Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PILOCARPINE”

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

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

At least 415 records · Page 23Linked to original sources
PubMed1986

Dilute solutions of phenylephrine and pilocarpine in the diagnosis of disordered autonomic innervation of the iris. Observations in normal subjects, and in the syndromes of Horner and Holmes-Adie.

A standardized method of testing irideal sensitivity to 1% phenylephrine and 0.05% pilocarpine is described, and a quantitative basis for pupillary neurotransmitter "supersensitivity" established. In a normal 20-year-old subject the pupillary diameter increases in bright light by no more than 2.1 mm 1 h after ocular application of phenylephrine; this figure should be adjusted for age since "phenylephrine sensitivity" of the iris increases by 0.23 mm per decade. The pupillary diameter, when measured in darkness, has normally decreased by less than or equal to 1.4 mm within 30 min of administration of pilocarpine. Differences in drug-induced diameter alterations between pairs of pupils should not normally exceed 0.7 mm for phenylephrine or 0.4 mm for pilocarpine. Seventy one percent of sympathetically denervated or decentralized (Horner's) pupils and 41% of parasympathetically denervated ("tonic") pupils are abnormally responsive or "supersensitive" to dilute solutions of phenylephrine and pilocarpine respectively. Supersensitivity to these agents is therefore a useful but not invariable diagnostic feature of disturbed irideal innervation.

Adie Syndrome↗
PubMed1986

Pilocarpine for the treatment of xerostomia associated with salivary gland dysfunction.

A double-blind placebo-controlled study was conducted to evaluate the efficacy of orally administered pilocarpine in treating oral dryness caused by salivary gland hypofunction. At low dosages, pilocarpine increased the production of saliva by parotid and submandibular and/or sublingual glands and relieved the sensation of oral dryness. The quantity and composition of pilocarpine-stimulated secretions were similar to saliva produced in response to gustatory stimulation with citrate. In appropriate patients, pilocarpine is a safe, easily administered, effective therapy to relieve xerostomia by increasing natural salivary function.

Aged↗
PubMed1978

Pilocarpine, food deprivation, and induction of mouse killing by cats.

Effects of three treatments that induce mouse killing by rats were examined with cats. Food deprivation induced about 50% killing after 24 hr and almost 100% killing by 27 hr. Pilocarpine (at doses of 1.0 mg/kg that produced marked side-effects, and whether or not methyl atropine pretreatment blocked those side-effects) and chlordiazepoxide (at doses of 1.0--2.0 mg/kg) did not induce any killing. Pilocarpine produced a dose-related inhibition of spontaneous mouse killing (as it does in rats), but this was antagonised by methyl atropine. The side-effects of pilocarpine and chlordiazepoxide did not seem to account for their failure to induce killing. In contrast with food deprivation, the mechanisms by which pilocarpine and chloridazepoxide induce killing in rats may not have homologs in cats.

Aggression↗
PubMed1990

The effects of amphetamine and pilocarpine on the release of ascorbic and uric acid in several rat brain areas.

Linear sweep voltammetry was used to investigate the effects of amphetamine (which enhances the release of dopamine) and/or pilocarpine (a cholinergic agonist) on the release of ascorbic acid and uric acid in brain areas differing in dopamine and acetylcholine concentrations. In caudate, nucleus accumbens, and hippocampus, the magnitude of the amphetamine-induced increase in ascorbic acid was roughly correlated with dopamine content of the brain area tested. Cingulate cortex was a notable exception; the increase in ascorbic acid was greater than that in nucleus accumbens. Pilocarpine produced the greatest increase in ascorbic acid in cingulate cortex, even though cingulate cortex has the lowest acetylcholine concentration of the brain areas tested. Except for cingulate cortex, the ascorbic acid data were consistent with the hypothesis that amphetamine and pilocarpine release different pools of ascorbic acid. The uric acid data were consistent with the hypothesis that amphetamine and pilocarpine release the same pool of uric acid. The unexpected findings in cingulate cortex may point to an important role of ascorbic acid in this brain area.

Amphetamine↗
PubMed1991

D-2 agonists protect rodents against pilocarpine-induced convulsions by stimulating D-2 receptors in the striatum, but not in the substantia nigra.

