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PubMed2003

Selective 5-HT1A antagonists WAY 100635 and NAD-299 attenuate the impairment of passive avoidance caused by scopolamine in the rat.

Systemic administration of the muscarinic-receptor antagonists atropine and scopolamine produces cognitive deficits in humans, nonhuman primates and rodents. In humans, these deficits resemble symptoms of dementia seen in Alzheimer's disease. The passive avoidance (PA) task has been one of the most frequently used animal models for studying cholinergic mechanisms in learning and memory. The present study examined the ability of two selective 5-HT(1A) receptor antagonists WAY 100635 and NAD-299 (robalzotan) and two acetylcholinesterase (AChE) inhibitors tacrine and donepezil to attenuate the impairment of PA retention caused by the nonselective muscarinic receptor antagonist scopolamine in the rat. Although demonstrating differences in their temporal kinetics, both WAY 100635 and NAD-299 attenuated the impairment of PA caused by scopolamine (0.3 mg/kg s.c.). Donepezil did not block the PA deficit caused by the 0.3 mg/kg dose of scopolamine, but it prevented the inhibitory effects of the 0.2 mg/kg dose of scopolamine. In contrast, tacrine was effective vs both the 0.2 and 0.3 mg/kg doses of scopolamine. These results indicate that (1). a functional 5-HT(1A) receptor antagonism can attenuate the anterograde amnesia produced by muscarinic-receptor blockade, and (2). the AChE inhibitors tacrine and donepezil differ in their ability to modify muscarinic-receptor-mediated function in vivo. These results suggest that 5-HT(1A) receptor antagonists may have a potential in the treatment of cognitive symptoms in psychopathologies characterized by reduced ACh transmission such as Alzheimer's disease.

Animals↗

PubMed2006

Scopolamine induces disruption of latent inhibition which is prevented by antipsychotic drugs and an acetylcholinesterase inhibitor.

The fact that muscarinic antagonists may evoke a psychotic state ('antimuscarinic psychosis'), along with findings of cholinergic alterations in schizophrenia, have kindled an interest in the involvement of the cholinergic system in this disorder. Latent inhibition (LI) is a cross-species phenomenon manifested as a poorer conditioning of a stimulus seen when the stage of conditioning is preceded by a stage of repeated nonreinforced pre-exposure to that stimulus, and is considered to index the capacity to ignore irrelevant stimuli. Amphetamine-induced LI disruption and its reversal by antipsychotic drugs (APDs) is a well-established model of positive symptoms of schizophrenia. Here, we tested whether the muscarinic antagonist scopolamine would disrupt LI and whether such disruption would be reversed by APDs and by the acetylcholinesterase inhibitor physostigmine. The results showed that scopolamine at doses of 0.15 and 0.5 mg/kg disrupted LI, and that this effect was due to the action of the drug in the pre-exposure stage, suggesting a role of muscarinic transmission in attentional processes underlying LI. Both the typical and the atypical APDs, haloperidol and clozapine, reversed scopolamine-induced LI disruption when given in conditioning or in both stages, but not in pre-exposure, indicating that the mechanism of antipsychotic action in this model is independent of the mechanism of action of the propsychotic drug. Scopolamine-induced LI disruption was reversed by physostigmine (0.05 and 0.15 mg/kg), which was ineffective in reversing amphetamine-induced LI disruption, pointing to distinct mechanisms underlying LI disruption by these two propsychotic drugs. The latter was further supported by the finding that unlike amphetamine, the LI-disrupting doses of scopolamine did not affect activity levels. We propose scopolamine-induced LI disruption as a model of cholinergic-related positive symptoms in schizophrenia.

Acetylcholine↗

PubMed1999

Laboratory confirmation of scopolamine co-intoxication in patients using tainted heroin.

