatory for the development of the pathological events. We suggest that pilocarpine-induced seizures cause an unmasking or strengthening of synaptic contacts within the recurrent subicular network.

Animals↗

Mechanistic and quantitative evaluation of precorneal pilocarpine disposition in albino rabbits.

The low ocular bioavailability of topically applied pilocarpine is attributed to extensive precorneal drug loss in conjection with the resistance to corneal penetration. Several elements of precorneal loss were reported earlier, but a complete mechanistic understanding has not been available. The present study was designed to gain a better understanding of the mechanisms governing pilocarpine disposition in the precorneal areas as well as the relative influence of these parameters on ocular drug bioavailability. Radioactive pilocarpine and glycerin solutions were instilled into the precorneal area of the albino rabbit eye under various experimental conditions, and the drug concentration in the lacrimal lake was monitored as a function of time. The results demonstrated that nonconjunctival loss of pilocarpine, vasodilation due to the drug, and lacrimation due to vehicle formulation are additional aspects of precorneal drug disposition. The individual influence of all precorneal loss parameters on drug bioavailability was then assessed using a mathematical model formulated from experimental findings on both precorneal and intraocular drug disposition. Drainage and vasodilation, as well as nonconjunctival pilocarpine loss, exerted major influences on drug loss at the absorption site.

Administration, Topical↗

Does salivary gland scintigraphy predict response to pilocarpine in patients with post-radiotherapy xerostomia?

This study was undertaken to determine whether standard salivary gland scintigraphy may be used for the objective assessment of salivary gland sialogogues, in particular oral pilocarpine, in the treatment of post-radiotherapy xerostomia. Nine patients, with xerostomia following radiotherapy to the head and neck region underwent salivary gland scintigraphy with technetium-99m pertechnetate (40 MBq) both before and following 1 month of oral pilocarpine (5 mg tds). For each scan, the percentage uptake in the first 14 min, the peak uptake, time to peak uptake and the percentage of activity excreted following lemon juice stimulation were calculated. The results were correlated with the subjective response as assessed by questionnaire and visual analogue scale. We found no correlation between subjective response and any of the four scan parameters analysed. We could not identify any parameter that predicted those patients who would respond to pilocarpine. In addition, only one parameter, the percentage of activity excreted following stimulation, correlated with previous dose of radiotherapy to the gland. In conclusion, in this study salivary gland scintigraphy did not appear to correlate with or predict response to oral pilocarpine. However, future studies might consider performing salivary gland scintigraphy prior to radiotherapy as well as at differing time points following the commencement of pilocarpine.

Administration, Oral↗

Effects of pilocarpine- and kainate-induced seizures on thyrotropin-releasing hormone biosynthesis and receptors in the rat brain.

The expression of mRNA coding for prepro-thyrotropin releasing hormone (preproTRH) was estimated in the rat brain in two animal models of limbic seizures, evoked by systemic administration of pilocarpine (400 mg/kg ip) or kainate (12 mg/kg ip). As shown by an in situ hybridization study, after 24h both pilocarpine- and kainate-induced seizures profoundly increased the preproTRH mRNA level in the dentate gyrus. After 72h, the preproTRH mRNA level was back to control values. Kainate-treated rats showed an elevated level of TRH in the hippocampus, septum, frontal and occipital cortex after 24 and 72h, whereas in the striatum and amygdala the TRH level was raised after 72h only. In the hypothalamus, TRH levels was lowered after 3 and 24h, and returned to the control after 72h. Pilocarpine-induced seizures also elevated the TRH level after 72h in the majority of the above structures, except for the hypothalamus and amygdala where no changes were found at any time point. A radioreceptor assay showed that kainate decreased the Bmax value of TRH receptors in the striatum and hippocampus after 3 and 24h, respectively, and had no effect on the Kd values. In contrast, pilocarpine-induced seizures lowered the Bmax of TRH receptors in the striatum, hippocampus and piriform cortex after 72h only, and decreased Kd values in the striatum, amygdala and frontal cortex. These data showed that pilocarpine- and kainate-induced seizures enhanced likewise preproTRH mRNA in the dentate gyrus; on the other hand, they differed with respect to time- and structure-related changes in TRH tissue levels and TRH receptors. These differences may have functional significance in TRH-dependent control mechanism of the seizure activity in these two models of limbic epilepsy.

Amygdala↗

Compliance with topical pilocarpine treatment.