This study employed the pilocarpine model of epilepsy to determine the relative systemic anticonvulsant potencies of five different D-2 agonists in the mouse, and to investigate the site of anticonvulsant action of LY 171555 in the rat's brain following intracerebral microinjection. Control mice pretreated with saline developed motor seizures when challenged with pilocarpine (400 mg/kg, 11/13 convulsed). D-2 agonists protected mice against pilocarpine-induced seizures in the rank order of potency PHNO greater than pergolide greater than greater than lisuride = LY 171555 much greater than RU 24213, with ED50 values ranging from 0.17 mg/kg for PHNO to greater than 4.5 mg/kg for RU 24213. The response to LY 171555 was abolished by the D-2 blocker metoclopramide (1.25 mg/kg), but not by the D-1 antagonist SCH 23390 (0.25 mg/kg). All D-2 agonists induced head-down sniffing and forward locomotion, consistent with central D-2 activation. LY 171555 (ED50 0.19 mg/kg), but not RU 24213 (ED50 greater than 4.5 mg/kg), was similarly efficacious in the rat. When injected into both hemispheres of the conscious rat via indwelling cannulae, intrastriatal saline failed to afford protection against the convulsant action of pilocarpine (600 mg/kg, 13/15 convulsed), whereas LY 171555 did (1 microgram, 1/12 convulsed). Intrastriatal RU 24213 (1 microgram per side) was without effect (7/10 convulsed). Similarly, no protection resulted when saline (15/16 convulsed) or LY 171555 (1 microgram, 17/23 convulsed) were delivered into both nigras. It is concluded that in this model of limbic seizures in the mouse and rat, D-2 agonists exert a powerful anticonvulsant effect which is mediated by D-2 receptors in the striatum, but not by D-2 receptors in the substantia nigra.

Animals↗
PubMed1992

Roles of gender and gonadectomy in pilocarpine and clonidine analgesia in rats.

Central and systemic morphine analgesia as well as both opioid and nonopioid forms of swim analgesia display gender differences with male rats showing greater magnitudes of analgesia than female rats. Since nonopioid swim analgesia is dependent upon muscarinic cholinergic and alpha 2-noradrenergic mechanisms, the present study evaluated in rats whether gender, adult gonadectomy or estrous phase altered analgesia induced by either the muscarinic cholinergic receptor agonist, pilocarpine or the alpha 2-noradrenergic receptor agonist, clonidine. Pilocarpine (1-10 mg/kg) analgesia was significantly greater in male rats. Female rats displayed 7-fold and 3-fold rightward shifts in peak analgesia on the tail-flick and jump tests respectively. Clonidine (100-500 micrograms/kg) analgesia was significantly greater on both nociceptive tests in males, but only produced a 2-fold rightward shift in peak analgesia in females on the jump test. Whereas castration failed to shift either dose-response curve, ovariectomy mitigated the gender differences in pilocarpine and clonidine analgesia. Both pilocarpine and clonidine analgesia were not altered by estrous phase changes. These data indicate that gender differences in analgesia are not specific to opioid systems.

Analgesics↗
PubMed1993

Paradoxical facilitation of pilocarpine-induced seizures in the mouse by MK-801 and the nitric oxide synthesis inhibitor L-NAME.

The sensitivity of pilocarpine-induced seizures to NMDA receptor blockade with MK-801, or to inhibition of synthesis of the second messenger nitric oxide (NO) with N omega-nitro-L-arginine methyl ester (L-NAME), was studied in mice. The NO precursor L-arginine (100-500 mg/kg, IP) and L-NAME (1-125 mg/kg, IP) had no overt effects on animals' behaviour by themselves, while MK-801 (0.1-0.8 mg/kg, IP) caused motor excitability at low doses and sedation and paraplegia at high ones. Contrary to expectation, MK-801 and L-NAME failed to protect mice against limbic motor seizures induced by pilocarpine (400 mg/kg, IP), and L-arginine was not proconvulsant in mice challenged with a threshold convulsant dose of the cholinomimetic (100 mg/kg, IP). Surprisingly, both MK-801 and L-NAME were found to be proconvulsant when injected in conjunction with 100 mg/kg pilocarpine, and in both cases this convulsant action synergised with that produced by the dopamine D1 agonist SK&F38393 (10 mg/kg, IP). Concomitant administration of L-arginine (500 mg/kg) prevented the convulsant effect of 5 mg/kg L-NAME but was ineffective against 25 mg/kg L-NAME and MK-801. It is concluded that glutamate, acting through the NMDA receptor and NO production, normally suppresses epileptogenesis in the mouse pilocarpine model of limbic epilepsy.

