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PubMed1994

Reproducibility of measurements by laser scanning tomography in eyes before and after pilocarpine treatment.

We measured the optic disc topography of ten eyes from ten normal, healthy volunteers before and 1 h after pilocarpine treatment, using the Heidelberg Retina Tomograph. The mean age of the volunteers was 26.4 years, and the mean pupil diameter before and after pilocarpine treatment was 5.5 mm and 3.2 mm, respectively. We collected a series of five to ten consecutive topographic images of the optic disc for each eye, before and after treatment. The mean coefficients of variation of the measurements for the three randomly selected topographic images before pilocarpine treatment were 7.28% (1.25-15.15%) for cup volume and 7.33% (1.44-15.24%) for mean depth inside the cup margin. After treatment, the means were 12.25% (3.24-21.80%) and 12.88% (0.66-21.71%), respectively. Statistically significant differences were observed (P < 0.05) between the pre- and post-treatment coefficients of variation. These results suggest that care should be taken to evaluate the disc changes in eyes treated with pilocarpine.

Adult↗
PubMedDate not supplied

Ultrasound biomicroscopic morphometry of the anterior eye segment before and after one drop of pilocarpine.

PURPOSE: To measure anterior eye-segment morphometric data using ultrasound biomicroscopy. This is a new high-frequency, high-resolution ultrasound method enabling the visualisation of the anterior segment of the living eye with magnification similar to a light microscope. METHODS: Thirteen morphometric parameters of the anterior eye segment were measured before and after the application of one drop of pilocarpine in 10 eyes of 5 persons, using a Zeiss-Humphrey Ultrasound Biomicroscope at a frequency of 50 MHz. In each session, 3 morphometric parameters in the central images (corneal thickness, anterior chamber depth, pupillary diameter) were measured 4 times, and 10 parameters in the radial images (scleral thickness, angle-opening distance, trabecular-iris angle, trabecular-ciliary process distance [TCPD], iris thickness, 1, 2 and 3, iris-ciliary process distance, iris-lens contact distance [ILCD], iris elevation) were measured on the 3, 6 and 9 o'clock meridians three times each. RESULTS: Statistically significant changes were noted in the following parameters: pupillary diameter, iris thickness 1 and 2, and TCPD were decreased, while ILCD was increased after pilocarpine. Wide chamber angles showed a tendency to become narrower and narrow ones to become wider after pilocarpine. CONCLUSION: One drop of pilocarpine caused significant changes in the anterior eye segment morphology. Not only the pupillary diameter decreased but iris thickness and trabecular-ciliary process distance were also decreased simultaneously. At the same time the contact surface between the lens and iris increased significantly. Ultrasound biomicroscopy gives new morphometric image information about the anterior eye segment which is not available using conventional gonioscopy or ophthalmic echography.

Administration, Topical↗
PubMed1979

Altered pilocarpine- or chlorpromazine-induced catalepsy after long-term treatment with cholinergic drugs.

Long-term administration of the cholinergic drug pilocarpine attenuates the catalepsy induced by an acute injection of pilocarpine or the deopamine antagonist chlorpromazine. Similar results (i.e., tolerance to pilocarpine and cross-tolerance to chlorpromazine) were noted in mice chronically treated with the cholinesterase inhibitor physostigmine but not in mice chronically treated with neostigmine, a cholinesterase inhibitor which does not penetrate the central nervous system. Mice maintained on the anticholinergic scopolamine showed the opposite effect; there was an increase in the sensitivity to the catalepsy induced by pilocarpine or chlorpromazine. The results suggest that long-term changes in cholinergic receptors may indirectly alter the behavioral effects of drugs which act via dopamine.

Animals↗
PubMed1981

Effect of muscimol, a central GABA receptor agonist, on the catalepsy, striatal homovanillic acid increase, and analgesia induced by pilocarpine in rats.

