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PubMed1988

Response of heart rate to atropine and left ventricular function in Chagas' heart disease.

Chagasic patients may have a normal or abnormal response of heart rate to atropine. To determine if this response to atropine is related to the degree of left ventricular dysfunction, we studied 33 patients with a positive complement fixation test for Chagas' disease. Eleven subjects, with atypical chest pain and negative complement fixation test, were used as controls (sero-negative). Left ventricular wall motion and the left ventricular volumes were determined by ventricular cineangiography. Coronary arteriography was also performed. The sero-negative subjects had normal left ventricular wall motion and the left ventricular diastolic volume was 88 +/- 24 ml/m2. The response of heart rate to atropine was 50 +/- 8 (mean +/- SD) (range 40-65 beats/min). On the basis of the response to atropine, the chagasic patients were divided into groups with a normal response (greater than 40 beats/min) and those with an abnormal response (less than 40 beats/min). Sixty five per cent of those with a normal response had left ventricular apical aneurysms. The left ventricular end-diastolic volume was not significantly different from the sero-negative subjects (96 +/- 26 ml/m2). Six patients (30%) had a left ventricular diastolic volume between 110 and 140 ml/m2. Sixty two per cent of those chagasic subjects with an abnormal response had diffuse left ventricular hypokinesis, and the left ventricular end-diastolic volume was 192 +/- 49 ml/m2 (P less than 0.01). The response of heart rate and the left ventricular diastolic volume were inversely correlated in the chagasic patients (r = -0.88, P less than 0.01). Our results indicate that myocardial damage and the degree of left ventricular dilatation are more severe in chagasic patients with an abnormal response of their heart rate to atropine. Furthermore, the inverse correlation between these two variables is highly indicative of a relationship between the response of heart rate to atropine and the degree of left ventricular dysfunction.

Adult↗
PubMed1992

Reduction by pyridostigmine pretreatment of the efficacy of atropine and 2-PAM treatment of sarin and VX poisoning in rodents.

This study concerned the effect of pyridostigmine pretreatment on (a) the antidotal efficacy of atropine and 2-PAM in sarin, tabun, and VX poisoning in mice and guinea pigs and on (b) the oxime-induced reactivation of VX-inhibited whole blood acetylcholinesterase (AChE) of guinea pigs. One hour prior to organophosphate (OP) challenge with sarin, tabun, or VX, animals were given oral doses of pyridostigmine to induce approximately 30 and 60% inhibition of whole blood AChE; controls received vehicle. Mice were challenged im and guinea pigs sc with the OP compounds. Treatment with atropine (11.2 mg/kg to mice; 32 mg/kg to guinea pigs) plus 2-PAM (25 mg/kg) was given im at 10 sec postchallenge in mice and 1 min postchallenge in guinea pigs. In the reactivation experiments, pyridostigmine or saline was given im to guinea pigs 30 min prior to VX (8.24 micrograms/kg, sc), atropine (16 mg/kg) was given im at 1 min, and 2-PAM (25 mg/kg) at 16 min postchallenge. Pyridostigmine significantly enhanced the efficacy of atropine and 2-PAM against tabun in both species. In contrast, pyridostigmine reduced or did not increase the efficacy of atropine and 2-PAM against sarin or VX in both species. Recovery of VX-inhibited AChE by 2-PAM was decreased significantly in pyridostigmine pretreated animals. The results suggest that pyridostigmine pretreatment may adversely effect the efficacy of atropine and 2-PAM as antidotes for VX and sarin intoxication.

Acetylcholinesterase↗
PubMed1987

Motor activity of the rat duodenum in vivo: evidence for the existence of an atropine-resistant peristalsis.

The motor activity of the proximal duodenum has been investigated by means of a balloon method in urethane-anaesthetized rats. A series of atropine- (1 mg/kg i.v.) or hexamethonium- (20 mg/kg i.v.) sensitive rhythmic contractions can be demonstrated in the rat duodenum which represents a peristaltic reflex mediated by intramural cholinergic neurons. The atropine-sensitive peristaltic reflex is transiently suppressed by intravenous DMPP (0.1 mg/kg) GABA (3 mg/kg) or noradrenaline (10 micrograms/kg). In rats pretreated with guanethidine (20 mg/kg s.c.) plus naloxone (2 mg/kg i.v.) and theophylline (2 mg/kg i.v.) a second type of peristaltic reflex which is atropine-resistant but hexamethonium-sensitive can be demonstrated. These findings indicate that in the rat small intestine a peristaltic activity can be sustained by both atropine-sensitive and atropine-resistant mechanism, which may explain failure of atropine to affect intestinal motility in conscious rats.

