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PubMed1975

The long-acting Ocusert-pilocarpine system in the management of glaucoma.

The Ocusert-pilocarpine devides with seven days' therapeutic duration were compared with pilocarpine eye drops for efficacy and ocular tolerance in the management of glaucoma in 16 patients. Magnitude of pressure reduction with release rates of 20 mcg. and 40 mcg. of pilocarpine per hour were as effective in the treatment of glaucoma as 2 per cent and 4 per cent pilocarpine eye drops, respectively. Ocular tolerance and retention in the human eyes were good. There were no appreciable side effects other than the occasional sudden leakage phenomenon encountered. Further refinement of the Ocusert-pilocarpine device to reduce the incidence of leakage would not only ensure precision in the rate of drug release, but would also expand its clinical application.

Acetazolamide↗
PubMed2001

Acquisition and retrieval of conditioned taste aversion is impaired by brain damage caused by two hours of pilocarpine-induced status epilepticus.

The effect of Cavalheiro's pilocarpine model of epileptogenesis upon conditioned taste aversion (CTA), an important example of nondeclarative memory, was studied in adult Long Evans rats. Deterioration of CTA was studied during the silent period between pilocarpine-induced status epilepticus (SE) and delayed spontaneous recurrent seizures. SE was elicited by i.p. injection of pilocarpine (320 mg/kg ) and interrupted after 2 hours by clonazepame (1 mg/kg i.p.). Peripheral cholinergic symptoms were suppressed by methylscopolamine (1 mg/kg i.p.), administered together with pilocarpine. CTA was formed against the salty taste of isotonic LiCl. In the experiment of CTA acquisition, the CTA was formed and tested during the silent period after SE. In the experiment of CTA retrieval, the CTA was acquired before SE and the retrieval itself was tested during the silent period. Retrieval of CTA acquired before SE was impaired more than the retrieval of CTA formed during the silent period. Our findings indicate that epileptic seizures can disrupt even non-declarative memory but that CTA formed by the damaged brain can use its better preserved parts for memory trace formation. Ketamine (50 mg/kg i.p.) applied 2 min after the onset of pilocarpine-induced status epilepticus protected memory deterioration.

Animals↗
PubMed2003

[Action of miosis of 1% pilocarpine liposome in rabbits].

OBJECTIVE: To compare the action of miosis of 1% pilocarpine liposome with 1% pilocarpine solution in rabbits. METHODS: 18 white rabbits were randomly divided into 3 groups. Test group received 1% pilocarpine liposome, positive control group received 1% pilocarpine solution, negative control group received liposome. Each eye drop instilled into left eye of rabbits and sterile saline solution instilled into right eye as control. The pupil diameter was measured at time intervals of beginning, 0.25, 0.5, 1, 2, 3, 4, 5, 7 hours. RESULTS: The mean pupil diameter change of 3 groups in both eyes was not significant (P > 0.05) at beginning. The strongest action of miosis took place 0.25 h in positive control group and 0.5 h in test group after instillation. The dilation of pupil in both groups took place 1 h and 3 h, and the restoration of pupil in both groups took place at 5 h and 7 h. The mean pupil diameter of negative control group was not significant in seven hours. CONCLUSIONS: The results suggest that 1% pilocarpine liposome improves the bioavailability and prolong the duration of its action.

Animals↗
PubMed1992

Inhibition of outflow facility and accommodative and miotic responses to pilocarpine in rhesus monkeys by muscarinic receptor subtype antagonists.

The muscarinic receptor subtype antagonists 4-diphenylacetoxy-N-methylpiperidine methobromide (4-DAMP), 11-[(2-[diethylamino)methyl]-1- piperidinyl)acetyl]-5,11-dihydro-6H-pyrido[2,3- b][1,4]benzodiazepine-6-one (AF-DX 116) and pirenzepine were used to inhibit the outflow facility and accommodative and miotic responses to near-maximal intracameral doses of pilocarpine in the living rhesus monkey eye. The pharmacologic M3 antagonist 4-DAMP was the most potent inhibitor of all three responses, with IC50 values of 41.7 nM for outflow facility (vs. 40.9 microM pilocarpine), 19.8 nM for accommodation (vs. 40.9 or 81.8 microM pilocarpine) and 3.2 nM for miosis (vs. 4.1 microM pilocarpine). The M1 antagonist pirenzepine was at least 30-fold less potent, with IC50 values of 2.2 microM for outflow facility, 1.4 microM for accommodation and 0.1 microM for miosis. The M2 antagonist AF-DX 116 was the least potent by far, with IC50 values of 15.5 microM for outflow facility, 14.2 microM for accommodation and 1.5 microM for miosis. The results suggest that these three functional responses to pilocarpine are all mediated through an M3 receptor subtype.

