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PubMed1985

Concentration-dependent precorneal loss of pilocarpine in rabbit eyes.

Precorneal loss of pilocarpine was studied in pigmented and albino rabbits. We instilled 25 microliter of isotonic pilocarpine solution, pH 6.4, into rabbit eyes and monitored drug concentration in the precorneal tear film. Increased concentration (0.2% - 2.0%) of pilocarpine accelerated precorneal drug loss from the tear film from 0.686 min-1 to 1.064 min-1. This increase was mainly due to induced lacrimation. Polyvinyl alcohol (1.4%) retarded precorneal loss of pilocarpine. The rate of loss was the same in pigmented and albino rabbits. The effects of the changed precorneal loss of pilocarpine on corneal drug absorption are discussed.

Animals↗
PubMed2006

Involvement of CYP2A6 in the formation of a novel metabolite, 3-hydroxypilocarpine, from pilocarpine in human liver microsomes.

Pilocarpine is a cholinergic agonist that is metabolized to pilocarpic acid by serum esterase. In this study, we discovered a novel metabolite in human urine after the oral administration of pilocarpine hydrochloride, and we investigated the metabolic enzyme responsible for the metabolite formation. The structure of the metabolite was identified as 3-hydroxypilocarpine by liquid chromatography-tandem mass spectrometry and NMR analyses and by comparing to the authentic metabolite. To clarify the human cytochrome P450 (P450) responsible for the metabolite formation, in vitro experiments using P450 isoform-selective inhibitors, cDNA-expressed human P450s (Supersomes; CYP1A2, -2A6, -2B6, -2C9, -2C19, -2D6, -2E1, and -3A4), and liver microsomes from different donors were conducted. The formation of 3-hydroxypilocarpine in human liver microsomes was strongly inhibited (>90%) by 200 microM coumarin. Other selective inhibitors of CYP1A2 (furafylline and alpha-naphthoflavone), CYP2C9 (sulfaphenazole), CYP2C19 [(S)-mephenytoin], CYP2E1 (4-methylpyrazole), CYP2D6 (quinidine), and CYP3A4 (troleandomycin) had a weak inhibitory effect (<20%) on the formation. The highest formation activity was expressed by recombinant CYP2A6. The K(m) value for recombinant CYP2A6 was 3.1 microM, and this value is comparable with that of human liver microsomes (1.5 microM). The pilocarpine 3-hydroxylation activity was correlated with coumarin 7-hydroxylation activity in 16 human liver microsomes (r = 0.98). These data indicated that CYP2A6 is the main enzyme responsible for the 3-hydroxylation of pilocarpine. In conclusion, we identified a novel metabolite of pilocarpine, 3-hydroxypilocarpine, and we clarified the involvement of CYP2A6 in the formation of this molecule in human liver microsomes.

Aryl Hydrocarbon Hydroxylases↗
PubMed1976

A comparison of the pupilloconstrictor effect of pilocarpine solution administered to the conjunctival sac as a single drop or as a continuous infusion in normal subjects.

Pilocarpine was administered into the conjunctival sac of normal volunteers by single-drop administration or by continuous infusion of a solution to the inner canthus by means of a fine Silastic tube. Using pupilloconstriction as a measure of response it was shown that infusion with a 0-01 per cent solution of pilocarpine was as effective as a single drop of 0-5 per cent pilocarpine. The response to the single drop was faster at onset. It was demonstrated that at pH 7-2 pilocarpine was more effective than at acid pH. The infusion method is simple to use, comfortable for long periods, has potential for reducing the need for frequent drop administration and for reducing the total amount of drug administered, and could be used for drugs other than pilocarpine.

Administration, Topical↗
PubMed1978

Topical atenolol versus pilocarpine: a double-blind study of the effect on ocular tension.