Animals↗
PubMed1988

Effects of atropine and glycopyrrolate on neuromuscular transmission in the rat phrenic nerve-diaphragm preparation.

1. The effects of atropine and glycopyrrolate on neuromuscular transmission and on muscle contraction, were studied, in the rat diaphragm preparation, by analyzing their effects on the indirectly (and directly)-elicited twitch (0.2 Hz), tetanic (50 Hz for 20 sec duration), post-tetanic twitch responses (at 5 sec after the tetanus), and on the phenomenon of post-tetanic twitch potentiation (PTP), which is thought to be of a presynaptic origin, i.e. due to increased transmitter release. 2. Atropine (0.001-10 microM) increased the indirectly-elicited twitch tension by 22 +/- 2.1% (control 0.9 +/- 0.1 g, P less than 0.02), the tetanus by 15 +/- 1.1% (control 3.9 +/- 0.7 g, P less than 0.05), the post-tetanic twitch response by 33 +/- 3.1% (control 1.2 +/- 0.1 g, P less than 0.01) and the PTP value by 36 +/- 1.9% (control 33 +/- 2.3%, P less than 0.01, means +/- SEM = 6). 3. Atropine (0.001-10 microM) had little effect on the directly-elicited twitch tension, but in high concentrations (e.g. 20 microM), it blocked the twitch tension. 4. In contrast, glycopyrrolate (0.1-100 microM) had little effect on the twitch tension (direct or indirect), but it significantly reduced the tetanus (by 38 +/- 3.5%, P less than 0.01), the post-tetanic twitch response (by 17 +/- 1.2%, P less than 0.05) and the PTP values (by 24 +/- 3.1% P less than 0.02). 5. In the presence of hemicholinium (1.3 microM) the responses to atropine and glycopyrrolate were altered (decreased), indicating a possible action on presynaptic mechanism of transmission. 6. It is concluded that atropine and glycopyrrolate produce different (opposite) effects at the rat neuromuscular junction, atropine enhances whereas glycopyrrolate depresses neuromuscular transmission. The effects of these two antimuscarinic drugs may be exerted at the presynaptic nerve terminals, i.e. on presynaptic muscarinic receptors, which are involved in the feedback mechanism of transmitter release.

Animals↗
PubMed1995

Effect of atropine on cyanide-induced acute lethality in mice.

The effects of atropine on acute lethality induced by cyanide were investigated in mice. The LD50 value of cyanide (s.c. injection) was 8.4 (7.6-9.3) mg/kg. However, the LD50 value of cyanide (s.c.) was significantly increased by 1.5-fold when atropine (32 mg/kg) was injected s.c. in mice. Furthermore, the combined administration of atropine (32 mg/kg), Ca2+ (500 mg/kg) and sodium thiosulfate (1 g/kg) tremendously increased the LD50 value by 5.6-fold in mice although sodium thiosulfate or Ca2+ alone increased the LD50 2.5- or 1.5-fold. On the other hand, although the LD50 value of cyanide (intracerebroventricular injection (i.v.t.)) was 52.0 (47.4-57.0) micrograms/brain, the LD50 value of cyanide (i.v.t.) was significantly increased by 1.3- or 1.61-fold in mice 10 min after s.c. injection of atropine (32 mg/kg) or Ca2+ (500 mg/kg). Furthermore, the combined administration of atropine and Ca2+ increased the LD50 value of cyanide by 2.1-fold. These results suggest that atropine inhibits cyanide-induced acute lethality and promotes the antagonistic effect of thiosulfate and Ca2+ in mice.

Animals↗
PubMed1987

Pharmacological properties of the atropine-resistant contraction of the carp (Cyprinus carpio) intestinal bulb induced by transmural stimulation.