Using an unobtrusive eyedrop medication monitor, we measured compliance with topical pilocarpine treatment in a sample of 184 patients. The eyedrop monitor recorded electronically the date and time of each pilocarpine administration over a four- to six-week period. The subjects administered a mean +/- S.D. of 76.0% +/- 24.3% of the prescribed pilocarpine doses. Eleven patients (6%) took less than one quarter and 28 patients (15.2%) took less than one half of the prescribed administrations. In contrast, when the subjects were interviewed they reported taking a mean +/- S.D. of 97.1% +/- 5.9% of the prescribed pilocarpine doses. As determined by the monitor, 45 patients (24.5%) had at least one day per month with no administrations of pilocarpine; 56 subjects (30.4%) compressed the doses during the daytime hours, leaving an interval between the night dose and the morning dose the next day of 12 hours or more. The rate of compliance was significantly higher (P less than .0001) in the 24-hour period preceding the return appointment than in the entire observation period.

Aged↗

Effects of aminophylline and 2-chloroadenosine on seizures produced by pilocarpine in rats: morphological and electroencephalographic correlates.

The effects of 2-chloroadenosine, aminophylline, bicuculline, beta-carboline-3-carboxylic acid methylester and Ro 15-1788 on seizures produced by pilocarpine were examined in rats. In animals pretreated with aminophylline at doses of 25-100 mg/kg, non-convulsant dose of pilocarpine, 100 mg/kg, resulted in severe motor limbic seizures, which rapidly developed into the status epilepticus. Electroencephalographic monitoring showed progressive evolution of seizure activity with initial high-voltage fast activity followed by high-voltage spiking and electrographic seizures. Morphological analysis of frontal forebrain sections with light microscopy demonstrated widespread damage to the hippocampal formation, thalamus, amygdala, olfactory cortex, substantia nigra and neocortex. Bicuculline, 2 mg/kg, beta-carboline-3-carboxylic acid methylester, 5 mg/kg, and Ro 15-1788, 50 mg/kg, did not augment seizures produced by pilocarpine, 100 mg/kg. 2-Chloroadenosine, 5 and 10 mg/kg, blocked the appearance of behavioral and electrographic seizures produced by pilocarpine, 380 mg/kg, and prevented the occurrence of brain damage. The results indicate that purinergic mechanisms are involved in the buildup of pilocarpine-induced convulsions and seizure-related brain damage in rats.

2-Chloroadenosine↗

Effects of the substance P antagonist [D-Arg1,D-Pro2,D-Trp7,9,Leu11]SP on miosis caused by echothiophate iodide or pilocarpine hydrochloride.

The anticholinesterase agent echothiophate iodide (EI) and the cholinergic agent pilocarpine hydrochloride (pilocarpine), drugs commonly used in glaucoma therapy, cause miosis in rabbits as well as in man. In rabbits the miotic effect decreases after a few days of treatment, a phenomenon possibly due to a drug-induced decrease in the number of muscarinic receptors. However, the muscarinic pupillary contraction caused by stimulation of the retina with light is intact. In this investigation the miosis caused by the doses of EI was found to be very resistant to muscarinic or nerve blockade but inhibited by the substance P (SP) analog [D-Arg1,D-Pro2,D-Trp7,9, Leu11]SP, which seems to be a SP/SPLI blocker in the rabbit pupillary sphincter. Miosis caused by pilocarpine was partly inhibited by muscarinic blockade and partly by the SP blocker. In eyes treated with EI topically twice daily for three weeks, SP or the red pepper extract capsaicin, a releaser of SP-like immunoreactivity (SPLI), had less miotic effect than in control eyes. Capsaicin caused more pronounced miosis in eyes treated with topical pilocarpine for three weeks than in controls. The radioimmunoassay technique did not reveal a significant change in the amount of SPLI in the retinas or iris-ciliary bodies from EI-treated eyes as compared with the controls. It is concluded that, besides cholinergic miosis, EI causes non-muscarinic miosis, probably by release of SP or a related substance and that pilocarpine may have similar effects.

Animals↗

Effects of cooling on the contractile response of the rat tracheal muscle to pilocarpine in vitro.