Topical atenolol (a beta1-adrenoceptive antagonist), pilocarpine, and placebo were tested in a randomised double-blind crossover trial of 8 patients with ocular hypertenion. Atenolol (2% 3 times a day) caused a fall in intraocular pressure (IOP) comparable to that achieved by topical application of pilocarpine (2% 3 times a day). The decrease in IOP by each compound was demonstrable on the second day of application and was significantly (P is less than 0.05) reduced on the seventh and 14th days of treatment. The combination of 2% pilocarpine and 2% atenolol administered 15 minutes apart (3 times a day) lowered the IOP significantly from the second day of treatment, and this reduction persisted throughout the trial period of 14 days. This combined of treatment, treatment lowered the IOP more than either substance alone. However, this further decrease was statistically significant only on the 14th day of treatment (atenolol versus atenolol + pilocarpine, P is less than 0.05). No change of the episcleral venous pressure was observed after 14 days' treatment with either atenolol or pilocarpine alone, or combined.

Adult↗
PubMed1979

Piloplex, a new long-acting pilocarpine polymer salt. A: Long-term study.

Thirty eyes of 15 patients with open-angle glaucoma were followed up for a period of up to 1 year while being treated with Piloplex eye drops containg a new long-acting pilocarpine polymer salt. Average morning intraocular pressure (IOP) values during treatment with pilocarpine hydrochloride administered 4 times daily was 20.5 mmHg. Average morning IOP values during Piloplex medication administered only twice daily were 19.8 to 18.2 mmHg (range of averages on 14 sessions). These findings indicate the lower average pressure during Piloplex medication and show its prolonged hypotensive effect. Both medications contained an equivalent total daily amount of pilocarpine. Throughout the 1-year study period no adverse side effects were reported, and only 1 patient complained of local sensitivity reaction. Visual disturbances characteristic of pilocarpine eye drops were reduced from 3 times a day on pilocarpine hydrochloride 4 times daily to once a day on Piloplex twice daily.

Aged↗
PubMed1992

Systemic pilocarpine increases deposition of and decreases responsiveness to inhaled carbachol in sheep.

The purpose of this study was to determine whether excessive airway secretions could serve as a barrier function against inhaled particulate matter. To increase airway secretions, six conscious sheep were treated with pilocarpine (0.8 mg/kg i.v.). Pilocarpine increased pulmonary resistance (RL) and total aerosol deposition within five breaths (AD5) as determined by the rebreathing of an inert monodisperse aerosol. When RL had returned to baseline, AD5 remained elevated [21 +/- 2% (SE), P < 0.05] and tracheal secretions were increased (237 +/- 77%, P < 0.05) above the values before pilocarpine administration. A carbachol aerosol dose-response curve was carried out at this time and compared with a control carbachol dose-response curve by calculating the dose of carbachol required to increase RL by 400% (PD400). Mean PD400 was increased postpilocarpine by 53 +/- 18 (P < 0.05) and 85 +/- 25% (P < 0.05) when normalized for increased aerosol deposition. Thus, pilocarpine decreased airway responsiveness to inhaled carbachol despite increasing aerosol deposition. The pilocarpine-induced airway hyporesponsiveness to inhaled carbachol is consistent with the hypothesis that excessive secretions have a protective role in the airways.

Administration, Inhalation↗
PubMed1998

Ictal epileptiform activity in the CA3 region of hippocampal slices produced by pilocarpine.

Pilocarpine, a muscarinic agonist, produces status epilepticus that is associated with the later development of chronic recurrent seizures. When applied to rat hippocampal slices, pilocarpine (10 microM) produced brief (<200 ms) epileptiform discharges that resembled interictal activity that occurs between seizures, as well as more prolonged synchronous neuronal activation that lasted seconds (3-20 s), and was comparable to ictal or seizures-like discharges. We assessed the factors that favored ictal patterns of activity and determined the biophysical properties of the ictal discharge. The probability of observing ictal discharges was increased when extracellular potassium ([K+]o) was increased from 5 to 7.5 mM. Raising [K+]o to 10 mM resulted in loss of ictal patterns and, in 20 of 34 slices, desynchronization of epileptiform activity. Making the artificial cerebrospinal fluid (ACSF) hyposmotic favored ictal discharges at 5 mM [K+]o, but shifted 7.5 mM [K+]o ACSF patterns to interictal discharges or desynchronized activity. Conversely, increasing osmolality suppressed ictal patterns. The pilocarpine-induced ictal discharges were blocked by atropine (1 microM, n = 5), a muscarinic antagonist, and pirenzepine (1 microM, n = 6), a selective M1 receptor antagonist. Kainate/alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid receptor blockade stopped all epileptiform activity (n = 8). The N-methyl--aspartate antagonist ,-2-amino-5-phosphonovaleric acid (100 microM, n = 34) did not change the pattern of epileptiform activity but significantly increased the rate of interictal discharges and prolonged the duration of ictal discharges. The ictal discharge was characterized intracellularly by a depolarization that was associated with action potential generation and persisted as a membrane oscillation of 4-10 Hz. The ictal oscillations reversed in polarity at -22.7 +/- 2.2 mV (n = 11) with current-clamp recordings and -20.9 +/- 3.1 mV (n = 7) with voltage-clamp recordings. The reversal potential of the ictal discharge in the presence of the gamma-aminobutyric acid-A blocker bicuculline (10 microM, n = 6) was -2.2 +/- 2.6 mV and was significantly different from that measured without bicuculline. Bicuculline added to 7.5 mM [K+]o and 10 microM pilocarpine did not cause epileptiform activity to change pattern but significantly increased the rate of interictal discharges and prolonged the ictal discharge duration. Both synaptic and nonsynaptic mechanisms are important for the generation of ictal patterns of epileptiform activity. Although the synchronous epileptiform activity produced by pilocarpine required fast glutamate-mediated synaptic transmission, the transition from an interictal to ictal pattern of activity depended on [K+]o and could be influenced by extracellular space.