Accommodation, Ocular↗
PubMed2004

[Mossy fiber sprouting and synapse formation in the dentate gyrus of temporal lobe epilepsy rats induced by pilocarpine].

OBJECTIVE: To investigate the relationship between mossy fiber axon sprouting (MFS), synaptic reorganization in the dentate gyrus, and the mechanism of chronic temporal lobe epilepsy induced by pilocarpine. METHODS: The mossy fiber sprouting and synapse formation were observed in rats after the acute status epileticus and chronic spontaneous temporal lobe epilepsy induced by pilocarpine using in situ hybridization of GAP-43 mRNA (a marker of MFS), an immunohistochemical staining of synaptophysin (P38, a marker of synaptogenes), and Neo-Timm staining. RESULTS: In hippocampus granule cell, there was a significant increase in the GAP-43mRNA levels measured 6 - 12 h after the end of status epileticus induced by pilocarpine. In contrast, synaptophysin immunoreactivity progressively increased in the molecular layer of the dentate gyrus from 7 d, which was in line with the Neo-Timm stain results that revealed a time-dependent growth of aberrant MFS into the dentate inner molecular layer. The GAP-43 mRNA levels in pilocarpine treated animals were significantly decreased after status epileticus. CONCLUSION: These results provide evidence for newly formed excitatory recurrent circuits, which might constitute a structural basis for chronic enhanced excitation and epileptogenesis in the hippocampus of pilocarpine-treated rats.

Animals↗
PubMedDate not supplied

A randomized study to assess the effectiveness of orally administered pilocarpine during and after radiotherapy of head and neck cancer.

BACKGROUND: This prospective randomized study was undertaken to assess the effectiveness of oral pilocarpine chloratum (Salagen) during and after radiotherapy. PATIENTS AND METHODS: Between October 1999 and December 2003, 66 patients received 60 Gy of irradiation to their head and neck cancer. Half of the patients received 5 mg oral pilocarpine 3 times a day from the beginning of radiotherapy over a period of 12 weeks. The control group received similar doses of pilocarpine only in the second 6 weeks following irradiation. Patient saliva secretion was recorded, and a visual analog scale measuring overall and daily xerostomia, difficulty in sleeping, speaking, eating and wearing dentures was employed. RESULTS: Pilocarpine, given concomitantly with radiotherapy, statistically improved the salivary flow and induced better patient comfort by the end of radiotherapy. Patient comfort and symptoms related to xerostomia greatly decreased compared to patients receiving pilocarpine after irradiation in the second 6-week period of therapy. The patients' quality of life, saliva production and symptoms related to xerostomia showed significant progress by the end of the 12 weeks. CONCLUSION: The results suggest that stimulated salivary glands suffer less decrease in saliva production during radiotherapy. The stimulated saliva flow reduced the side-effects of irradiation.

Administration, Oral↗
PubMed2006

Effect of pilocarpine during radiation therapy: results of RTOG 97-09, a phase III randomized study in head and neck cancer patients.

Radiation therapy is an important curative modality in the treatment of patients with head and neck cancer. However, radiation-induced changes in the oral cavity, such as xerostomia and mucositis, are among the most debilitating treatment sequelae experienced by patients undergoing radiation therapy, and attempts at ameliorating these side effects have been poor at best. Pilocarpine has been approved for post-radiation xerostomia, and the effect of its use during radiation therapy on salivary flow, xerostomia, mucositis, and quality of life (QOL) was assessed in a phase III study conducted by the Radiation Therapy Oncology Group (RTOG 97-09). In total, 245 evaluable patients were randomized to pilocarpine or placebo. Selected patients were required to have > or = 50% of the volume of the major salivary glands receive > or = 50Gy; to agree to provide stimulated and unstimulated samples of saliva (measured in g) before treatment, at the end of treatment, and 3 and 6 months after completion of radiation therapy; and to complete the University of Washington Head and Neck Symptom Scale. Following the completion of radiation therapy, the average unstimulated salivary flow was statistically greater in the pilocarpine group, whereas no difference was noted following parotid stimulation. There was no effect on the amelioration of mucositis. The results of the QOL scales did not reveal any significant difference between the pilocarpine and placebo groups with regard to xerostomia and mucositis. The significant difference in unstimulated salivary flow supports the concomitant use of oral pilocarpine to decrease radiation-associated xerostomia. However, the absent correlation between improved salivary flow and QOL scores is of some concern (though not a new finding) and may be related to the existence of comorbidities and the lack of effect on mucositis.