1. The pharmacological properties of the atropine-resistant contraction of the carp intestinal bulb induced by transmural stimulation were investigated. 2. In the presence of atropine (1 microM), transmural stimulation caused frequency-dependent (2-50 Hz) contraction which was abolished by tetrodotoxin (780 nM). 3. The atropine-resistant contraction was not decreased by tubocurarine (5 microM), hexamethonium (100 microM), carteolol (5 microM) and phentolamine (5.4 microM). 4. In vitro pretreatment with guanethidine (10 microM for 1 hr) markedly decreased the noradrenaline and adrenaline contents of the carp intestinal bulb. The atropine-resistant contraction was not affected by pretreatment with guanethidine. 5. Diphenhydramine (1 microM), methysergide (3 microM) and naloxone (1 microM) did not decrease the atropine-resistant contraction, indicating that histamine, 5-hydroxytryptamine and opioid peptides were not involved in the atropine-resistant response. 6. These results indicate that a non-cholinergic, non-adrenergic excitatory nerve is present in the carp intestinal bulb. The neurotransmitter mediating the excitatory response could not be identified.

Animals↗
PubMed2004

A randomized trial of atropine regimens for treatment of moderate amblyopia in children.

OBJECTIVE: To compare daily atropine to weekend atropine as prescribed treatments for moderate amblyopia in children younger than 7 years. DESIGN: Prospective, randomized multicenter clinical trial (30 sites). PARTICIPANTS: One hundred sixty-eight children younger than 7 years with amblyopia in the range of 20/40 to 20/80 associated with strabismus, anisometropia, or both. INTERVENTION: Randomization either to daily atropine or to weekend atropine for 4 months. Partial responders were continued on the randomized treatment until no further improvement was noted. MAIN OUTCOME MEASURE: Visual acuity (VA) in the amblyopic eye after 4 months. RESULTS: The improvement in VA of the amblyopic eye from baseline to 4 months averaged 2.3 lines in each group. The VA of the amblyopic eye at study completion was either (1) at least 20/25 or (2) better than or equal to that of the sound eye in 39 children (47%) in the daily group and 45 children (53%) in the weekend group. The VA of the sound eye at the end of follow-up was reduced by 2 lines in one patient in each group. Stereoacuity outcomes were similar in the 2 groups. CONCLUSIONS: Weekend atropine provides an improvement in VA of a magnitude similar to that of the improvement provided by daily atropine in treating moderate amblyopia in children 3 to 7 years old. This article contains additional online-only material available at http://www.ophsource.com/periodicals/ophtha.

Amblyopia↗
PubMed1999

Effect of atropine on QT prolongation and torsade de pointes induced by intracoronary acetylcholine in the long QT syndrome.

We recently reported a marked QT prolongation and torsade de pointes (TDP) induced by an intracoronary acetylcholine (ACh) administration in patients with long QT syndrome, but the mechanism was not determined. In the present study, the effect of atropine on the ACh-induced QT prolongation and TDP was studied in long QT syndrome. Nine patients with congenital long QT syndrome were studied. ACh at doses of 20, 50, and 100 microg were injected in a stepwise manner into the left main coronary artery, and the changes in the QT interval were measured. In 4 of the 9 patients, ACh administration at a dose of 100 microg was repeated after an intravenous atropine administration at a dose of 0.5 mg. The QT intervals were measured using 12-lead electrocardiograms, and the data were compared before and after atropine administration. The coronary angiograms were normal and coronary spasm was not induced by ACh in all patients. The intracoronary administration of ACh at a dose of 100 microg significantly prolonged the corrected QT interval (QTc), from 511 +/- 26 to 629 +/- 40 ms (p <0.05). In 5 of the 9 patients, TDP was induced and was spontaneously terminated within 10 seconds (n = 4) or required direct-current shock (n = 1). After atropine administration, intracoronary ACh at the same dose resulted in no QT prolongation, and the QTc interval remained unchanged (525 +/- 29 vs 520 +/- 21 ms before and after atropine), and no TDP was induced. These findings indicate that the muscarinic receptor is involved in ACh-induced QT prolongation and TDP, both of which were prevented by the atropine administration.

Acetylcholine↗
PubMed1983

Efficacy of atropine as an endoscopic premedication.

To determine the efficacy of atropine as an endoscopic premedication, we prospectively evaluated in double-blind fashion 196 elective endoscopies performed on 189 consecutive consenting patients. Group 1 (95 endoscopies) received meperidine, 1.5 mg/kg, intramuscularly 30 min prior to endoscopy. Group 2 (101 endoscopies) additionally received atropine, 0.6 mg, in the same injection. Endoscopy was performed by one of two investigators using a 13-mm fiberoptic instrument. Endoscopists and patients filled out postendoscopy questionnaires. Both endoscopists (p less than 0.01) and patients (p less than 0.05) noted less oral secretions after atropine. Endoscopists noted less gastric motility after atropine (p less than 0.05) and guessed correctly whether or not atropine had been given in two thirds of cases. They noted no overall difference, however, in the ease of the endoscopy (p greater than 0.05). Moreover, there were no differences in the patients' assessments of the acceptability of the procedure between the two groups (p greater than 0.05). We concluded that although atropine does not improve patients' tolerance for the examination or the endoscopists' ability to do an adequate examination, it does objectively decrease the amount of gastric motility and oral secretions. This latter effect could potentially decrease the hazard of aspiration, but such a benefit could not be demonstrated in our series.