BACKGROUND: First described in 1995, at least 325 patients with a history of heroin use have since required emergency medical evaluation in several eastern US cities, because of an anticholinergic toxidrome following use of heroin. This co-intoxication has been alleged to result from an atropine-like compound. We report the clinical findings and laboratory analysis of one of several individuals who presented to our Emergency Department during this epidemic. CASE REPORT: A 23-year-old male was one of 3 patients brought to the Emergency Department due to agitated behavior after insufflating heroin. Following physical and chemical restraint, vital signs were pulse 134 bpm, BP 160/90 mm Hg, RR 24/min, and T 37.3 degrees C. Physical examination was remarkable for dilated pupils 8-9 mm without nystagmus, along with dry mouth, decreased bowel sounds, and flushed dry skin. A bladder catheter was placed and 500 mL of urine was obtained. Electrocardiogram revealed sinus tachycardia only. Additional sedation was required for 12 hours until normal mental status returned. A small sample of the "heroin" used was obtained and analyzed. Scopolamine was confirmed by gas chromatography-mass spectrometry. Further evidence of scopolamine intoxication was supported by identifying scopolamine in the urine of this patient. CONCLUSION: Gas chromatography-mass spectrometry revealed scopolamine to be the cause of anticholinergic findings in a patient following use of tainted heroin. It is unclear whether scopolamine is an adulterant or contaminant in this heroin. Patients with anticholinergic findings following use of heroin may be co-intoxicated with scopolamine.

Adult↗

PubMed1990

Systemic absorption of ocular scopolamine in patients.

The systemic absorption of scopolamine 0.25% eyedrops given unilaterally was quantitated in eight patients following therapeutic drug application. Another set of eight patients received placebo drops to study the effect of scopolamine on heart rate, blood pressure and salivation. Scopolamine was rapidly and efficiently absorbed after its ocular administration. The peak plasma scopolamine concentration of 550 +/- 60 pg/ml was reached within 15 minutes in all but two patients. Ocular scopolamine did not affect patients blood pressure or heart rate when compared to patients in the placebo group. Thirty minutes after administration of scopolamine the salivary secretion was slightly but insignificantly reduced.

Absorption↗

PubMed1999

Transdermal scopolamine alters phasic REM activity in normal young adults.

Transdermal scopolamine has been widely used for the prevention of motion-sickness by travelers due to its potent anticholinergic effects and the ease of administration. Nevertheless, its effects on sleep physiology are not known, despite the wellknown fact that the administration of scopolamine as an injection or an oral form could influence the sleep architecture, especially prolonging rapid eye movement (REM) sleep latency and shortening duration of REM sleep. This study aimed to measure the influence of transdermal scopolamine on REM sleep in order to examine whether it affects REM sleep as in the previous studies. We studied eight young healthy male adults polysomnographically for three nights including one adaptation night in a double blind crossover design and compared REM sleep-related variables between sleeps with and without scopolamine patch of 1.5 mg. We found no differences in tonic REM sleep measures such as REM duration and REM latency, but phasic REM sleep measures such as total REM activity (p < 0.05) and total REM density (p < 0.05) were significantly suppressed by the transdermal scopolamine; REM densities of the first (p < 0.05) and the second (p < 0.05) REM sleep periods as well as REM activity of the fourth REM sleep period (p < 0.05) were decreased significantly on the scopolamine patch nights compared with placebo patch nights. These results suggest that phasic REM components reflect cholinergic mechanism in the central nervous system (CNS) even at the lowest commercial dose, and could be useful markers of CNS cholinergic activities in the future research.

Adult↗

PubMed2002

The efficacy and safety of transdermal scopolamine for the prevention of postoperative nausea and vomiting: a quantitative systematic review.