Female↗
PubMed1989

D-1 dopamine agonist administration reduces the threshold for convulsions produced by pilocarpine.

Focal, limbic seizures were produced by systemically administered pilocarpine (200 mg/kg, i.p.); as previously described this dose produces limbic stereotypies but neither convulsions nor seizure-related brain damage. The pretreatment, 5 minutes prior pilocarpine, with the D-1 agonist SKF 38393 (-ED50 = 1 mg/kg; i.p.) induced convulsions similar to those produced by a higher, convulsant dose of pilocarpine. On the other hand, the pretreatment with the D-2 agonist LY 171555 failed to induce convulsions. The D-1 receptor antagonist SCH 23390 prevented the convulsions induced by SKF 38393 plus pilocarpine (200 mg/kg). This study indicates that D-1, but not D-2, receptor stimulation converts subconvulsant doses of pilocarpine into convulsant ones.

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

gamma-Glutamyltranspeptidase activity of rat submandibular gland after pilocarpine stimulation.

gamma-glutamyltranspeptidase (gamma-GT) activity of the rat submandibular gland was studied after pilocarpine stimulation. After a single i.p. dose pilocarpine or physiologic saline the animals were sacrificed in intervals within 24 h p.i. The glands were homogenized and enzyme activity was calculated by measuring the release of p-nitroanilid per minute where rates of product formation were linear towards time and DNA-concentration. The specific activity of gamma-GT rapidly declined after pilocarpine injection until 3-6 h p.i. when a plateau stage was seen. During 6-24 h p.i. the gamma-GT activity slowly increased but never reached the original level. The controls receiving physiologic saline showed only a slight reduction of gamma-GT activity. However, in the control animals the initial level of enzyme activity was restored after 24 h. A depletion of cellular glutathione by pilocarpine is unlikely to explain the decrease of gamma-GT activity observed. The results indicate that pilocarpine affects the enzyme itself.

Animals↗
PubMed1979

[The pressure reducing effects of pilocarpin in combination with Dipivalyl-epinephrine in glaucoma simplex (author's transl)].

We compared in two controlled studies the effect of pilocarpine 1% with the effect of pilocarpine 1% combined with 0,05% or 0,1% dipivalyl-epinephrine in patients with open-angle glaucoma. The pressure reducing effect of pilocarpine 1% was significantly increased and prolonged by the combination with dipivalyl-epinephrine. 0,1% dipivalyl-epinephrine + pilocarpine 1% did not have a more significant pressure reducing effect in our patients than 0,05% dipivalyl-epinephrine + pilocarpine 1%, but the reduction of pressure persisted longer. It is a considerable advantage in glaucoma therapy to diminish or to avoid systemic and local side effects of epinephrine due to very low concentrations of dipivalyl-epinephrine.

Double-Blind Method↗
PubMed1979

[Effect of spasmolytics on cathartic activity of pilocarpine, 5-HT and prostaglandlin E2 in mice (author's transl)].

Effects of autonomic, anti-histaminic, anti-5HT drugs, papaverine and morphine on cathartic activity of spasmogens such as pilocarpine, 5-HT and prostaglandin E2 (PGE2) were tested by giving these drugs to mice subcutaneously. Mice used were male dd strain weighing 20 +/- 2 g and the catharatic effect was evaluated by the all or none method. The cathartic effect by pilocarpine was inhibited markedly by anti-cholinergic drugs such as atropine and diphenhydramine, but not by hexamethonium and methysergide. Therefore, the action of pilocarpine was found to be direct on the acetylcholine receptors. The catharatic effect by 5-HT was inhibited significantly by hexamethonium and methysergide. Atropine inhibited the cathartic effect of 5-HT, but the inhibitory activity was lower by about one hundredth than that on pilocarpine-induced diarrhea. It is suggested that 5-HT has dual sites of actions and there are less cholinergic and specific serotonergic actions. The cathartic effect by PGE2 was inhibited by anticholinergic, anti-5HT and ganglion blocking agents. PGE2 appears to possess the same mode of action as both pilocarpine and 5-HT. Papaverine inhibited little the cathartic effect of all three spasmogens, while morphine had a potent and nonspecific inhibitory effect on the cathartic action of all three spasmogens.