Adolescent↗
PubMed1995

A placebo-controlled trial using intravenous atropine as an adjunct to conscious sedation in pediatric esophagogastroduodenoscopy.

BACKGROUND: The usefulness of intravenous atropine as an adjunct to conscious sedation in pediatric esophagogastroduodenoscopy remains an unresolved issue. METHODS: This prospective, double-blind, randomized study examined 101 patients, who were randomized to receive either intravenous atropine 0.02 mg/kg (maximum 0.4 mg) or a placebo of normal saline solution prior to the procedure. RESULTS: The mean maximum heart rate during the procedure and the percentage of time that the heart rate was more than 1 standard deviation above mean for age was significantly greater in the atropine group as compared to the placebo group (p < 0.0005). There was no significant difference between groups in the amount of secretions noted, gastric motility, retching or vomiting, facial flushing, or dysphoria. There were no causes of significant bradycardia or hypotension in either group. There was a significant number of patients greater than 5 years of age and receiving meperidine and atropine (as compared with meperidine and placebo) whose arterial oxygen saturation dropped below 90% during the procedure (p = 0.0485). CONCLUSIONS: We found that the use of atropine when used as an adjunct to conscious sedation in children undergoing upper endoscopy did not increase the safety of the procedure or provide significant benefits. We do not recommend the routine use of atropine for upper endoscopy in pediatric patients.

Adjuvants, Anesthesia↗
PubMed1997

Serum anticholinergic activity and behavior following atropine sulfate administration in the rat.

Anticholinergic agents such as atropine and scopolamine have long been suggested to produce delirium-like states in humans and experimental animals. Evidence for an anticholinergic mechanism in the pathogenesis of human delirium has accumulated, leading to studies of the behavioral effects of the anticholinergic drug atropine in animals. The current study addresses the adequacy of animal models of delirium in terms of sensitivity, specificity and pharmacological relevance. A multiple fixed-ratio fixed-interval reinforcement schedule was used to test the effects of relatively low doses of atropine on behavior in rats. Additionally, total serum anticholinergic activity (SAA) was measured under dose and time course conditions identical to those used in the behavioral study. Atropine reduced high and low rates of responding in a dose-dependent manner, and SAA increased in a dose dependent manner. SAA at atropine doses of 0.1 mg/kg to 1.0 mg/kg was similar to that found in delirious humans. These behavioral and serum level data suggest that relatively low doses of atropine, substantially below those used in previous attempts to model delirium using rats, may be more pharmacologically relevant to delirium and may minimize non-specific peripheral effects of this drug.

Animals↗
PubMed1981

Cycloplegic refraction in esotropic children. Cyclopentolate versus atropine.

Retinoscopy was performed on a population of predominantly white esotropic children younger than 5.5 years with cyclopentolate 1% and atropine 1.0%. Atropine 1.0% revealed +0.34 diopters more hyperopia than cyclopentolate 1.0%, when the mean differences between the two drugs were examined. Mean difference analysis would probably indicate that atropine retinoscopy was unnecessary. However, 22% of the children had +1.0 diopters or more of hyperopia uncovered by atropine. This significant subpopulation suggests that in young patients with esotropia, an atropine refraction is essential to uncover the maximum amount of hyperopia. Almost all of this subgroup with +1.00 or greater hyperopia had an initial cyclopentolate retinoscopy of +2.00 diopters or more. Therefore, retinoscopy using atropine cycloplegia becomes even more important in this population. There was a trend for the greater differences to be in children older than age 2 years. However, these values were not statistically significant.

Accommodation, Ocular↗
PubMed1991

Systemic atropine administration during cardiac arrest does not cause fixed and dilated pupils.

