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At least 199 records · Page 11Linked to original sources
PubMed1997

Primary argon laser trabeculoplasty vs pilocarpine 2% in primary open angle glaucoma: two years follow-up study.

In a prospective study, the efficacy of argon laser trabeculoplasty (ALT) was evaluated and compared with pilocarpine 2% as primary treatment in newly diagnosed primary open angle glaucoma (POAG). Out of 38 patients with POAG included in this study, one eye each of 36 patients underwent ALT, and one eye each of 26 patients received pilocarpine 2% every 8 hours. The mean pre-treatment IOP was 25.48 +/- 4.13 mmHg in ALT group and 24.47 +/- 3.51 mmHg in the pilocarpine group. The mean post treatment IOP at 2 year follow was 18.2 +/- 2.55 mmHg in ALT group and 18.27 +/- 2.22 mmHg in the pilocarpine group. Post treatment IOP was significantly lower than pre-treatment IOP in both ALT and pilocarpine groups. The post treatment fall in IOP showed no significant difference in ALT versus pilocarpine 2% at various follow up intervals (p > 0.05). This study showed equal efficacy of ALT and pilocarpine 2% as initial therapy of POAG.

Administration, Topical↗
PubMed1998

A multicenter study comparing dorzolamide and pilocarpine as adjunctive therapy to timolol: patient preference and impact on daily life.

BACKGROUND: A multicenter, 4-week, two-period crossover study, comparing 2% dorzolamide three times daily to 2% pilocarpine four times daily as adjunctive therapy to 0.5% timolol twice daily, was conducted on 81 patients with elevated intraocular pressure (IOP). The treatments were evaluated for patient preference, tolerability, impact on daily life, IOP control, and visual-field changes. METHODS: The Comparison of Ophthalmic Medications for Tolerability questionnaire was used to assess patient preference, as well as the perception of side effects and activity limitations resulting from the study medications. IOP measurements and visual-field examinations were obtained at baseline and at the end of each crossover period. RESULTS: Of the 77 patients who participated in both periods, 63 (82%) preferred dorzolamide. Patients who expressed a preference preferred dorzolamide over pilocarpine by a ratio of more than 10:1. Patients reported less interference with their daily life because of side effects and activity limitations while receiving dorzolamide than while receiving pilocarpine. Dorzolamide and pilocarpine were comparably effective in lowering IOP (16% to 17%). Also, significantly more patients reported adverse experiences and discontinued therapy as a result of adverse experiences while receiving pilocarpine than while receiving dorzolamide. CONCLUSION: The results of this multicenter study support those of two previous single-center studies; these results show that dorzolamide was greatly preferred over pilocarpine and had better tolerability and less adverse impact on patients' daily lives than pilocarpine.

Adrenergic beta-Antagonists↗
PubMed1999

Pilocarpine tablets for the treatment of dry mouth and dry eye symptoms in patients with Sjögren syndrome: a randomized, placebo-controlled, fixed-dose, multicenter trial. P92-01 Study Group.

BACKGROUND: Patients with Sjögren syndrome (SS) experience slowly progressive infiltration of lacrimal and salivary glands by mononuclear cells. This leads to diminished secretions, with resultant symptoms of xerostomia and xerophthalmia. Although pilocarpine hydrochloride tablets are currently indicated for the treatment of radiation-induced xerostomia, their effects on dry mouth or dry eyes in patients with SS are unclear. OBJECTIVE: To assess the safety and efficacy of pilocarpine (Salagen) tablets as symptomatic treatment for dry mouth and dry eyes caused by SS in a multicenter, doubleblind, placebo-controlled trial. METHODS: After providing written informed consent, 373 patients with primary or secondary SS and clinically significant dry mouth and dry eyes were randomized to receive 2.5-mg pilocarpine, 5-mg pilocarpine, or placebo tablets 4 times daily for 12 weeks. Symptoms were assessed by questionnaires with visual analog scales or categorical checkboxes. Whole-mouth salivary flow rates were measured. RESULTS: A significantly greater proportion of patients in the 5-mg pilocarpine group showed improvement compared with the placebo group (P< or =.01) in global assessments of dry mouth, dry eyes, and other symptoms of dryness (P< or =.05). Salivary flow was significantly increased 2- to 3-fold (P<.001) after administration of the first dose and was maintained throughout the 12-week study. The most common adverse effect was sweating, and no serious drug-related adverse experiences were reported. CONCLUSION: Administration of 5-mg pilocarpine tablets 4 times daily (20 mg/d) was well tolerated and produced significant improvement in symptoms of dry mouth and dry eyes and other xeroses in patients with SS.