Animals↗
PubMedDate not supplied

Separation and analysis of pilocarpine, isopilocarpine, and pilocarpic acid by reverse phase liquid chromatography: collaborative study.

A method for separating and determining pilocarpine and 2 degradation products was developed and subjected to collaborative study. Pilocarpine, isopilocarpine, and pilocarpic acid were isolated on a reverse phase liquid chromatographic phenyl bonded column and detected by UV spectrophotometry at 220 nm. Nine collaborators received commercial samples labeled to contain 2, 1, and 0.5% pilocarpine and a 2% practice sample. The collaborative results for pilocarpine were excellent; coefficients of variation ranged from 3.20 to 4.10%. The method was adopted official first action for determination of the active component, pilocarpine, in the presence of isopilocarpine and pilocarpic acid. Although quantitative results for the degradation products were not as good, the method is suitable as a limits test for these substances.

Chromatography, Liquid↗
PubMed1995

Pilocarpine-associated allograft rejection in postkeratoplasty patients.

Corneal allograft rejection is a major cause of graft failure. Identifying possible risk factors for rejection may improve chances for successful outcome. We report three cases of graft rejection associated with the use of post-operative pilocarpine at different concentrations. Pilocarpine was used to treat persistent epithelial defects or raised intraocular pressure. The patients were managed until their rejection episodes resolved. In each case, graft rejection ensued in a quiet eye after initiating treatment with pilocarpine, without other change in medications. Each graft rejection episode resolved with discontinuation of pilocarpine and administration of prednisolone acetate. We propose that if pilocarpine does indeed diminish corneal allograft immune privilege and enhance graft rejection, the mechanisms may include induced intraocular inflammation and altering of anterior chamber associated immune deviation. This is the first report implicating a topical ophthalmic medication with possible corneal allograft rejection.

Aged↗
PubMedDate not supplied

Effect of nifedipine on lithium-pilocarpine-induced seizures in the rats.

Recent studies have shown that lithium pretreatment of rats potentiates the convulsant effect of pilocarpine. A large body of evidence support the hypothesis that calcium channel antagonists possess antiepileptic properties in various models of epilepsy. This study was designed to investigate effect of calcium channel antagonist, nifedipine on lithium-pilocarpine-induced convulsions in rats. Pretreatment of rats with nifedipine (5 or 10 mg/kg) as well as with a calcium channel agonist BAY k-8644 (2 mg/kg) increased convulsant effect induced by lithium and pilocarpine. The facilitating effect of nifedipine on lithium-pilocarpine-induced convulsions was prevented by pretreatment with a cholinergic antagonist atropine. It can be concluded that nifedipine facilitates convulsions in lithium-pilocarpine model of epilepsy and that cholinergic system may be involved in this effect.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1996

The effect of a medication alarm device on patient compliance with topical pilocarpine.

BACKGROUND: This study was performed to investigate the use of an electronic medication alarm device (Prescript TimeCap) to enhance compliance in glaucoma patients taking pilocarpine. METHODS: Thirteen subjects were selected who had been diagnosed with open-angle glaucoma and were receiving 1 drop of pilocarpine solution 4 times a day in both eyes. For each subject, the study was divided into 2 30-day phases, one with the medication alarm device and the other without. Thus, each subject served as his or her own control. Compliance was measured based on the amount of pilocarpine used and by patient questionnaire. In addition, the subjects completed a post-study questionnaire regarding the ease of use of the TimeCap and whether it helped them remember to take their medication. RESULTS: When subjects used the TimeCap, they administered an average of 2.867 g (P < 0.0001) more pilocarpine over the 30 days than during the period without it. Subjects also estimated a significant difference in compliance level, 95.8 percent with the alarm device versus 83.1 percent without it (p < 0.01). All subjects reported no difficulty using the TimeCap, and all reported that it helped them remember to take their medication. CONCLUSIONS: These results are highly suggestive that the TimeCap is an effective compliance aid for glaucoma patients on pilocarpine.

Administration, Topical↗
PubMed1997

Changes in hippocampal circuitry after pilocarpine-induced seizures as revealed by opioid receptor distribution and activation.