Muscimol, a structural analog of GABA, significantly potentiated pilocarpine-induced analgesia in rats, but failed to alter pilocarpine-induced catalepsy. It also failed to affect pilocarpine-elicited increase in homovanillic acid levels in the striatum. These findings suggest that the potentiation of pilocarpine-induced analgesia by muscimol is unrelated to an interaction of the GABAergic system with the striatal cholinergic or dopaminergic systems.

Analgesics↗
PubMed1994

Long-term effects of glaucoma therapy with 4% pilocarpine gel on corneal clarity and endothelial cell density.

Corneal thickness measurements and endothelial cell counts were carried out in 34 patients undergoing treatment for glaucoma with 4% pilocarpine gel between 18 to 78 months after initiation of therapy. The corneal thickness and endothelial cell population were found to be within normal limits in all cases except two, one patient with increased corneal thickness who had recently undergone cataract and glaucoma filtering surgery and another patient with decreased cell count who had an old endothelial scar sustained prior to pilocarpine gel therapy. There was a very close correlation for both of these parameters noticed in patients treated with pilocarpine gel and in age-matched control group of patients with glaucoma. The present study has shown that there are no adverse corneal effects with pilocarpine gel therapy.

Adolescent↗
PubMed1981

A physiologically based pharmacokinetic model for the intraocular distribution of pilocarpine in rabbits.

This report presents a mathematical model which has been developed to describe the intraocular disposition of pilocarpine following topical dosing in rabbits. The model uses experimentally determined parameters such as rates of tissue uptake of drug and equilibrium distribution coefficients. Differential mass balance equations for pilocarpine in the cornea, aqueous humor, iris-ciliary body, and lens were written and solved numerically. Measured tear concentrations, following topical dosing wih pilocarpine, were fit by a monoexponential curve and used as the forcing function of the model. By using a combination of known physiological and experimentally determined parameters, predictions of intraocular tissue levels of pilocarpine were made. These predictions were then compared to experimentally determined concentration-time profiles.

Animals↗
PubMed1994

The mechanism of histamine release induced by pilocarpine from different tissues: studies on rat peritoneal mast cells.

Pilocarpine releases histamine from mast cells of cat submandibular gland and rat liver. In the salivary gland, histamine is released into the saliva and venous outflow. Atropine blocks the salivation, but not histamine release from the submandibular gland into the blood. Histamine release from the gland could be due to a direct action of pilocarpine on tissue mast cells or to an indirect action of mediators (acetylcholine and peptides). These hypotheses were further investigated in our present studies on rat peritoneal mast cells. Our results show: (1) histamine release from rat peritoneal mast cells induced by pilocarpine (ED50 = 1.7 x 10(-2) mol/l) occurs at 1000-fold higher concentrations than by substance P (ED50 = 1.7 x 10(-5) mol/l) and in 6.5-fold higher concentrations than by atropine (ED50 = 2.6 x 10(-3) mol/l), (2) pilocarpine injected directly into the rat peritoneal cavity causes histamine release from peritoneal mast cells in 1.8-fold higher concentrations than from isolated rat peritoneal mast cells. These results would support the hypothesis that histamine release from cat submandibular gland is caused by peptidergic co-transmission during the stimulation of the organ.

Animals↗
PubMed1993

Restoration of brain myo-inositol levels in rats increases latency to lithium-pilocarpine seizures.

Lithium pretreatment in rats potentiates the epileptogenic effects of pilocarpine and other cholinergic agonists. In order to determine if this effect of lithium could be reversed by myo-inositol, rats were pretreated with intracerebroventricular (ICV) injections of myoinositol, artificial CSF or L-chiro-inositol. Lithium chloride, 3 meq/kg was administered intraperitoneally 20-24 h prior to the subcutaneous injection of pilocarpine, 20 or 30 mg/kg. In both experiments, myo-inositol significantly prolonged the latency to the appearance of clonic seizures and lowered the pilocarpine seizure score. myo-Inositol prevented the development of clonic seizures in 50% of the rats receiving pilocarpine, 20 mg/kg. The levels of cortical myo-inositol in rats injected with myo-inositol were approximately double those of the CSF and L-chiro-inositol groups.