2-Amino-5-phosphonovalerate↗
PubMed2003

Central muscarinic receptors signal pilocarpine-induced salivation.

Although cholinergic agonists such as pilocarpine injected peripherally can act directly on salivary glands to induce salivation, it is possible that their action in the brain may contribute to salivation. To investigate if the action in the brain is important to salivation, we injected pilocarpine intraperitoneally after blockade of central cholinergic receptors with atropine methyl bromide (atropine-mb). In male Holtzman rats with stainless steel cannulas implanted into the lateral ventricle and anesthetized with ketamine, atropine-mb (8 and 16 nmol) intracerebroventricularly reduced the salivation induced by pilocarpine (4 micro mol/kg) intraperitoneally (133 + 42 and 108 + 22 mg/7 min, respectively, vs. saline, 463 + 26 mg/7 min), but did not modify peripheral cardiovascular responses to intravenous acetylcholine. Similar doses of atropine-mb intraperitoneally also reduced pilocarpine-induced salivation. Therefore, systemically injected pilocarpine also enters the brain and acts on central muscarinic receptors, activating autonomic efferent fibers to induce salivation.

Acetylcholine↗
PubMed2004

Oral pilocarpine for treatment of opioid-induced oral dryness in healthy adults.

Pilocarpine induces a profuse flow of saliva when administered orally, but effects on drug-induced oral dryness have not been examined. The aim of this trial was to investigate if pilocarpine increases production of saliva in individuals suffering from dry mouth due to treatment with opioids. Sixty-five individuals were enrolled in a randomized, double-blind, placebo-controlled trial. The subjects received tramadol (50 mg t.d.s.) to induce oral dryness, and were thereafter assigned to one of three groups. Secretion rate of saliva was measured before and after tramadol, and after the oral administration of pilocarpine (5 mg), placebo, or no treatment. Baseline characteristics did not differ among the groups (mean +/- SEM: 0.37 +/- 0.06 mL/min), and tramadol lowered the secretion at the same level in all groups (0.15 +/- 0.02 mL/min). Pilocarpine increased the flow above that observed with placebo (0.66 +/- 0.19 vs. 0.15 +/- 0.02 mL/min). Thus, pilocarpine re-establishes the flow of saliva in the state of tramadol-induced oral dryness.

Administration, Oral↗
PubMed2004

Bilateral anterior thalamic nucleus lesions and high-frequency stimulation are protective against pilocarpine-induced seizures and status epilepticus.