UNLABELLED: The role of scopolamine administered via transdermal therapeutic systems in the prevention of postoperative vomiting, nausea, and nausea and vomiting is unclear. We performed a systematic search for full reports of randomized comparisons of transdermal scopolamine with inactive control. Dichotomous data were extracted. In the meta-analysis, relative risks and numbers-needed-to-treat/harm were calculated with 95% confidence intervals (CI). In 23 trials, 979 patients received transdermal scopolamine, and 984 patients received placebo. Sensitivity analyses were performed using restricted data for truncated control event rates (40%-80%) and for large trials. With these data, the relative risks for postoperative vomiting (five reports), nausea (five reports), nausea and vomiting (eight reports), and rescue treatment (three reports) were 0.69 (95% CI, 0.58-0.82), 0.69 (95% CI, 0.54-0.87), 0.76 (95% CI, 0.66-0.88), and 0.68 (95% CI, 0.54-0.85), respectively. This means that of 100 patients who receive transdermal scopolamine, approximately 17 will not experience postoperative vomiting who would have done so had they all received a placebo. However, 18 of 100 patients will have visual disturbances, eight will report dry mouth, two will report dizziness, one will be classified as being agitated, and 1-13 patients who are prescribed transdermal scopolamine will not use it correctly. The timing of application does not alter efficacy. IMPLICATIONS: Of 100 patients who receive transdermal scopolamine, approximately 17 will not vomit in the postoperative period who would have done so had they all received a placebo. However, 18 of 100 patients will have visual disturbances, and eight will report dry mouth. Incorrect use further limits its efficacy.

Administration, Cutaneous↗

PubMed1997

Physostigmine reversal of scopolamine-induced hypofrontality.

The muscarinic receptor antagonist scopolamine produces a transient memory deficit in healthy humans. This deficit has been offered as a model of the cholinergic deficit of Alzheimer's disease (AD). However, we have previously shown that scopolamine produces a deficit of cortical perfusion maximal in the frontal lobe, dissimilar to the parietal cortex deficit characteristic of AD. The current experiment was aimed at replicating and extending this observation by critically testing the central cholinergic origin of both cognitive and perfusion deficits. Nine healthy subjects participated in regional cerebral blood flow (rCBF) measurements at baseline, after scopolamine (7.2 micrograms/kg i.v.), and after both physostigmine (22 micrograms/kg i.v.) and neostigmine (7 or 11 micrograms/kg i.v.). rCBF was quantified by the xenon 133 inhalation method. As expected, scopolamine reduced cortical perfusion, mainly in the frontal cortex, and produced a memory deficit. Physostigmine, but not neostigmine, reversed all three variables partially or completely. These results support the hypothesis that all three consequences of scopolamine, namely, reduction of mean flow, frontal deficit, and memory impairment, are cholinergically mediated. Furthermore, because neostigmine poorly crosses the blood-brain barrier, these findings confirm that the effect is centrally mediated and cannot be explained by peripheral effects. However, they also confirm the frontal cortex locus of action for both scopolamine and its reversal by physostigmine and therefore suggest a major dissimilarity to the characteristic rCBF appearance of AD. This study extends our previous preliminary findings with tacrine and strengthens the suggestion that only nicotinic receptors are associated with the characteristic parietal deficit of AD.

Acetylcholine↗

PubMed1986

Premedication for day-case surgery: double-blind comparison of ketobemidone + dimethylaminodiphenylbuten (A-29) and morphine + scopolamine.

A double-blind comparison of the effect of Ketogan (ketobemidone and A-29, an anticholinergic and spasmolytic agent) and morphine + scopolamine as premedication was performed in 113 women admitted for abortion and in 114 women admitted for gynaecological dilatation and curettage. Anaesthesia was thiopentone and nitrous oxide and oxygen, occasionally supplemented with enflurane. It was found that 1 ml morphine + scopolamine (10 mg + 0.4 mg) was more sedative than 1 ml ketogan (ketobemidone 5 mg + A-29 25 mg). After ketogan there was less nausea and dryness of the mouth before induction of anaesthesia than after morphine + scopolamine. Ketogan had the same tranquillizing effect but less hypnotic effect preoperatively than morphine + scopolamine. During the 3-h postoperative observation period the patients premedicated with ketogan woke up significantly sooner and had more pain than those given morphine + scopolamine. More patients required postoperative antiemetics in the ketogan-premedicated group than in the morphine + scopolamine-premedicated group.

Abortion, Legal↗

PubMed1992

Scopolamine effects on visual information processing, attention, and event-related potential map latencies.