OBJECTIVES: Systemic administration of atropine during CPR may postpone brain death determination because of its reputed ability to produce fixed and dilated pupils. We studied the effect of atropine administered in the usual doses as an adjunct to endotracheal intubation and for cardiac arrest to determine if it would interfere with neurological assessment. DESIGN: Two groups of children were studied. Group 1 consisted of 28 patients who received atropine (0.03 +/- 0.003 mg/kg) prior to endotracheal intubation. Group 2 consisted of 21 patients previously without evidence of brainstem disease who suffered a witnessed arrest and had prompt return of spontaneous circulation and received an atropine dose of 0.03 +/- 0.01 mg/kg. RESULTS: In group 1, pupillary size averaged 4.02 +/- 0.78 mm before and 4.75 mm +/- .84 mm after atropine (P less than .001). In group 2, the pupillary examination was conducted 30 minutes after return of spontaneous circulation. The pupillary diameter was 4.80 +/- 0.91 mm. All pupils were reactive to light in both groups. CONCLUSION: Atropine administration in conventional dose causes slight pupillary dilation but does not abolish pupillary light reactivity.

Adolescent↗
PubMed1984

Atropine: animal models.

Bradyarrhythmias, with or without hypotension, may be associated with acute myocardial infarction, especially inferior. The early use of atropine in the management of sinus bradycardia, with associated hypotension, spurred a continuing controversy that has found only partial solution in animal models. Experimentally there is increased sensory and autonomic motor activity with acute coronary occlusion. For example, in the cat, increased cholinergic activity was evidenced by the absence of bradycardia with atropinization and vagotomy, although these pretreatments accelerated the onset of significant ventricular arrhythmias. Atropine in experimentally infarcted dogs increased ischemia, while elevated heart rates reduced the threshold for ventricular fibrillation (VF) and vagal stimulation increased the threshold for VF, largely independent of heart rate. Specific clinical studies failed to support much of the animal data, although reports of tachyarrhythmias and VF resulting from the administration of atropine extended the controversy. The animal models, in the main, failed to mimic the clinical situation, for: 1) pentobarbital, with its propensity to alter some autonomic reflexes, dominated earlier work; 2) relatively large doses of atropine were employed; 3) the animals were presumed to be free of coronary and cardiac disease, factors known to influence autonomic reflexes; and 4) vagotomy and atropinization commonly preceded the acute occlusion.

Animals↗
PubMed2003

Comparative efficacy of diazepam and avizafone against sarin-induced neuropathology and respiratory failure in guinea pigs: influence of atropine dose.

This investigation compared the efficacy of diazepam and the water-soluble prodiazepam-avizafone-in sarin poisoning therapy. Guinea pigs, pretreated with pyridostigmine 0.1 mg/kg, were intoxicated with 4LD(50) of sarin (s.c. route) and 1 min after intoxication treated by intramuscular injection of atropine (3 or 33.8 mg/kg), pralidoxime (32 mg/kg) and either diazepam (2 mg/kg) or avizafone (3.5 mg/kg). EEG and pneumo-physiological parameters were simultaneously recorded. When atropine was administered at a dose of 3 mg/kg, seizures were observed in 87.5% of the cases; if an anticonvulsant was added (diazepam (2 mg/kg) or avizafone (3.5 mg/kg)), seizure was prevented but respiratory disorders were observed. At 33.8 mg/kg, atropine markedly increased the seizure threshold and prevented early respiratory distress induced by sarin. When diazepam was administered together with atropine, seizures were not observed but 62.5% of the animals displayed respiratory difficulties. These symptoms were not observed when using avizafone. The pharmacokinetic data showed marked variation of the plasma levels of atropine and diazepam in different antidote combination groups, where groups receiving diazepam exhibited the lowest concentration of atropine in plasma. Taken together, the results indicate that avizafone is suitable in therapy against sarin when an anticonvulsant is judged necessary.

Animals↗
PubMed2000

Dobutamine-atropine stress echocardiography and dipyridamole sestamibi scintigraphy for the detection of coronary artery disease: limitations and concordance.