OBJECTIVE: The thalamus is thought to play an important role in secondary generalization of seizures. The aim of the present study was to investigate the influence of anterior thalamic nucleus lesions and high-frequency stimulation in the pilocarpine model of secondarily generalized seizures in rats. METHODS: Adult Wistar rats underwent unilateral (n = 7) or bilateral anterior nucleus thalamotomies (n = 10), or unilateral (n = 4) or bilateral (n = 9) anterior thalamic nucleus stimulation through implanted electrodes. Control animals (n = 9) received bilateral implants but no stimulation. Seven days after these procedures, animals were provided pilocarpine (320 mg/kg intraperitoneally) to induce seizures and status epilepticus (SE). Electrographic recordings from hippocampal and cortical electrodes were evaluated, and ictal behavior was assessed. RESULTS: In the control group, 67% of the animals developed SE 15.3 +/- 8.8 minutes after pilocarpine administration. Neither unilateral anterior nucleus lesions nor stimulation significantly reduced the propensity or latency for developing seizures and SE. Bilateral thalamic stimulation did not prevent SE (observed in 56% of the animals), but it significantly prolonged the latency to its development (48.4 +/- 17.7 min, P = 0.02). Strikingly, no animal with bilateral anterior nucleus thalamotomies developed seizures or SE with pilocarpine. CONCLUSION: Bilateral anterior thalamic nuclear complex stimulation and thalamotomies were protective against SE induced by pilocarpine.

Animals↗
PubMed2000

Pilocarpine for radiation-induced xerostomia in head and neck cancer.

This article examines the use of pilocarpine hydrochloride for radiation-induced xerostomia in patients with head and neck cancer. Four randomized controlled trials involving 401 patients met the authors' predefined inclusion criteria and were critically appraised. Three studies used topical pilocarpine as a mouthwash. Outcome measurements were both quantitative and qualitative. The studies reported statistically significant differences in favour of pilocarpine-stimulated treatment groups. Subjective improvements in feelings of oral dryness, speaking and chewing were reported in all studies. However, sample sizes varied and in all cases sampling methods were poorly defined. The pilocarpine doses tested produced side effects, but those reported were easily tolerated. The persistent findings of symptomatic improvement following pilocarpine use merit consideration, but there is insufficient evidence from these studies alone to generalize results to the wider population.

Head and Neck Neoplasms↗
PubMed2005

Comparison of sweat rate during graded exercise and the local rate induced by pilocarpine.

Centrally stimulated sweat rate produced by graded exercise until exhaustion was compared to the local sweat rate induced by pilocarpine, often used as a sweating index for healthy individuals. Nine young male volunteers (22 +/- 4 years) were studied in temperate environment in two situations: at rest and during progressive exercise with 25 W increases every 2 min until exhaustion, on a cycle ergometer. In both situations, sweating was induced on the right forearm with 5 ml 0.5% pilocarpine hydrochloride applied by iontophoresis (1.5 mA, 5 min), with left forearm used as control. Local sweat rate was measured for 15 min at rest. During exercise, whole-body sweat rate was calculated from the body weight variation. Local sweat rate was measured from the time when heart rate reached 150 bpm until exhaustion and was collected using absorbent filter paper. Pharmacologically induced local sweat rate at rest (0.4 +/- 0.2 mg cm-2 min-1) and mean exercise-induced whole-body sweat rate (0.4 +/- 0.1 mg cm-2 min-1) were the same (P > 0.05) but were about five times smaller than local exercise-induced sweat rate (control = 2.1 +/- 1.4; pilocarpine = 2.7 +/- 1.2 mg cm-2 min-1), indicating different sudorific mechanisms. Both exercise-induced whole-body sweat rate (P < 0.05) and local sweat rate (P < 0.05) on control forearm correlated positively with pilocarpine-induced local sweat rate at rest. Assuming that exercise-induced sweating was a result of integrated physiological mechanisms, we suggest that local and whole-body sweat rate measured during graded exercise could be a better sweating index than pilocarpine.

Adult↗
PubMed1983

Stimulation of amylase and sialic acid releases from dog submandibular gland slices by pilocarpine or high K+ medium: a possible role of calmodulin for their releases.

The mechanism of amylase and sialic acid releases stimulated by pilocarpine or high K+ medium was investigated in the slices of dog submandibular glands. The release of both amylase and sialic acid was dose-dependently increased by pilocarpine and a considerable release was observed at pilocarpine concentrations of more than 1 microM. Similar effects were observed when K+ concentration in the medium was increased and the maximal response was observed at 75 mM K+. The release of amylase and sialic acid by pilocarpine or K+ considerably decreased by removing Ca2+ from the medium and the slices. The release of amylase in the Ca2+-deficient slices was nearly recovered by the addition of 2.5 and 5.0 mM Ca2+, whereas that of sialic acid was recovered by only 60-75%. Ca2+ inhibitors, La3+ and verapamil, and calmodulin inhibitors, trifluoperazine, prenylamine, and W-7, significantly inhibited the release of amylase and sialic acid induced by the stimulants. These results suggest that the release of amylase and sialic acid stimulated by pilocarpine or K+ is dependent on the presence of Ca2+, and that the activation of calmodulin is involved in the process of the release.

