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PubMed1995

[Use of high doses of atropine during dipyridamole echocardiography: safety and efficacy of the combined test].

BACKGROUND: Recent reports demonstrated an increased accuracy of dipyridamole echocardiography test with the intravenous infusion of 0.25 to 1 mg of atropine in 1-4 consecutive administrations at the end of the test. The effect of higher doses of atropine during dipyridamole echocardiography, potentially able to further increase heart rate and myocardial oxygen consumption, has not been evaluated. The aim of the study was to evaluate the effect of high doses of atropine during dipyridamole echocardiography and to investigate the possible pharmacological interference between dipyridamole and atropine. METHODS: One-hundred consecutive patients (M = 81, F = 19; mean age 58 yrs) without inducible wall motion abnormalities at 14th minute of a high-dose (0.84 mg/Kg in 10') dipyridamole echocardiography test were studied. Seventy-five patients referred to the test in pharmacological wash-out were randomly divided in three groups: 25 patients (Group 1) received 10 mcg/Kg of atropine in 60"; 25 patients (Group 2) received 15 mcg/Kg of atropine in 120"; 25 patients (Group 3) received 20 mcg/Kg of atropine in 120"; moreover, 25 patients with a full-dose oral beta-blocker therapy (Group 4) received 20 mcg/Kg of atropine in 120". Atropine was infused during the 15th and 16th minute of the test. Heart rate (HR) changes and new wall motion abnormalities induced by atropine were considered and compared for each Group. In 60 patients (15 randomly selected from each Group) the effect on mean HR and R-R interval (msec) of the same dose of atropine infused during dipyridamole echocardiography was evaluated in resting conditions 24 hours apart. RESULTS: The dipyridamole-atropine test was well tolerated and accomplished in all patients. HR increased significantly in all Groups of patients in comparison with pre-atropine HR values (Group 1: +14 +/- 8 b/m', p < 0.0001; Group 2: +19 +/- 8 b/m', p < 0.0001; Group 3: +22 +/- 9 b/m', p < 0.0001; Group 4: +19 +/- 8 b/m', p < 0.0001; Groups 2, 4 vs Group 1: p = 0.03, Group 3 vs Group 1: p = 0.002). No patients in Group 1 (0%), 3 patients in Groups 2 and 3 (12%), and 5 patients in Group 4 (20%) showed new wall motion abnormalities after atropine infusion (Group 4 vs Group 1: p = 0.06). Effects of atropine on HR and mean R-R interval were significantly more pronounced in resting conditions than during dipyridamole test (HR: +25 +/- 11 vs +18 +/- 9 b/m', p < 0.001; R-R: -256 +/- 122 vs -127 +/- 68 msec, p < 0.0001). CONCLUSIONS: High doses of atropine during dipyridamole echocardiography test are safe and more effective for induction of new wall motion abnormalities than usual doses, particularly in patients tacking beta-blockers. The likelihood of an antagonistic mechanism between atropine and endogenous, dipyridamole-induced adenosine on sinus node is supported from our results.

Administration, Oral↗
PubMed1987

Alterations in the effects of atropine on the behavior of pigeons following chronic administration.

The acute effects of atropine (0.01-1.0 mg/kg) on pigeons' key-pecking maintained under a variable-interval (VI) 60-sec schedule of food reinforcement were determined. Atropine decreased key-peck rates in a dose-dependent manner. A rate-decreasing dose of physostigmine, an acetylcholinesterase inhibitor, was studied in combination with the range of atropine doses. The rate reduction produced by physostigmine was attenuated by some doses of atropine. An atropine dose which decreased key-peck rates was then administered to the pigeons every day after their experimental sessions (chronic post-session phase). During this regimen, the dose-effect curves for atropine and the combination of atropine and physostigmine were redetermined. Atropine was then given chronically prior to experimental sessions (chronic pre-session phase), and the dose-effect curves for atropine and the combinations of atropine and physostigmine were determined again. The pigeons became tolerant to the rate-reducing effects of atropine following chronic post-session administration. Physostigmine's effect alone was unchanged following chronic atropine administration for two pigeons, and was slightly greater for a third. The rate reduction caused by physostigmine was attenuated across a wider range of atropine doses in the two pigeons for which the effect of physostigmine alone was unchanged. The atropine/physostigmine interaction curve for the third pigeon was shifted to the right following chronic post-session atropine administration. No further changes in effects of either atropine alone or in combination with physostigmine were seen following chronic pre-session atropine administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Effects of different concentrations of atropine on controlling myopia in myopic children.