The pilocarpine model of temporal lobe epilepsy was used to study the time-dependent changes in dentate gyrus circuitry after seizures. Seizures caused a decrease in mu- and delta-opioid receptor immunoreactive (MOR-IR and DOR-IR, respectively) neurons in the hilus and MOR-IR neurons in the granule cell layer. Additionally, diffuse DOR-IR, MOR-IR, and GABA immunoreactivities (GABA-IR) were increased in the inner molecular layer. Using the in vitro hippocampal slice preparation to study the physiological consequences of the anatomical changes, we found that the disinhibitory effects of the mu-opioid receptor agonist [D-Ala2, MePhe4,Gly-(ol)5]-enkephalin (DAMGO) and the GABAA receptor antagonist bicuculline were greatly depressed 5-13 d after pilocarpine injection but returned to control levels within 6 weeks. The amplitudes of monosynaptic evoked IPSCs and the effects of DAMGO on this parameter were also slightly decreased 5-13 d after pilocarpine injection but significantly increased at 6 weeks. DAMGO significantly decreased the mean amplitude of spontaneous IPSCs (sIPSCs) at 6 weeks after pilocarpine injection but not in controls. The delta-opioid receptor agonist [D-Pen2,5]-enkephalin (DPDPE) principally inhibited excitatory transmission in saline-treated animals without affecting either sIPSCs or evoked IPSCs. The DPDPE-induced inhibition of excitatory transmission became more pronounced at 6 weeks after pilocarpine injection. These results illustrate the anatomical reorganization and functional changes in dentate gyrus circuitry evident in an animal model of temporal lobe epilepsy and provide evidence of compensatory changes after trauma to the hippocampal formation.

Animals↗
PubMed1998

Administered and endogenously released kappa opioids decrease pilocarpine-induced seizures and seizure-induced histopathology.

The effects of kappa opioids on seizures and seizure-induced histopathology were investigated with the pilocarpine model of temporal lobe epilepsy. Rats treated with the kappa opioid receptor agonist U50488h before pilocarpine showed: 1) increased seizure latency; 2) decreased seizure duration; 3) decreased mossy fiber sprouting; and 4) increased hilar neuron survival when compared with rats pretreated with saline. Behavioral effects of U50488h were blocked by the kappa opioid receptor antagonist norbinaltorphimine (nBNI), whereas the changes caused by U50488h in the histological response to pilocarpine were not blocked by nBNI. Rats treated with nBNI before pilocarpine exhibited: 1) increased incidence of seizures; 2) increased mossy fiber sprouting; and 3) increased hilar neuron loss when compared with rats treated with pilocarpine alone. These changes suggest a protective role of endogenously released kappa opioids in this seizure model. The location of functional kappa opioid receptors in the rat dentate gyrus was documented electrophysiologically to enable correlation with kappa opioid effects on histopathology. The kappa selective agonist, U69593, reversibly decreased the amplitude of excitatory postsynaptic potentials in the middle molecular layer of the dentate gyrus from the ventral but not the more dorsal portion of the hippocampal formation. Thus, kappa opioids decreased the severity and incidence of behavioral seizures and secondarily decreased seizure-induced histopathology via the decreased incidence of seizures.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1998

Normal variation in, and effect of 2% pilocarpine on, intraocular pressure and pupil size in female horses.

OBJECTIVE: To determine normal variation in, and effect of 2% pilocarpine hydrochloride on, intraocular pressure (IOP) and pupil size in female horses during a specified period. ANIMALS: 10 female horses with normotensive eyes. PROCEDURE: IOP and horizontal and vertical pupil size were measured on a single day between 8 AM and 8 PM at hours 0, 0.5, 1, 2, 4, 6, 8, 10, and 12. Measurements were repeated after single- dose application of 2% pilocarpine to both eyes. IOP and pupil size were measured at 8 AM and noon in a 5-day experiment of twice-daily application of 2% pilocarpine. RESULTS: Variation in IOP and pupil size was not significant between 8 AM and 8 PM. Change in IOP or pupil size after a single dose of 2% pilocarpine also was not significant. In the multiple-dose experiment, the IOP at noon on the fifth day was significantly higher than the IOP in the morning on the first and second days. The IOP in the morning on the fifth day was significantly higher than the IOP in the morning and at noon on the first and second days. The IOP at noon on the fourth day was significantly higher than the morning IOP on the first and second days and at noon on the first day. The decrease in vertical pupil size was significant. CONCLUSIONS: Between 8 AM and 8 PM, variation in IOP and pupil size in normotensive eyes of horses is not significant. Two percent pilocarpine does not significantly change IOP between 8 AM and 8 PM in clinically normal horses after a single dose or multiple twice-daily applications. After multiple twice-daily applications, a trend toward an increase in IOP was seen, and the decrease in vertical pupil size was significant.

Animals↗