Adult↗
PubMed1978

A proposed pilocarpine therapeutic test.

For the pilocarpine therapeutic test that we have devised, one drop (0.1 ml) of 2% pilocarpine hydrochloride (an arbitrarily chosen concentration) is instilled in the glaucomatous eye to be treated, and the intraocular pressure is measured hourly for four hours. If the IOP does not fall below 24 mm Hg, which is our chosen pressure limit, the response is considered to be inadequate therapeutically. Our study showed that if an inadequate therapeutic response is obtained, initiation of treatment with 2% pilocarpine is not indicated, since in patients with such a response, continued treatment with 2% pilocarpine will be ineffective in controlling IOPs on subsequent clinical visits. In only those cases of patients with an adequate response to the pilocarpine therapeutic test (with a fall in pressure below 24 mm Hg) was there the likelihood of having the glaucoma controlled with continued 2% pilocarpine treatment.

Glaucoma↗
PubMed1987

Pilocarpine antagonizes prostaglandin F2 alpha-induced ocular hypotension in monkeys. Evidence for enhancement of Uveoscleral outflow by prostaglandin F2 alpha.

Twice daily topical application of 50 micrograms of prostaglandin F2 alpha tromethamine to cynomolgus monkey eyes produced significant ocular hypotension lasting at least six hours, with the intraocular pressure (IOP) falling between 35% and 50%, ie, to about 8 to 10 mm Hg, following the seventh dose. A single topical application of 1 mg of pilocarpine hydrochloride produced a much smaller IOP reduction and strong, probably maximal accommodation, both of which lasted at least eight hours. When prostaglandin F2 alpha-treated eyes were given pilocarpine before the seventh dose of prostaglandin F2 alpha, accommodation and IOP responded as in eyes receiving pilocarpine only. Atropine sulfate pretreatment of eyes receiving pilocarpine and prostaglandin F2 alpha completely prevented pilocarpine-induced accommodation and inhibition of ocular hypotension induced by prostaglandin F2 alpha. We hypothesize that (1) prostaglandin F2 alpha reduces IOP by increasing uveoscleral drainage of aqueous humor, and (2) pilocarpine pretreatment contracts the ciliary muscle, obliterating the intramuscular spaces and closing off the uveoscleral drainage pathway and thus physiologically blocking the effect.

Accommodation, Ocular↗
PubMed2000

Cell damage and neurogenesis in the dentate granule cell layer of adult rats after pilocarpine- or kainate-induced status epilepticus.

Dentate granule cells are generally considered to be relatively resistant to excitotoxicity and have been associated with robust synaptogenesis after neuronal damage. Synaptic reorganization of dentate granule cell axons, the mossy fibers, has been suggested to be relevant for hyperexcitability in human temporal lobe epilepsy and animal models. A recent hypothesis suggested that mossy-fiber sprouting is dependent on newly formed dentate granule cells. However, we recently demonstrated that cycloheximide (CHX) can block the mossy-fiber sprouting that would otherwise be induced by different epileptogenic agents and does not interfere with epileptogenesis in those models. Here, we investigated cell damage and neurogenesis in the dentate gyrus of pilocarpine- or kainate-treated animals with or without coadministration of CHX. Dentate granule cells were highly vulnerable to pilocarpine induced-status epilepticus (SE), but were hardly damaged by kainate-induced SE. CHX pretreatment markedly reduced the number of injured neurons after pilocarpine-induced SE. Induction of SE dramatically increased the mitotic rate of KA- and KA + CHX-treated animals. Induction of SE in animals injected with pilocarpine alone led to 2-7-fold increases in the mitotic rate of dentate granule cells as compared to 5- and 30-fold increases for pilocarpine + CHX animals. We suggest that such increased mitotic rates might be associated with a protection of a vulnerable precursor cell population that would otherwise degenerate after pilocarpine-induced SE. We further suggest that mossy-fiber sprouting and neurogenesis of granule cells are not necessarily linked to one another.