Amylases↗
PubMedDate not supplied

A solid colloidal drug delivery system for the eye: encapsulation of pilocarpin in nanoparticles.

The present study was undertaken in order to encapsulate pilocarpin into nanoparticles. Two principally different methods for manufacturing these particles were investigated. Firstly, pilocarpin was dissolved in an aqueous medium in which the polymerization was carried out, and secondly, the polymerizing monomer was kept saturated with the drug solution under acidic conditions resulting in an incorporation into the nanoparticles in an aqueous environment. The amount of pilocarpin that could be incorporated into the nanoparticles was found to be largely influenced by the temperature at which the nanoparticles were produced and by the stabilizers used. At low temperatures, up to 60 per cent of pilocarpin nitrate could be encapsulated into butylcyanoacrylate nanoparticles using emulsion polymerization techniques. Larger amounts of pilocarpin could not be incorporated because of the hydrophilicity of the salts of this drug. The physico-chemical characteristics of the nanoparticles are reported: the particle size and morphology were determined by scanning and transmission electron microscopy and photon correlation spectrometry. The average particle size was about 100 nm. The results obtained in this study show that photon correlation spectrometry is a suitable method for the sizing of nanoparticles.

Colloids↗
PubMedDate not supplied

Pilocarpine-induced salivary secretion, kinin system and nitric oxide in rats.

In anaesthetized rats, intraperitoneal injection of pilocarpine (0.1 to 1 mg.Kg-1) induced a dose-dependent flow of saliva. During salivation by pilocarpine (0.5 mg.Kg-1), the blood content of submaxillary glands was not significantly increased but the blood volume of the animals was reduced. The salivary flow rate induced by pilocarpine was similar in normal and kininogen-deficient rats. L-NG-nitro-arginine (L-NOARG, 35 mg.Kg-1), a nitric oxide synthesis inhibitor, increased the salivary flow elicited by pilocarpine (0.5 mg.Kg-1). L-NOARG did not modify the blood volume loss but decreased the blood content of the submaxillary glands. The volume of salivary secretion induced by isoproterenol (250 mg.Kg-1) was lower in kininogen-deficient rats than in normal rats. It was significantly reduced by HOE 140 (2 mg.Kg-1), a bradykinin antagonist. L-NOARG increased the salivary flow induced by isoproterenol during the ten first minutes of collection but suppressed it thereafter. We concluded that kinins are not involved in the stimulating effect of pilocarpine on rat salivary glands but these peptides would participate to the development of the salivation induced by isoproterenol in rats. Nitric oxide contributes to the control of the vascular tone in rat salivary glands. The influence of L-NOARG on salivation would be explained by its effects on blood pressure and vascular resistances.

Amino Acid Oxidoreductases↗
PubMed1987

Effect of orally administered pilocarpine on ruminal characteristics and nutrient digestibility in cattle.

Four barren Holstein cows weighing 637 kg were fed a 45% concentrate diet plus the following amounts of pilocarpine: 1) 0 mg/kg; 2) 1 mg/kg; 3) 2 mg/kg; 4) 4 mg/kg body weight in a 4 X 4 Latin square design. Cows were administered the treatments for a 14-d adaptation period followed by an 8-d collection period. Digestibility of dry matter, crude protein, cellulose, and hemicellulose were determined during the first 3 d of the collection period. Ruminal liquid volume, volatile fatty acids, NH3N, bacterial mass production, viable bacteria, cellulolytic bacteria, liquid dilution rate, and particulate rate of passage were measured during the remainder of the collection period. As pilocarpine increased from 0 to 4 mg/kg body weight, digestibility of dry matter and cellulose increased by 8.5%. Digestibility of crude protein increased by 6.1%. Digestibility of hemicellulose was unchanged. Ruminal liquid volume was unchanged by treatment, whereas liquid dilution rate and particulate rate of passage increased 30% as pilocarpine increased. Ruminal volatile fatty acid concentrations and proportion were unchanged by treatment. Ruminal pH increased 4.2% and NH3N decreased by 37% as pilocarpine increased. Percent cellulolytic and bacterial mass production tended to increase as pilocarpine increased.