Although 1% atropine effectively slows myopia progression, it is associated with adverse effects, including photophobia, blurred near vision, and poor compliance. We investigated whether lower doses of atropine would control myopia progression. One hundred and eighty-six children, from 6 to 13 years of age, were treated each night with different concentrations of atropine eye drops or a control treatment for up to 2 years. The mean myopic progression in each of the groups was 0.04 +/-0.63 diopter per year (D/Y) in the 0.5% atropine group, 0.45+/-0.55 D/Y in the 0.25% atropine group, and 0.47+/-0.91 D/Y in the 0.1% atropine group. All atropine groups showed significantly less myopic progression than the control group (1.06+/-0.61 D/Y) (p<0.01). Our study also showed that 61% of students in the 0.5% atropine group, 49% in the 0.25% atropine group and 42% in the 0.1% atropine group had no myopic progression. However, 4% of children in the 0.5% atropine group, 17% in the 0.25% atropine group, and 33% in the 0.1% atropine group still had fast myopic progression (>-1.0 D/Y). In contrast, only 8% of the control group showed no myopic progression and 44% had fast myopic progression. These results suggest that all three concentrations of atropine had significant effects on controlling myopia; however, treatment with 0.5% atropine was the most effective.

Adolescent↗
PubMed2006

Effects of intravitreally and intraperitoneally injected atropine on two types of experimental myopia in chicken.

Atropine, a non-selective muscarinic receptor antagonist, is currently the most potent agent used to prevent myopia in animal models and children. However, the ocular target tissues are not well defined. To learn more about the effect of atropine on experimental myopia, atropine was applied both intravitreally and systemically (intraperitoneally) to chickens wearing either negative lenses or light diffusers. Furthermore, the effect of ipsilateral intravitreal atropine on myopia development in the saline-treated fellow eye was studied. Monocular intravitreal injections of atropine were performed daily for a period of 4 successive days, starting at day 8 post-hatching. Fellow eyes received saline injections. Chicks were fitted with -7D lenses, either over the atropine-injected eyes only (unilateral "lens-induced myopia (LIM)"), or over both eyes (bilateral LIM). Other groups of chicks were fitted with translucent diffusers over the atropine-injected eyes (unilateral "form deprivation myopia (FDM)"). Finally, atropine was intraperitoneally injected for 4 days in chicks that wore monocularly -7D lenses. Refractive errors (RE) were measured with infrared photoretinoscopy and axial length (AL) with A-scan ultrasonography. Atropine prevented development of myopia in both unilateral LIM and FDM in a dose-dependent fashion. Fifty percent inhibition of myopia was observed at a dose of 25 microg (unilateral LIM) or 90 microg atropine (bilateral LIM) and complete inhibition at 750 microg; in unilateral FDM, 50% inhibition occurred at 2.5 microg and almost 100% inhibition at 250 microg. Interestingly, at the highest dose of atropine (2500 microg), the treated eyes became even more hyperopic compared to the saline-injected contralateral eyes with normal visual experience. In the bilateral LIM model, atropine suppressed development of myopia in both the treated and the saline-injected control eye. However, about 8.3 times higher doses were necessary to achieve comparable contralateral suppression. Since this ratio is lower than the vitreous volume to blood volume ratio (about 1:23 in young chicks), it seems unlikely that systemic dilution of the intravitreally injected drug can fully account for the contralateral suppression. Intraperitoneal injection inhibited myopia development only at the highest dose (2500 microg) but, strikingly, this inhibition was still less when the same dose was provided through the vitreous of the fellow eye. Both eyes seem to be coupled by a yet unknown, perhaps neuronal pathway. Estimations of the scleral concentrations of atropine after intravitreal injection are compatible with the assumption that the suppression of myopia by atropine occurs by direct inhibition of scleral chondrocytes.

Animals↗
PubMed2003

Stability of atropine sulfate prepared for mass chemical terrorism.