Animals↗
PubMed1993

Use of pilocarpine during head and neck radiation therapy to reduce xerostomia and salivary dysfunction.

BACKGROUND: Salivary gland hypofunction commonly develops during radiation therapy to the head and neck region. This study evaluated whether the sialogogue pilocarpine given during radiation therapy may reduce the severity of xerostomia and salivary dysfunction. METHODS: Nine patients requiring head, neck, or mantle radiation therapy participated in this double-blind, placebo-controlled trial. The patients took either 5 mg of pilocarpine or placebo four times daily for 3 months, beginning the day before radiation therapy. Subjective complaints and salivary functions were assessed. RESULTS: The pilocarpine-treated group had a lower frequency of oral symptoms during treatment than the placebo-treated group. Although salivary flow decreased in all patients, the pilocarpine-treated group had smaller reductions in flow. No drug effect was observed in glands that were irradiated completely. Thus, pilocarpine appeared to stimulate salivary tissues outside the radiation field. CONCLUSIONS: These results suggest that stimulation with pilocarpine may reduce the severity of salivary dysfunction and associated oral symptoms during radiation therapy.

Adult↗
PubMedDate not supplied

Mast cell degranulation, hepatic glycogen depletion, and hyperglycemia in Compound 48/80 or pilocarpine-treated rats.

Blood glucose, hepatic glycogen, and mean carotid blood pressure were determined in anesthetized Sprague-Dawley rats receiving an i.v. infusion of Compound 48/80, pilocarpine, or Ringer's solution as a control. Histochemical determinations of the integrity and number of hepatic mast cells and hepatic glycogen content also were performed at the light microscopic level, and the results compared to those from rats whose livers were treated topically with each of these compounds. Compound 48/80 produced a marked decrease in mean carotid blood pressure, while pilocarpine produced a slight increase in this parameter. Injection of either Compound 48/80 or pilocarpine provoked an increase in blood glucose and a decrease in hepatic glycogen as well as in the number of hepatic mast cells. Infusion produced no change in glycogen within cardiac or skeletal muscle. The application of Compound 48/80 or pilocarpine to the surface of the liver evoked no alteration in the histochemical appearance of hepatic glycogen. However, the topical application of these substances elicited a significant decrease in the number of Falck-Hillarp-positive hepatic mast cells. Blood glucose was higher in rats that survived 30 min or more after injection of either compound. However, glucose levels were significantly higher in rats that survived 30 min or longer following Compound 48/80 infusion than in those surviving pilocarpine treatment. These results provide evidence that the i.v. injection of Compound 48/80 or pilocarpine causes: (a) hyperglycemia; (b) depletion of hepatic glycogen, and (c) a concomitant decrease in the number of Falck-Hillarp-positive mast cells. The degree of hyperglycemia appeared to correlate with the length of survival of the rats and to be independent of the hyper- or hypotensive effects elicited by either chemical.

Animals↗
PubMed1976

Simultaneous determination of pilocarpine and isopilocarpine in pharmaceutical preparations by liquid chromatography.