Animals↗
PubMed1993

Disordered dopamine neurotransmission in the striatum of rats undergoing pilocarpine-induced generalized seizures, as revealed by microdialysis.

In this study rats were fitted with a concentric dialysis probe in one striatum and extracellular concentrations of dopamine and HVA measured by reverse phase high performance liquid chromatography. Injections of saline or the D1 agonist SKF 38393 (30 mg/kg) did not affect the releases of these compounds. On the other hand, the D2 agonist LY 171555 (0.5 mg/kg) inhibited the release of both dopamine and HVA, whilst amphetamine (1 mg/kg) increased the output of dopamine but not HVA. Treatment with 200 mg/kg pilocarpine caused minimal signs of epileptic activity and did not affect striatal dopamine neurotransmission. Concomitant administration of SKF 38393 (30 mg/kg) to this dose of pilocarpine greatly facilitated the incidence and severity of motor seizures, which were accompanied by an irregular pattern of dopamine release and a significant rise in HVA overflow. Similar results were obtained with rats made to convulse with 400 mg/mg pilocarpine, and to a lesser extent if these animals were first pretreated with a protective dose of LY 171555 (0.5 mg/kg). It is concluded that dopamine neurotransmission in the striatum is disrupted in rats undergoing a pilocarpine-induced motor seizure, and that the extent of this disruption increases as the seizure becomes more severe. An irregular release of dopamine could signify a loss of sensorimotor control by the striatum, which might conceivably contribute to the intractability of the seizure. An increase in the dialysate concentrations of metabolite and not dopamine, is consistent with a heightened glutamate-stimulated release of dopamine from a discrete striatal pool, caused by the seizure spreading through the cortex and activating the cortico-striatal system.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1993

Glutamate-dopamine interactions in the production of pilocarpine motor seizures in the mouse.

An assortment of glutamate antagonists with differing selectivities for NMDA and AMPA-type glutamate receptors, were tested for their effects in the mouse pilocarpine model of complex partial seizures. MK 801 (0.1-0.8 mg/kg) and high doses of HA 966 (50 mg/kg) were proconvulsant, whilst CGP 40116 (1-8 mg/kg) and low doses of HA 966 (0.4-10 mg/kg) inhibited pilocarpine-induced convulsions. CPP (5-20 mg/kg) and NBQX (1-50 mg/kg) were without effect. The dopamine D1 agonist SKF 38393 (10 mg/kg) facilitated the convulsant effects of low-dose pilocarpine (100 mg/kg). MK 801 (0.1-0.2 mg/kg) and HA 966 (50 mg/kg) interacted synergistically with SKF 38393 to promote the proconvulsant effects of D1 stimulation, whilst CPP (10-20 mg/kg) and HA 966 (10 mg/kg) had the opposite effect. CGP 40116 and NBQX were without effect. These results show that the convulsant qualities of MK 801 and SKF 38393, that have been detected in animal models of Parkinson's disease, can be reproduced in the pilocarpine model of epilepsy. Whilst the glutamate antagonists all interact synergistically with SKF 38393 to improve its antiparkinson activity, only MK 801 and high doses of HA 966 similarly potentiate the convulsions associated with D1 stimulation. An appropriate mixture of a glutamate antagonist and a D1 agonist could theoretically be used beneficially in the treatment of Parkinson's disease, without causing epilepsy as a side effect.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1975

Comparative distribution of pilocarpine in ocular tissues of the rabbit during administration by eyedrop or by membrane-controlled delivery systems.