Experiments were designed to determine the effect of cooling on the contractile response of rat tracheal strip-chain preparation to the partial agonist pilocarpine. The preparation was suspended in an organ bath containing Krebs bicarbonate solution for isometric tension recording. A decrease of the bath temperature from 37 to 30, 20 or 10 degrees C (cooling) did not affect or inhibited the contractile response of the trachea caused by pilocarpine (1-100 microM), while it augmented the carbachol (0.1-1 microM)-induced response. At 37 degrees C, the pilocarpine (3-100 microM)-induced contraction was relatively resistant to removal of extracellular Ca2+ or to the Ca2+ entry blocker, verapamil (1 microM). Similar results were also obtained for the carbachol (0.3-10 microM)-induced response. On the other hand, the affinity of pilocarpine for the tracheal muscarinic receptors, determined from its dissociation constant (KA), was significantly decreased at a lower temperature. It is concluded from these observations that cooling-induced subsensitivity of the rat tracheal muscle to pilocarpine is mainly associated with a decrease in the affinity of the agonist for muscarinic receptors.

Animals↗

Dopamine D1 and D2 receptors mediate opposite functions in seizures induced by lithium-pilocarpine.

The effect of selective dopamine receptor blockade on epileptic activity was tested in rats, using the lithium-pilocarpine seizure model. One day after lithium pretreatment, systemic administration of the dopamine D1 antagonist, SCH 23390, prevented the convulsive activity induced by either 10 or 15 mg/kg of pilocarpine in a dose-dependent manner as revealed by behavioral and electroencephalographic alterations. No anticonvulsant effect was observed when SCH 23390 was injected at the same time as lithium and 24 h prior to pilocarpine. Furthermore, the D2 antagonists, raclopride and haloperidol, potently reduced the threshold for convulsions induced by 10 mg/kg of pilocarpine, following lithium pretreatment. Neither dopamine D1 nor D2 antagonists altered the limbic stereotypies induced by pilocarpine, supporting the view that the dopamine system is primarily involved in the mechanisms of convulsion generation and seizure spreading. These results indicate that dopamine receptor subtypes exert opposite functions on the regulation of convulsive activity.

Animals↗

Effects of drugs on the initiation and maintenance of status epilepticus induced by administration of pilocarpine to lithium-pretreated rats.

The ability of various drugs to prevent the onset of status epilepticus induced by administration of the muscarinic agonist, pilocarpine, to lithium-pretreated rats was determined. Motor limbic seizures and status epilepticus occurred in 100% of rats administered pilocarpine (30 mg/kg, s.c.) 20 h after pretreatment with lithium (3 meq/kg, i.p.). The latency to spike activity and to status epilepticus was 20 +/- 1 min and 24 +/- 1 min, respectively. Atropine, diazepam, phenytoin, carbamazepine, phenobarbital, paraldehyde, and L-phenylisopropyladenosine (L-PIA) prevented all phases of seizure activity induced by lithium/pilocarpine treatment. The initiation of status epilepticus was significantly prolonged by pretreatment with sodium valproate. These findings indicate that the seizures induced by administration of lithium and pilocarpine accurately model generalized tonic-clonic epilepsy. The anticonvulsant activity of L-PIA was prevented by prior treatment with the adenosine antagonist, theophylline. The latency to spike and seizure activity was decreased by theophylline, indicating that endogenous adenosine may have a tonic inhibitory influence on cholinergic neurons. Atropine, diazepam, phenobarbital, phenytoin, sodium valproate, L-PIA, and carbamazepine did not interrupt seizure activity when administered 60 min after pilocarpine (approximately 35 min after initiation of status epilepticus). When rats were administered paraldehyde at this time, status epilepticus was rapidly terminated and all rats survived. Thus, status epilepticus induced by lithium and pilocarpine provides a seizure model that is not responsive to conventional anticonvulsants.

Animals↗

High-performance liquid chromatographic determination of pilocarpine hydrochloride and its degradation products using a beta-cyclodextrin column.

A high-performance liquid chromatographic (HPLC) method for the determination of pilocarpine, isopilocarpine, pilocarpic acid and isopilocarpic acid was developed. A beta-cyclodextrin column achieved the separation in less than 10 min. Baseline resolution of all four compounds permitted the determination of each degradation product in the presence of pilocarpine. The calibration graphs for each compound were linear, and pilocarpine degradation products could be determined without a correction for the ultraviolet detector response using a pilocarpine standard. A comparison of beta-cyclodextrin separation with the USP HPLC method demonstrated similar results for pilocarpine contents in several commercial ophthalmic formulations.

Chromatography, High Pressure Liquid↗