Animals↗
PubMed2006

Erythropoietin preconditioning on hippocampus neuronal apoptosis following status epilepticus induced by Li-pilocarpine in rats through anti-caspase-3 expression.

UNLABELLED: Selective neuronal loss following status epilepticus (SE) was first described just under 100 years ago. The acute pathology following SE was shown to be 'ischemic cell change' and was assumed to arise through hypoxia/ischemia. Recently, erythropoietin (Epo) has been shown to have potent anti-apoptosis activity in central nervous system neurons in animal models of ischaemic injury. AIMS: In this report, in order to determine Epo preconditioning on hippocampus neuronal apoptosis, we examined caspase-3 expression following SE caused by Li-pilocarpine in rats. SETTINGS AND DESIGN: Animals were classified into three groups: EP group (pilocarpine group), rhEpo-pilocarpine group and control group. Four hours after preconditioning with Epo intraperitoneally, pilocarpine hydrochloride was administered intraperitoneally and observed for behavioral manifestations of SE. The animals were sacrificed at one hour after SE onset. MATERIALS AND METHODS: At the above-mentioned time point, animals were deeply anesthetized and were perfused through the left ventricle. Detection of hippocampus neuronal apoptosis was performed with caspase-3 immunohistochemical technique on three groups. To further confirm which cell population upregulates caspase-3, brain sections were stained for NeuN (green) and caspase-3 (red). STATISTICAL ANALYSIS: ANOVA and Fisher's post hoc test was used. RESULTS: Quatification of hippocampus neurons revealed that the number of caspase-3-positive cells in the CA1/CA3 area and dentate gyrus(DG) of three groups had a significant difference. In comparison with control group, there was an increase by 74% and 534%, 42% and 272% in the CA1/CA3 area and DG of EP group and rhEpo-treated group respectively. There was a decrease by 18% and 26% in the CA1/CA3 area and DG of rhEpo-treated group compared with those in EP group. In addition, colocalization of caspase-3 with NeuN was shown. CONCLUSIONS: Systemic rhEpo therapy reduced caspase-3 expression in SE induced by Li-pilocarpine.

Animals↗
PubMed1999

The dorzolamide/timolol combination versus timolol plus pilocarpine: patient preference and impact on daily life. United States Patient Preference Study Group. International Patient Preference Study Group.

PURPOSE: To compare the 2.0% dorzolamide/0.5% timolol fixed combination (COSOPT; Merck & Co., Whitehouse Station, NJ) to 0.5% timolol plus 2.0% pilocarpine given concomitantly, and to determine patient preference, tolerability, and impact on daily life in patients with elevated intraocular pressure (IOP). METHODS: Two multi-center, randomized, cross-over, observer masked studies were conducted, one in the United States (97 patients) and one in Europe (93 patients). The Comparison of Ophthalmic Medications for Tolerability questionnaire was used to assess patient preference and perception of side effects and activity limitations resulting from study medications. Intraocular pressure was measured before and 2 hours after the morning dose of study medication (hour 0 and hour 2). RESULTS: In both studies, among patients with a preference, the combination was preterred to timolol plus pilocarpine by a ratio of 4 to 1. The most commonly cited reason for this preference was side effects. Patients in both studies also reported that the combination interfered significantly less with daily life in terms of side effects and activity limitations. They also reported missing significantly fewer doses of study medication while taking the combination and being significantly more satisfied with it. The efficacy of these two treatments was not significantly different, based on IOP measurements at hour 0 and 2 hours after administration. Patients reported significantly more adverse events while receiving timolol plus pilocarpine in both studies, and in the U.S. study, significantly more patients discontinued therapy while receiving timolol plus pilocarpine than while receiving the combination. CONCLUSION: Compared with timolol plus pilocarpine, patients preferred the combination of 2% dorzolamide/0.5% timolol, and reported less interference in daily activities, better tolerability, and better compliance with therapy.

Activities of Daily Living↗