A liquid chromatographic assay method is described for the simultaneous determination of pilocarpine and isopilocarpine in pharmaceutical preparations. The method involves separation of the isomers on a high-resolution ion-exchange column, followed by detection of pilocarpine and isopilocarpine by UV absorption in the 217-nm region. The specificity of the method is such that pilocarpine and isopilocarpine can be assayed separately in the presence of one another and in the presence of the excipients commonly found in commercial pilocarpine solutions. Its sensitivity for isopilocarpine is at least 25 ppm (independent of the concentration of pilocarpine). In contrast, USP methods lack both specificity and sensitivity. It is concluded that this method is applicable to the routine analysis of commercial pilocarpine preparations and is an improvement over the official methods.

Chromatography↗
PubMed1976

Effect of topically applied pilocarpine on tear film pH.

Changes in tear film pH were observed during the 1st hr after instillation of pilocarpine in various dosage forms to the rabbit eye. In anesthetized rabbits, with periodic blinking induced electrically, commercial formulations of pilocarpine salts applied as drops or a spray acutely lowered tear film pH by 1.1-1.6 pH units. The pH remained below pretreatment levels for 45-greater than 60 min after instillation. Pilocarpine base, administered continuously at the rates of 20 or 80 mug/hr from ocular therapeutic systems, had little or no effect on tear film pH in this same animal preparation. The reduction in tear film pH produced by pilocarpine eyedrops or spray solution is attributable to the acid pH and buffer capacity of these solutions. Delivery of pilocarpine base without pH change was achieved with ocular therapeutic systems, because the drug (pKa = 7.07) was delivered free, or virtually so, of excipients. These observed differences in tear film pH after application may partially explain the four- to eightfold reduction in total effective pilocarpine dose with ocular therapeutic systems compared to eyedrops or spray, since the cornea is less permeable to ionized than to unionized molecules.

Administration, Topical↗
PubMed1976

Subnanogram assay for pilocarpine in biological fluids.

A method for the determination of pilocarpine was developed in which the imidazole ring of pilocarpine was acylated with heptafluorobutyric anhydride, using triethylamine as a catalyst. After cleanup, the pilocarpine derivative was analyzed using GLC with electron-capture detection. The limit of sensitivity was 25-50 pg of pilocarpine, which had been subjected to the derivatization and cleanup procedures. The method was specific for pilocarpine, with the isopilocarpine derivative eluting prior to the pilocarpine derivative.

Animals↗
PubMed1993

Expression of c-fos protein in the experimental epilepsy induced by pilocarpine.

The expression of the c-fos proto-oncogene, as estimated by immunohistochemistry of the FOS nuclear protein, was studied in both focal and generalized seizures induced in rats by systemic administration of pilocarpine. Focal seizures, as indicated by the occurrence of stereotyped oral movements, chewing and sniffing, were evoked by either a subconvulsant dose of pilocarpine (200 mg/kg) or the association of a convulsant dose of pilocarpine (400 mg/kg) with SCH 23390, a selective D-1 dopamine receptor antagonist. This seizure pattern resulted in FOS accumulation in certain limbic areas, namely, the piriform cortex, amygdala, and olfactory tubercle. On the other hand, in rats developing generalized seizures, accumulation of FOS was also found in hippocampus, cingulate cortex, frontal cortex, striatum, accumbens, as well as in certain thalamic nuclei. Generalized seizures, including motor limbic seizures and status epilepticus, were induced by either a convulsant dose of pilocarpine (400 mg/kg) or a low dose of pilocarpine (15-200 mg/kg) combined with either lithium or the D-1 selective agonist SKF 38393. These findings indicate a close correlation between the sequence of behavioural alterations induced by pilocarpine and the proto-oncogene activation. The results provide the basis for mapping the areas of origin and the pathways of generalization of seizure activity. As shown by the effects of dopamine receptor agonists and antagonists, the process of generalization appears to be controlled by the dopamine system.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1988

Desensitization of the isolated bovine iris sphincter muscles by pilocarpine.