Animals↗
PubMed1993

Enhanced pilocarpine-induced oral activity responses in neonatal 6-OHDA treated rats.

Neonatal destruction of rat nigrostriatal dopaminergic fibers results in an enhanced oral activity response to both dopamine (DA) D1 and serotonin (5-HT) agonists. Because cholinergic systems represent another one of the neural circuits involved in oral behavior, it was of interest to determine whether muscarinic receptors might also be sensitized in the lesioned rats. At 3 days after birth, rats were pretreated with desipramine HCl (20 mg/kg, IP) 1 h before 6-hydroxydopamine (6-OHDA) HBr (100 micrograms in each lateral ventricle) or saline-ascorbic acid (0.1%) vehicle. Between 2 and 4 months, behavioral supersensitivity to a D1 agonist (SK&F 38393) and 5-HT agonist (m-chlorophenylpiperazine; m-CPP) was established before rats were challenged with the muscarinic receptor agonist, pilocarpine HCl (0.125 to 10.0 mg/kg, IP). The pilocarpine dose-effect curve was shifted to the left, with a maximal effect of 63.7 +/- 8.6 oral movements being produced by a 1.0 mg/kg pilocarpine HCl dose in the 6-OHDA lesioned rats, versus 15.0 +/- 2.4 oral movements in the control group (p < 0.001). The enhanced response to pilocarpine was attenuated by the muscarinic receptor antagonist, scopolamine HCl (0.1 mg/kg IP). These findings indicate that neonatal 6-OHDA treatment produces supersensitization of muscarinic receptors in rats.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1989

The muscarinic agonist pilocarpine inhibits DNA and interferon-gamma synthesis in peripheral blood mononuclear cells.

Lymphocyte basal DNA synthesis and proliferative responses to phytohemagglutinin (PHA) showed a dose-dependent (5 X 10(-5)-5 X 10(-3) M) inhibition by the muscarinic agonist pilocarpine, in contrast to the basal enhancing effect produced by the M2 muscarinic-nicotinic agonist carbachol. The effect of pilocarpine was reversed by both atropine (1 X 10(-6) M) and pirenzepine (1 X 10(-7)-1 X 10(-8) M), M1-M2 and M1 muscarinic antagonists, respectively. The effect of pilocarpine may thus be specific for the M1 muscarinic receptor. Pilocarpine also inhibited interferon-gamma (IFN-gamma)-PHA induced production, but was unable to reverse the pokeweed mitogen (PWM)-induced DNA synthesis. Distinct immunoregulatory activities are suggested for cholinergic muscarinic receptors M1 and M2.

Cells, Cultured↗
PubMed1994

Interictal discharges in the hippocampus of rats with long-term pilocarpine seizures.

Systemic administration of pilocarpine to adult rats induces an acute status epilepticus followed by spontaneous recurrent seizures after a 1-2-week silent period. We recorded field potentials in hippocampal slices obtained from rats with spontaneous recurrent seizures after pilocarpine-induced status. The frequency of the interictal discharges induced in these slices by 4-aminopyridine (4AP) was reduced and their duration was increased. Cutting the Schaffer collaterals caused interictal discharges in CA1 to disappear in normal rats and in rats 3 weeks after pilocarpine-induced status. However, 12 weeks after pilocarpine, these discharges remained in CA1 after such a cut but occurred at a lower frequency. These findings show that in rat hippocampi with a lesion similar to that of human Ammon's horn sclerosis some electrophysiological features of 4AP-induced interictal discharges are altered in comparison to those induced in normal hippocampi.

4-Aminopyridine↗
PubMed1992

High-performance liquid chromatographic determination of pilocarpine in plasma.

A high-performance liquid chromatographic procedure requiring neither derivatization nor complex sample work-up is reported for reproducibly and sensitively determining pilocarpine in plasma. Following stabilization of pilocarpine against in vitro hydrolysis using sodium fluoride, plasma samples were extracted and the extracts chromatographed on a 5-microns, low-carbon-load (6%) C18 reversed-phase column. The assay was linear between 10 and 300 ng/ml (r = 0.998). It had sufficient sensitivity to quantitate pilocarpine at concentrations as low as 10 ng/ml (signal-to-noise ratio > or = 4) using a 500-microliters sample. The assay appears to be the first published specifically for plasma determinations and has proven capable of supporting pharmacokinetics studies of pilocarpine disposition in the anesthetized dog.