We compared the patterns of pilocarpine distribution in the rabbit eye during two regimens that were comparably efficacious in human clinical use: an administration of 2% pilocarpine nitrate eyedrops, every six hours, for four and eight days, and a continuous delivery of pilocarpine for as long as eight days, at 20 mug/hr, from a membrane-controlled delivery system in the inferior cul-de-sac. Pilocarpine labeled with radioactive carbon (14C) was used as a tracer. With administration of eyedrops, 14C levels in ocular tissues rose and fell within each six-hour interval between eyedrops, but with the delivery system, 14C levels remained constant over the two- to eight-day period. In each tissue, the 14C level within the first hour after the most recently administered eyedrop always exceeded the constant level maintained by the delivery system. Three to six hours after eyedrop administration, the 14C levels in cornea, iris, and sclera were approximately equal to those maintained by the delivery system. However, in lens, vitreous humor, and conjunctiva, the 14C levels were always two to five times higher with eyedrop administration than with the delivery system. Only aqueous humor showed a significantly lower 14C level with eyedrops than with the delivery system, occurring late in the interval between eyedrops. Compared to eyedrop administration, the membrane-controlled delivery system produced drug levels in ocular tissues that were constant rather than variable with time, and appreciably lower in tissues where the drug made no known contribution to the reduction of pressure.

Administration, Topical↗
PubMed1975

Comparative pharmacologic effects of pilocarpine administered to normal subjects by eyedrops or by ocular therapeutic systems.

Normal volunteers used 1, 2, and 4% pilocarpine eyedrops, three times daily, or ocular therapeutic systems placed in the conjunctival cul-de-sac to control intraocular pressure. The systems continuously release 20 and 40 mug/hour of pilocarpine for one week. Although the amount of drug delivered to the eye from the ocular therapeutic system was one fifth that obtained from the eyedrops, the decrease of intraocular pressure was comparable. The ocular therapeutic systems produced small, constant effects on visual acuity, refractive error, and miosis that did not cause visual handicaps or require correction. The effects of eyedrops on these visual factors were large and varied and produced marked visual handicaps that were not correctable with spectacles. Despite its comparable hypotensive effect in normal subjects, continuous delivery of pilocarpine by means of an ocular therapeutic system elicits less severe side effects than pilocarpine eyedrops.

Adult↗
PubMed1986

Corneal changes during pilocarpine gel therapy.

Fifteen of 53 patients (28%) receiving long-term pilocarpine gel therapy were noted to have a subtle, diffuse superficial corneal haze. Results of a masked examination of patients using pilocarpine gel vs pilocarpine eyedrops and the finding of the haze unilaterally in patients using the gel unilaterally suggested that the haze is related to the pilocarpine gel. In most patients the haze persisted for two years after gel treatment was discontinued; the haze disappeared in two patients. Although patients remain asymptomatic with unaltered visual acuities, the long-term effect of this corneal change is unknown.

Conjunctiva↗
PubMed1982

Mechanisms of increase in amylase activity in rat submandibular and sublingual glands after administration of pilocarpine.

The increase in parotid rather than pancreatic-type amylase activity in the submandibular and sublingual glands of rats caused by administration of pilocarpine was abolished or diminished when pilocarpine was injected into rats which had been parotidectomized, sympathectomized by superior cervical ganglionectomy or pretreated with reserpine. These results suggest that the increases in amylase activity in the submandibular and sublingual glands by pilocarpine are not due to increase in enzyme synthesis, but to uptake of enzyme released into the blood in large quantities from the parotid gland and that the release from the parotid gland by pilocarpine is primarily mediated by sympathetic nerves.

Amylases↗
PubMed1986

Seizures produced by pilocarpine: neuropathological sequelae and activity of glutamate decarboxylase in the rat forebrain.

Morphological analysis of brains from rats receiving a convulsant dose of the muscarinic cholinergic agonist, pilocarpine hydrochloride (380 mg/kg), revealed a widespread damage to the forebrain as assessed by light microscopy 5-7 days after seizures. The substantia nigra, olfactory cortex, amygdala, hippocampus, septum, temporal cortex and thalamus underwent prominent morphological injury and cell loss. A concurrent assessment of the activity of L-glutamate decarboxylase (GAD), the gamma-aminobutyrate (GABA) synthesizing enzyme, demonstrated marked deficits in GAD activity in the brain regions undergoing morphological insult. Diazepam, 10 mg/kg, and scopolamine hydrochloride, 10 mg/kg, administered 30 min prior to the injection of pilocarpine, 380 mg/kg, prevented acute behavioral and electrographic, and long-term morphological and biochemical sequelae of seizures. These findings suggest that the muscarinic antagonist, scopolamine, and the anticonvulsant benzodiazepine, diazepam, may aid in preventing extensive brain damage related to pathological muscarinic cholinergic overactivity. The similarity of the topography of the damage and deficits in the GAD activity in brains of rats treated with pilocarpine indicates that GABAergic neurons are lost in the subregions of the brain preferentially sensitive to the convulsant action of pilocarpine.