We investigated the effect of pilocarpine on the bovine iris sphincter. This muscle contracted in a dose-dependent manner from 2 x 10(-6) M, with a maximal response at 3 x 10(-3) M. The ED50 values was (1.6 +/- 0.3) x 10(-4) M. Pilocarpine generated a desensitization while desensitization was not significant in the case of other cholinergic agents such as acetylcholine (Ach) and carbachol. Desensitization was profoundly increased in the presence of Ach, neostigmine or eserine: the responses to the second and third trials of pilocarpine were reduced to approximately 8-10% or 30% of the corresponding first responses. Pilocarpine reportedly releases transmitters and alters choline-acetyltransferase activity. These results taken together suggest that either variable Ach synthesis, inhibitory transmitter release or possible toxic action in high concentrations may be involved in the pilocarpine-induced responses of the bovine iris sphincter muscle. The desensitization and partial agonist-antagonist action of pilocarpine could not explain the characteristics of the bovine iris sphincter muscle.

Acetylcholine↗
PubMed1994

Pilocarpine-induced lysosomal enzyme secretion, from bovine trabecular meshwork cells.

It has long been held that pilocarpine-induced ciliary muscle contraction causes a mechanical change in the configuration of the trabecular meshwork, thereby increasing its fluid conductance. Though the results of many studies are consistent with this theory, other findings suggest a direct action of pilocarpine on the meshwork. We used cultured bovine trabecular meshwork (BTM) cells to study the cell biological effects of pilocarpine, chemically a weak base, and demonstrated increased vacuolization of the BTM cells after incubation with pilocarpine, reflecting a trapping of the protonated base inside the lysosomes. We also showed that pilocarpine enhanced the release of lysosomal hydrolases into the medium. We hypothesize that this is clinically relevant and that the pilocarpine-induced release of hydrolases modifies the extracellular matrix of the trabecular meshwork, thereby increasing its fluid conductance.

Animals↗
PubMed1988

The involvement of excitatory amino acid receptors within the prepiriform cortex in pilocarpine-induced limbic seizures in rats.

The prepiriform cortex (PPCx) shows high sensitivity to the epileptogenic action of chemo-convulsants and to the protective action of the NMDA receptor antagonist, 2-amino-7-phosphono-heptanoate (APH) against pilocarpine-induced (motor) limbic seizures in rats. In this study the interaction between agonists acting selectively on the three main excitatory amino acid receptor subtypes in the PPCx and the muscarinic agonist, pilocarpine, within the PPCx have been investigated. Kainate (KA) or quisqualate (QUIS) injected focally into the PPCx (100 pmoles or 5 nmoles per side respectively) induced motor limbic seizures when administered after a subconvulsant dose of pilocarpine (250 mg/kg, i.p.). KA, 100 pmoles injected into the same site in olfactory-bulboectomized rats (bulbectomy results in protection against pilocarpine-induced seizures) also facilitated seizures. However, activation of the NMDA receptor in the PPCx by focal injection of NMDA (250 fmoles-10 nmoles) failed to produce seizures after a subconvulsant dose of pilocarpine. Moreover NMDA in the same range of doses injected into the PPCx protected rats against the seizures induced by a fully convulsant dose of pilocarpine.

Animals↗
PubMed1977

Development and disappearance of subsensitivity to pilocarpine following a single administration of the irreversible anticholinesterase angent, DFP.

The present study examined the possibility that subsensitivity to pilocarpine might occur following a single injection of the irreversible anticholinesterase agent, DFP. In one experiment male Sprague-Dawley rats were trained to drink from experimental drinking chambers for 1/2 h per day. After establishment of baselines, pilocarpine hydrochloride (8 mg/kg) was injected i.p. 5 min before the drinking session. One week later DFP or the arachis oil vehicle (1 mg/kg) was injected intramuscularly and injections of pilocarpine were given at varying times thereafter. The suppression of water intake by this dose of pilocarpine was unaffected by pretreatment with arachis oil, but was markedly attenuated by pretreatment with DFP. This subsensitivity was first observed on the second day but had largely disappeared by the 14th day. DFP was found to have comparable effects on water intake and brain acetylcholinesterase activity when the injections were separated by 20 days. In a second experiment the hypothermic effects of pilocarpine were found to be reduced in rats acutely treated with DFP. These data establish that subsensitivity to pilocarpine occurs following a single administration of DFP. This subsensitivity could reflect a reduced sensitivity of postsynaptic receptors to acetylcholine, which may partially account for the behavioural recovery of the rats while acetylcholinesterase activity is still markedly depressed.