Animals↗
PubMed1996

Sensitive high-performance liquid chromatographic assay for pilocarpine in biological fluids using fluorescence derivatisation.

A sensitive assay for pilocarpine in biological fluids has been developed involving HPLC of a fluorescent derivative of 4-bromomethyl-7-methoxycoumarin. Pilosine as internal standard was added before the derivatisation step. The fluorescent derivatives were well resolved and separated from excess reagent and endogenous compounds on a cyanopropyl silica column. The detection limit of pilocarpine in biological fluids was 1.0 ng/ml and the assay was linear up to a concentration of 150 ng/ml. The assay was applied to a preliminary study of pilocarpine disposition in man after a single oral dose. This is the first report of pilocarpine excretion into saliva.

Chromatography, High Pressure Liquid↗
PubMed1994

Quantitative evaluation of neuronal loss in the dorsal hippocampus in rats with long-term pilocarpine seizures.

Systemic administration of the cholinergic agonist pilocarpine (350-400 mg/kg, i.p.) to rats induces acute behavioral and EEG status epilepticus followed by apparent complete neurological recovery. In rats receiving higher doses of pilocarpine (i.e., 380-400 mg/kg), recurrent seizures reappear 2-2.5 weeks later and continue to occur as long as the rats are kept alive. Stereological estimates of neurons in regions CA1, CA3 and the dentate granule cell layer in the dorsal hippocampus show a dose-dependent neuronal loss in the CA3 and CA1 subregions. The granule cell layer of the dentate gyrus is not affected. No progressive neuronal loss was observed in the regions studied after 3, 6 and 12 weeks during which the animals displayed spontaneous recurrent seizures. The temporal profile of the epileptic condition induced by pilocarpine and the resulting pattern of neuronal loss in the rat hippocampus are similar to those seen in many cases of human temporal lobe epilepsy. The neuronal loss is dose-dependent and primarily results from the acute pilocarpine-induced seizures as chronic seizures do not produce any measurable additional cell loss in the regions examined in the experimental model used in this study.

Animals↗
PubMed1994

Kappa opioid receptor agonists inhibit the pilocarpine-induced seizures and toxicity in the mouse.

Involvement of the kappa opioid receptor in regulation of the pilocarpine-induced seizures and neurodegeneration was studied in mice. Administration of pilocarpine (400 mg/kg i.p.) resulted in a sequence of behavioral alterations including motor limbic seizures. Pretreatment of mice with the selective kappa opioid receptor agonist U69,593 (2 and 20 mg/kg i.p.) or PD117,302 (0.1 and 1 mg/kg i.p.) increased the latency of motor seizures and decreased the seizure severity and mortality. Those effects were abolished in animals pretreated with the specific kappa opioid receptor antagonist nor-binaltorphimine (Nor-BNI, 10 mg/kg i.p.). Examination of frontal forebrain sections by light microscopy revealed widespread damage, especially within the hippocampal formation, in pilocarpine-treated mice. Both U69,593 and PD117,503 protected the integrity of hippocampal neurons, especially in the CA1 region, that effect being reversed by Nor-BNI. The above data indicate that activation of the kappa opioid receptor exerts an inhibitory effect on the pilocarpine-induced limbic seizures and neurotoxicity.

Analgesics↗
PubMed2006

The effect of timolol-dorzolamide and timolol-pilocarpine combinations on ocular blood flow in patients with glaucoma.

PURPOSE: To investigate the effect of timolol-dorzolamide and timolol-pilocarpine fixed combinations on retrobulbar vessel blood flow. DESIGN: Prospective, randomized, masked, crossover clinical trial. METHODS: Sixteen patients with primary open angle glaucoma, treated with timolol 0.5%, received timolol 0.5%-dorzolamide 2% and timolol 0.5%-pilocarpine 2% for four weeks each. Heart rate, blood pressure, intraocular pressure (IOP), and peak systolic (PSV) and end diastolic velocities (EDV) in ophthalmic, central retinal, and short posterior ciliary arteries were measured before and after each treatment, and resistivity index was calculated. RESULTS: The IOP was reduced (P < .01) by timolol-dorzolamide and, more effectively, timolol-pilocarpine combinations. In central retinal artery, the end diastolic velocity was increased by the timolol-dorzolamide combination (P < .01), resulting in higher end diastolic velocity and lower resistivity index values (both P < .01) compared with the timolol-pilocarpine combination. CONCLUSIONS: The timolol-dorzolamide combination increases the end diastolic velocity in central retinal artery, despite a lower intraocular pressure decrease, suggesting an effect on retinal circulation.