OBJECTIVES: We sought to compare dobutamine-atropine stress echocardiography (DASE) and dipyridamole Technetium 99-m (Tc-99m) sestamibi single photon emission computed tomography (SPECT) scintigraphy (DMIBI) for detecting coronary artery disease (CAD). BACKGROUND: Both DASE and DMIBI are effective for evaluating patients for CAD, but their concordance and limitations have not been directly compared. METHODS: To investigate these aims, patients underwent multistage DASE, DMIBI and coronary angiography within three months. Dobutamine-atropine stress echocardiography and stress-rest DMIBI were performed according to standard techniques and analyzed for their accuracy in predicting the extent of CAD. Segments were assigned to vascular territories according to standard models. Angiography was performed using the Judkin's technique. RESULTS: The 183 patients (mean age: 60 +/- 11 years, including 50 women) consisted of 64 patients with no coronary disease and 61 with single-, 40 with two- and 18 with three-vessel coronary disease. Dobutamine-atropine stress echocardiography and DMIBI were similarly sensitive (87%, 104/119 and 80%, 95/119, respectively) for the detection of CAD, but DASE was more specific (91%, 58/64 vs. 73%, 47/64, p < 0.01). Sensitivity was similar for the detection of CAD in patients with single-vessel disease (84%, 51/61 vs. 74%, 45/61, respectively) and multivessel disease (91%, 53/58 vs. 86%, 50/58, respectively). Multiple wall motion abnormalities and perfusion defects were similarly sensitive for multivessel disease (72%, 42/58 vs. 66%, 38/53, respectively), but, again, DASE was more specific than DMIBI (95%, 119/125 vs. 76%, 95/125, respectively, p < 0.01). Dobutamine-atropine stress echocardiography and DMIBI were moderately concordant for the detection and extent of CAD (Kappa 0.47, p < 0.0001) but were only fairly (Kappa 0.35, p < 0.001) concordant for the type of abnormalities (normal, fixed, ischemia or mixed). CONCLUSIONS: Dobutamine-atropine stress echocardiography and DMIBI were comparable tests for the detection of CAD. Both were very sensitive for the detection of CAD and moderately sensitive for the extent of disease. The only advantage of DASE was greater specificity, especially for multivessel disease. Dobutamine-atropine stress echocardiography may be advantageous in patients with lower probabilities of CAD.

Atropine↗
PubMed1999

Visual acuity after cycloplegia in children: implications for atropine penalization.

BACKGROUND: Atropinization of the sound eye is an alternative to patching in the treatment of amblyopia. Whether atropine treatment can induce a switch in fixation depends on the refractive error of the sound eye, visual acuity of the amblyopic eye, distance from the fixation target, and presence of any optical correction or penalization. General guidelines are needed on the basis of refractive error and visual acuity in the amblyopic eye to predict which patients may potentially benefit from atropine penalization. METHODS: Refractive error and visual acuity at distance (6 m) and/or at near (33 cm) were recorded in a normal eye of 126 consecutive children (mean age, 8.2 years), 30 to 60 minutes after receiving cyclopentolate 1%. Visual acuity was plotted versus refractive error at distance and at near, and best-fit curves were calculated. RESULTS: There was a consistent, reproducible relationship between refractive error and visual acuity after cycloplegia at both distance and near in healthy children. CONCLUSIONS: The results of this study can be used to quickly determine whether atropine penalization has the potential for success on the basis of a patient's visual acuity in the amblyopic eye and refractive error in the sound eye. When adequate hyperopia is present in the sound eye, one should consider testing for fixation preference or initiating a therapeutic trial of atropine. Those children with insufficient hyperopia in the sound eye relative to visual acuity in the amblyopic eye can be spared the time, expense, and potential side effects of atropine penalization.

Adolescent↗
PubMed2000

Solvent extraction coupled on-line to a reversed micellar mediated chemiluminescence detection system for trace-level determination of atropine.

A fast and sensitive method for the determination of atropine, an alkaloid closely related to cocaine, is proposed. The principles of on-line ion-pair formation of alkaloid-metal complexes and liquid-liquid extraction are applied to the chemiluminescence determination of atropine. On mixing with a reversed micellar medium of cetyltrimethylammonium chloride in dichloromethane-cyclohexane (1:1 v/v)-water (0.3 M Na2CO3) containing luminol, the ion-pair complex of tetrachloroaurate(III) with atropinium produced an analytical chemiluminescence signal when it entered the reversed micellar water pool. Using the reverse-flow injection and chemical conditions optimized for atropine in aqueous samples, a detection limit of 1 ng/mL was achieved and a linear calibration graph was obtained with a wide dynamic range from 10 ng/mL to 100 micrograms/mL. The proposed method is simple and provides a good precision with a relative standard deviation (n = 6) of ca. 3% at the atropine concentration of 100 ng/mL. After a preliminary study involving the potential interference from species of organic, inorganic, and metallic nature, the method was applied to the determination of atropine in artificial urine samples and of atropine and scopolamine in pharmaceutical formulations.

Atropine↗