Acetylcholinesterase↗
PubMed1981

Effects of scopolamine, pilocarpine, and oxotremorine on the exploratory behavior of two psychogenetically selected lines of rats in a complex maze.

Rats of two psychogenetically selected lines received pretest IP injections of scopolamine hydrobromide (0.25, 1.0, or 4.0 mg/kg), pilocarpine hydrochloride (3.0, 6.0, or 12.0 mg/kg) or oxotremorine sesquifumarate (0.2, 0.4 or 0.8 mg/kg) and were subsequently placed in a complex enclosed maze of the Dashiell type that included a small, central, illuminated arena. Animals receiving pilocarpine or oxotremorine injections were pretreated with methscopolamine to counter the peripheral actions of these muscarinic cholinergic agonists. Following vehicle injections, Roman High-Avoidance rats (RHA/Verh) were significantly more active, explored more maze sectors, and required less time to activate the initial 24 different photocell units uniformly distributed throughout the maze than Roman Low-Avoidance rats (RLA/Verh). Scopolamine, pilocarpine, and oxotremorine depressed locomotor activity, reduced the explored area, and increased the time required to activate the initial 24 different photocell units within this complex maze for both RHA/Verh and RLA/Verh rats. Although the doses of scopolamine injected were approximately equally effective in both rat lines (except for total maze activity), the RHA/Verh rats exhibited significant alterations in several measures of maze patrolling after treatment with the lowest dose of pilocarpine, whereas the RLA/Verh rats did not. In contrast, most of the RLA/Verh rats exhibited very pronounced tremors following treatment with the highest dose of oxotremorine, but none of the RHA/Verh rats did. These results demonstrate that manipulation of the central cholinergic system with scopolamine, pilocarpine, or oxotremorine, despite their different pharmacological mechanisms, impair maze patrolling. Furthermore, the results suggest that the two psychogenetically bred lines of rats investigated are differentially sensitive to central cholinergic manipulation with the muscarinic receptor agonists pilocarpine and oxotremorine.

Animals↗
PubMed1989

Comparison of different models for the testing of pilocarpine eyedrops using conventional eyedrops and a novel depot formulation (nanoparticles).

An objective in the development of ophthalmic formulations is the use of in vitro or animal models that closely resemble the clinical situation. For this reason, experiments with conventional pilocarpine nitrate eyedrops and a depot formulation of pilocarpine nitrate sorbed to poly (butylcyanoacrylate) nanoparticles were carried out. In vitro, the diffusion of pilocarpine through bovine cornea was measured using Edelhauser cells. In vivo, the rabbit aqueous humor concentration of pilocarpine and miosis were determined after application of the above formulations. In addition, intraocular pressure was measured. Since pilocarpine has little influence on intraocular pressure in healthy rabbits, the pressure had to be increased artificially. Three models were employed that are described in the literature, namely, the betamethasone model, the alpha-chymotrypsin model, and the water-loading model. Pilocarpine could be loaded onto nanoparticles by 15% but was rapidly released from the nanoparticles based on the bovine corneal experiment. Nanoparticles only enhanced the aqueous humor concentration at 30 min; this increase, however, led to a considerably extended period of miosis as well as a reduction in intraocular pressure. The duration of the action and the intensity of the response were different among the three models tested. According to the present results, the betamethasone model seems to represent the best correlation to the clinical situation.

Animals↗