We measured performance and event-related brain potential (ERP) map latencies in 12 subjects during four visual discrimination tasks to compare the timing of scopolamine effects on information processing and attention. "Topographic component recognition" found ERP map latencies at times of best fit with a component model map. This "common topography" criterion minimized topographic differences among conditions to facilitate latency interpretations. Scopolamine slowed N1 latency in all tasks, and P3 and reaction time in some tasks. The drug delayed responses to easy targets more than to hard targets. It also induced a disproportionate N1 delay for unilateral high spatial frequency gratings. Both effects reflect a scopolamine-induced impairment when processing targets that usually capture attention. Scopolamine also impaired accuracy for unilateral high spatial frequency gratings, and for gratings presented at probable locations, confirming and extending previous findings. Scopolamine-induced P1 and N1 delays showed that visual processing was affected. Several results were inconsistent with a serial stage model. We suggest that scopolamine both delays selected processes and impairs a processing mode based on automatic capture of attention, inducing more serial processing.

Adult↗

PubMed1978

Electrocorticographic effects of topically applied scopolamine.

The electrocorticographic effects of topically applied scopolamine were investigated in unanesthetized cats with high cervical transection. After subpial injection of 30 cumu scopolamine in concentrations of 10 to 20%, large amplitude intermittent sharp waves appeared in the electrocorticogram, which developed into long-lasting paroxysmal activity. This effect was antagonized by intravenous eserine, 0.1 mg/kg, when it was produced by topical scopolamine in low dosage. The acoustically evoked cortical response and the generalized epileptiform activity produced by topical succinylcholine disappeared after topical scopolamine in low dosage. It is suggested that the seizure-suppressing effect of scopolamine may be due to its cholinolytic action. The convulsive activity of topical scopolamine in high concentrations may be accounted for by its depolarizing, synchronizing, disinhibiting, and acetylcholine-releasing effects.

Administration, Topical↗

PubMed1997

Effect of low-dose scopolamine on autonomic control of the heart.

BACKGROUND: In low doses, scopolamine paradoxically enhances parasympathetic outflow to the heart. The mechanisms which mediate this action are not fully understood. Moreover, there are conflicting data regarding the potential role of sympathetic activity. This study in 17 healthy individuals was designed to characterize the influence of low dose transdermal scopolamine on the gain of the baroreflex and respiratory heart rate reflex and to determine the role of sympathetic activity. METHODS: The effect of scopolamine was analyzed in the time and frequency domain by computing heart rate variability indices. The gains of the respiratory heart rate reflex and the baroreflex were estimated simultaneously by means of a cardiovascular system identification approach using an optimized autoregressive moving average algorithm. Measurements were repeated in the upright posture to assess the influence of enhanced sympathetic activity. In six subjects ambulatory ECGs were recorded to determine whether there are diurnal variations of the effect of scopolamine. RESULTS: Scopolamine enhances vagal modulation of heart rate through both the respiratory-heart rate reflex and the baroreflex, as the gains of both were augmented by the drug in the supine and in the upright postures. CONCLUSIONS: Scopolamine increases parasympathetic cardiac control by augmenting the gain of the respiratory-heart rate and baroreflex. This action is not attenuated in the upright posture when sympathetic tone is increased.

Administration, Cutaneous↗

PubMed1986

Effects of transdermal scopolamine, alone or in combination with cimetidine, on total 24 hour gastric acid secretion in patients with duodenal ulcer.

Transdermal scopolamine is an antimuscarinic preparation approved for use in the United States for prevention of motion sickness. A recent study using this drug (0.5 mg/patch) suggested that enough scopolamine was absorbed through the skin to reduce basal gastric acid secretion in patients with duodenal ulcer. We have compared the effect of transdermal scopolamine and oral cimetidine (400 mg twice daily) in seven men with chronic duodenal ulcer, both alone and in combination, on acid secretion throughout an entire 24 hour period in a placebo-controlled, randomised, double blinded cross over study. The effect of these drugs on basal, interprandial, and nocturnal gastric juice volume and hydrogen ion concentration also was measured. Transdermal scopolamine had no significant effect on mean 24 hour acid secretion (placebo, 409.4 mmol/day; scopolamine, 364.0 mmol/day) nor did it have a significant effect on gastric juice volume or hydrogen ion concentration. The combination of transdermal scopolamine plus cimetidine was not more effective than cimetidine alone in reducing total 24 hour acid secretion (mean, 231.8 versus 235.3 mmol/day) nor in reducing gastric juice volume or hydrogen ion concentration.