Animals↗
PubMed1992

Dopaminergic modulation of pilocarpine-induced motor seizures in the rat: the role of hippocampal dopamine D1 receptors.

The present study addressed the role of dopamine D1 receptors in pilocarpine-induced motor seizures in rats. Bilateral pretreatment of the hippocampus with the D1 agonist SKF 38393 (0.1-5 micrograms) did not alter the animals' sensitivity to a threshold (200 mg/kg i.p.) or fully convulsant dose (600 mg/kg i.p.) of pilocarpine, as compared to hippocampal saline-treated controls. Similarly, direct injection of pilocarpine (200 micrograms per side) into both hippocampi elicited low level seizure activity that was not modified by SKF 38393, either coadministered (2 micrograms per side) or injected systemically (30 mg/kg i.p.). On the other hand, intrahippocampal microinjections of the D1 antagonist, SCH 23390 (2 micrograms per side), whilst unable to prevent epileptogenesis to 600 mg/kg pilocarpine, delayed the onset of seizures and reduced their severity. These results suggest that hippocampal dopamine lowers the seizure threshold by activating D1 receptors, an effect which is only disclosed by D1 receptor blockade and is not surmountable by additional D1 stimulation.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1985

The chronically pilocarpine-treated rat in the study of cystic fibrosis: investigations on submandibular gland and pancreas.

The chronically pilocarpine-treated rat has been proposed as an animal model for the disease cystic fibrosis, a generalized exocrinopathy. The effect of chronic pilocarpine treatment on structure, composition, and function of the acinar cells of rat submandibular gland and pancreas was investigated by electron microscopy, X-ray microanalysis, and biochemical analysis. The morphological effects of chronic pilocarpine treatment were most pronounced in the pancreas. The number and size of the zymogen granules was increased, and the granules had a less electron-dense appearance. X-ray microanalysis at the cellular level showed in both the submandibular gland and the pancreas a significant increase in calcium and a decrease in sodium. The increase in cellular calcium concentrations can be explained by an increase in the relative volume of secretory material in the cell (assessed by morphometry) and an increase in the local calcium concentration in the secretory material (assessed by X-ray microanalysis at the subcellular level). Chronic pilocarpine treatment caused a disturbance of glycolysis and energy metabolism in the submandibular gland, but no significant effects in this respect were noted in the pancreas. On the other hand, a nearly twofold increase of the pancreatic amylase activity was noted. The pancreas appeared somewhat hyperreactive towards cholinergic stimulation.

Animals↗
PubMed1993

Analysis of pilocarpine and its trans epimer, isopilocarpine, by capillary electrophoresis.

Capillary zone electrophoresis was used for the separation of pilocarpine from its epimer, isopilocarpine, using coated fused-silica capillaries of 20 cm x 25 microm I.D., 8 kV running voltage, migration buffer of 0.1 M sodium dihydrogenphosphate pH 8, detection at 217 nm and injection by electromigration. Injections of aqueous, acid and basic solutions were compared. Linearity of the signal for pilocarpine hydrochloride up to 200 microg ml(-1) in 0.05 M hydrochloric acid was obtained, using naphazoline nitrate as internal standard. Optimization of migration buffer pH using coated silica capillaries of 50 cm x 50 microm I.D. showed that at pH 6.9 pilocarpine can be separated from ++isopilocarpine. Inclusion of beta-cyclodextrin in the buffer allows full baseline separation of both epimers. The method was applied to the analysis of a commercial ophthalmic pilocarpine solution.

Buffers↗