Aged↗
PubMed2005

Seizure susceptibility in intact and ovariectomized female rats treated with the convulsant pilocarpine.

Despite numerous neuroendocrinological studies of seizures, the influence of estrogen and progesterone on seizures and epilepsy remains unclear. This may be due to the fact that previous studies have not systematically compared distinct endocrine conditions and included all relevant controls. The goal of the present study was to conduct such a study using pilocarpine as chemoconvulsant. Thus, age and weight-matched, intact or ovariectomized rats were tested to determine incidence of status epilepticus and to study events leading to status. Intact female rats were sampled at each cycle stage (proestrus, estrus, metestrus, or diestrus 2). Convulsant was administered at the same time of day, 10:00-10:30 a.m. Statistical analysis showed that there was a significantly lower incidence of status on the morning of estrus, but differences were attenuated in older animals. Ovariectomized rats were distinct in their rapid progression to status. These results show that the incidence of status in female rats following pilocarpine injection, and the progression to pilocarpine-induced status, are influenced by reproductive state as well as age. The hormonal milieu present specifically on the morning of estrus appears to decrease susceptibility to pilocarpine-induced status, particularly at young ages. In contrast, the chronic absence of reproductive steroids that characterizes the ovariectomized rat leads to a more rapid progression to status. This dissociation between incidence vs. progression provides new insight into the influence of estrogen and progesterone on seizures.

Animals↗
PubMed2005

Pilocarpine-induced shift of an accommodating intraocular lens: AT-45 Crystalens.

PURPOSE: To measure the shift of an accommodating plate-haptic intraocular lens (IOL) along the visual axis induced by ciliary muscle contraction after application of pilocarpine. SETTING: Department of Ophthalmology, Medical University of Vienna, Vienna, Austria. METHODS: Fifty-four eyes of 28 patients with age-related cataract comprised this prospective study. Each patient received an AT-45 silicone accommodating IOL (Crystalens, Eyeonics Corp.) after standardized cataract surgery. In a subgroup of 24 eyes, capsular bag fibrosis was reduced by extensive polishing of the anterior capsule with a slit cannula. Assessment included measurements of anterior chamber depth, assessed with partial coherence interferometry, before and after application of pilocarpine 2% and evaluation of near visual acuity 1 month and 3 months postoperatively. RESULTS: A slight backward shift of the IOL of 151 mum in the nonpolished group (P < .001) and 122 mum in the polished group (P < .005) could be detected after application of pilocarpine. Polishing the capsule did not influence IOL shift. The median near visual acuity with distance correction 1 month and 3 months postoperatively was J5 and J4, respectively, in the nonpolished group and J6 at both times in the polished group. CONCLUSIONS: Pilocarpine induced a counterproductive active backward shift of the AT-45 IOL. Polishing of the capsular bag had no impact on accommodative ability. The reading performance of patients with the AT-45 IOL patients at 1 and 3 months was not significantly different from that of with a standard IOL under similar testing methods.

Accommodation, Ocular↗
PubMed2004

Pilocarpine toxicity and the treatment of xerostomia.

Pilocarpine has been used as an ophthalmologic agent for decades; however, toxicity rarely has been reported in the medical literature. Oral pilocarpine tablets, as well as another muscarinic agent (cevimeline), have recently been approved for the treatment of dry mouth (xerostomia). We report a case of unintentional overdose of oral pilocarpine tablets that resulted in bradycardia, mild hypotension, and muscarinic symptoms in a patient with Sjogren's syndrome. The patient's symptoms were relieved with 0.5 mg intravenous atropine and she recovered uneventfully. The case is unique in that it is the first reported ingestion of oral pilocarpine tablets and the first dosing error reported for this indication. In addition, this case underscores the importance of communication between physician and patient and the resulting toxicity related to miscommunication.

Administration, Oral↗