Administration, Cutaneous↗

PubMed1996

Effect of low doses of scopolamine on RR interval variability, baroreflex sensitivity, and exercise performance in patients with chronic heart failure.

OBJECTIVE: To study the effect of transdermal scopolamine on heart rate variability, baroreflex sensitivity, and exercise performance in patients with heart failure and age matched healthy volunteers. DESIGN: Double blind, randomised, placebo controlled, crossover study. PATIENTS: 16 patients with chronic, stable heart failure due to ischaemic cardiomyopathy (mean (SEM) age 58 (2) years; mean (SEM) radionuclide left ventricular ejection fraction 28 (2)%; New York Heart Association class II-III) and eight age matched healthy controls. INTERVENTION: Transdermal scopolamine (500 micrograms delivered over 72 h) or a placebo patch was administered for 48 h. MAIN OUTCOME MEASURES: Indices of tonic and reflex cardiac vagal activity and exercise performance. RESULTS: In both groups scopolamine produced a reduction in the 24 h average heart rate and an increase in the time domain measures of heart rate variability. Both the incidence and severity of ventricular arrhythmias remained unchanged. Baroreflex sensitivity, evaluated by the phenylephrine technique, increased significantly (P < 0.001) with scopolamine in patients with heart failure (6.22 (2.81) ms/mm Hg) and in healthy volunteers (5.97 (2.20) ms/mm Hg) as did the amplitude of respiratory sinus arrhythmia, computed by autoregressive spectral analysis of 10 min electrocardiographic recordings (319.9 (123.5) and 657.3 (126.6) ms2 respectively, P < 0.001). While exercise performance did not change, heart rate at submaximal exercise was significantly reduced by scopolamine in each group. CONCLUSIONS: In patients with mild to moderate heart failure low doses of scopolamine increased tonic and reflex cardiac vagal activity. This was achieved without affecting exercise tolerance or the incidence and severity of ventricular arrhythmias.

Baroreflex↗

PubMed2001

The effects of dimenhydrinate, cinnarizine and transdermal scopolamine on performance.

We assessed the influence of dimenhydrinate, cinnarizine and transdermal scopolamine on the ability to perform simulated naval crew tasks. The effect of single doses of dimenhydrinate, 100 mg, cinnarizine, 50 mg, and one transdermal scopolamine patch on psychomotor performance was evaluated using a double-blind, placebo-controlled, randomized, crossover design in three separate studies. A total of 60 young naval crew (20 for dimenhydrinate, 15 for cinnarizine and 25 for transdermal scopolamine) underwent a battery of computerized and paper and pencil performance tests, and filled out a questionnaire on side-effects and well-being self-assessment. Dimenhydrinate significantly impaired decision reaction time and auditory digit span. Most of the subjects who took dimenhydrinate also reported a subjective decrease in well-being and general performance abilities. Cinnarizine and transdermal scopolamine did not affect performance abilities. Cinnarizine was free of significant side-effects. Dry mouth was the only significant side-effect of transdermal scopolamine. These findings could be explained by the well-known sedative properties of dimenhydrinate and not by a specific effect on any particular cognitive or motor function. Our results suggest that dimenhydrinate, 100 mg, adversely affects psychomotor function, whereas single doses of cinnarizine, 50 mg, and transdermal scopolamine appear to be free of side-effects on performance and seem to be a preferable anti-seasickness drug for use by a naval crew.

Administration, Cutaneous↗

PubMed2002

Nimodipine prevents scopolamine-induced impairments in object recognition.

The effects of acute administration of the dihydropyridine calcium channel antagonist, nimodipine, were studied on the actions of scopolamine in the object recognition test. Scopolamine at 0.125 mg/kg decreased the difference in the time spent exploring novel and familiar objects when given either 15 min before, or immediately after, exposure to objects. Administration of nimodipine at 10 mg/kg, or 1 mg/kg, at the same time as the scopolamine completely prevented the deleterious effects on memory in this task. This effect was seen when nimodipine and/or scopolamine were given prior to the object exposure and also when the drugs were given after the experience of seeing the objects. Nimodipine had no effects on performance when given in the absence of scopolamine. This lack of change in total time spent exploring the objects indicated that the effects of scopolamine and nimodipine were not due to changes in motor coordination or alertness. The results are discussed in the light of the role of cholinergic transmission in memory and the known actions of dihydropyridines on brain function.

Animals↗

PubMed1987

A controlled clinical trial of the addition of transdermal scopolamine to a standard metoclopramide and dexamethasone antiemetic regimen.

A randomized prospective clinical trial was conducted to evaluate the potential utility of adding transdermal scopolamine to a standard regimen of metoclopramide and dexamethasone for the prevention of cisplatin-induced emesis. Thirty-one patients who were about to receive their first cycle of chemotherapy, using a combination regimen including cisplatin at a dose greater than or equal to 60 mg/m2 were randomized to receive an antiemetic regimen of either metoclopramide and dexamethasone alone, or these two drugs plus transdermal scopolamine patches. The mean number of episodes of emesis was .63 +/- 1.31 in the 16 scopolamine-treated patients, and 2.27 +/- 2.66 in the 15 patients who did not receive scopolamine (P less than .01). The scopolamine appeared to inhibit extrapyramidal reactions to the metoclopramide, but the number of cases was too small for statistical significance. We conclude that the addition of transdermal scopolamine to a standard metoclopramide and dexamethasone antiemetic regimen provides additive benefit in the control of cisplatin-induced emesis.

Administration, Cutaneous↗

PubMed1989

Prophylactic transdermal scopolamine patches reduce nausea in postoperative patients receiving epidural morphine.

To evaluate the efficacy of prophylactic transdermal scopolamine in reducing nausea associated with postoperative epidural analgesia, we studied 32 healthy adult women undergoing major gynecologic surgery. The patients were randomized in a double blind fashion to receive either a cutaneous scopolamine patch or a visually identical cutaneous placebo patch. Postoperative analgesia was provided solely with epidural morphine. Nausea was treated with metoclopramide and droperidol. At 24 hours postoperatively, the mean nausea score was significantly lower with scopolamine than with placebo (1 +/- 2 vs 51 +/- 42, respectively, P less than 0.05). The number of patients reporting "zero nausea" was significantly greater with scopolamine patches than with placebo patches (13 vs 1, P less than 0.01). The mean number of times antiemetic drugs were administered per patient was lower with scopolamine than with placebo patches (0.2 +/- 0.4 vs 2.8 +/- 2.6, P less than 0.05). It is concluded that prophylactic transdermal scopolamine patches reduce nausea in postoperative patients receiving epidural morphine.

Administration, Cutaneous↗

PubMed1983

Circadian variation in susceptibility to the ambulation-increasing effect of scopolamine in mice.

Circadian variation in susceptibility to the ambulation-increasing effect of scopolamine in mice was investigated. The mice housed under a 12-hr light-dark situation (light period: 6:00-18:00 and dark period: 18:00-6:00) for 5 weeks were administered scopolamine HBr at 0.5 or 2 mg/kg s.c. at one of six times of the day (3:00, 7:00, 11:00, 15:00, 19:00 and 23:00), and the ambulatory activity was measured for 2 hr. Scopolamine induced a dose-dependent increase in the ambulatory activity. In addition, there was a clear circadian variation in the susceptibility to the ambulation-increasing effect of scopolamine. The highest and the lowest overall activity counts during the 2 hr observation period were found when the drug was administered at 3:00 and 15:00, respectively. The present results suggest that the susceptibility to scopolamine in mice is dependent on the time-of-day at which the drug is administered. The reasons which may induce this circadian variation in susceptibility to scopolamine are discussed.

Animals↗