BACKGROUND: Preparedness for chemical terrorism includes the procurement of the appropriate pharmacological antagonists. A large emphasis has been placed on having a sufficient quantity of atropine available to treat patients exposed to acetylcholinesterase inhibitors such as sarin. Severe exposures may necessitate the administration of large amounts of atropine and dictate the need to prepare significant quantities of extemporaneously compounded atropine solution to respond to mass numbers of casualties over the first 24-48 hours postexposure. OBJECTIVE: The objective of this project was to determine the stability of a 1 mg/mL atropine solution prepared in multidose IV solutions of 0.9% sodium chloride over a 72-hr period stored at varying temperatures. METHODS: Atropine sulfate solution 1 mg/mL in 0.9% sodium chloride was prepared from sterile pharmaceutical-grade atropine sulfate powder. Multidose bags of atropine sulfate (100 mL) were stored at controlled temperatures of 4 degrees C to 8 degrees C, 20 degrees C to 25 degrees C, and 32 degrees C to 36 degrees C for 3 days and covered with an amber occlusive cover to minimize exposure to light. Six samples from each bag were drawn at 6, 12, 24, 48, and 72 h after preparation and compared with a time zero control sample. The samples were assayed using United States Pharmacopeia/National Formulary (USP/NF) high-performance liquid chromatography (HPLC) methods for atropine sulfate injection. The USP standard of 95% for atropine sulfate stability was used as the primary endpoint. RESULTS: Atropine sulfate 1 mg/mL in 0.9% sodium chloride was stable for at least 72hr at 4 degrees C to 8 degrees C (percent initial concentration ranging from 96.5% to 103.4%), 20 degrees C to 25 degrees C (percent initial concentration ranging from 98.7% to 100.2%), and 32 degrees C to 36 degrees C (percent initial concentration ranging from 98.3% to 102.8%). Because the IV bags were protected from light during this study, we recommend this practice after preparing the atropine solution. CONCLUSIONS: The amount of atropine necessary to treat hundreds to thousands of victims of a chemical attack is immense. The extemporaneous preparation of atropine solution from pharmaceutical-grade powder eliminates concerns about the storage of excessive quantities of atropine. A 1 mg/mL solution is stable for at least 3 days, allowing for use during the most critical treatment periods after exposure.

Atropine↗
PubMed1987

Is atropine a pilocarpine antagonist in cases of eliminated parasympathetic innervation of the human parotid salivary gland?

1 Following denervation of the human parotid salivary gland, pilocarpine caused an intensified stimulant response on salivation and a stimulant effect of atropine on salivary secretion was revealed. However, despite its stimulant effect on salivary secretion, atropine retained its action in blocking the salivatory response to pilocarpine. 2 This dualism in the action of atropine is explained by an action on different muscarinic receptor sub-types, i.e. on some sub-types atropine behaves as an antagonist and on others as an agonist. 3 Under the particular conditions in which the studies were performed, pilocarpine neither prevented nor increased the subsequent paradoxical response to atropine. Moreover, when injected at the peak of the atropine salivatory response it caused neither addition nor synergism to the atropine response. 4 Following the simultaneous injection of both pilocarpine and atropine, atropine initially suppressed the effect of pilocarpine and then itself caused a powerful paradoxical salivation. 5 Pilocarpine injected at the end of the paradoxical secretory response to atropine caused no secretion indicating that atropine retained its antisecretory effect against pilocarpine. 6 The extent of pilocarpine secretory responses is dependent upon the presence or absence of atropine, whilst the atropine effect is independent of the presence of pilocarpine. This points to the presence of differing populations of cholinoreceptors to explain the agonist effects of pilocarpine and atropine.

Atropine↗
PubMed1976

The effects of atropine on atrio-ventricular conduction in patients with Wolff-Parkinson-White syndrome. Studies with His bundle electrogram.

The effects of atropine on normal and anomalous A-V pathways were investigated using HBE in 40 cases consisting of 25 subjects without pre-excitation (group I) and 15 cases with WPW syndrome (group II). In group I, A-H interval shortened with a mean decrease of 30% following the administration of atropine (p less than 0.001), while P-A and H-V intervals as well as QRS duration remained unchanged. In group II the electrocardiogram showed WPW syndrome pattern (pattern W) in 12, normalization (pattern N) in 1 and both patterns (pattern WN) in 2 cases during the control study. In 10 cases pattern W persisted after atropine. Atropine changed pattern W to WN in 2 cases, WN to W in 1, WN to N in 1 and N to WN in one case. P-d interval remained constant. Atropine had no effect on the conduction time within atrium. His-Purkinje system and anomalous A-V pathway, but accelerated the transmission through A-V node. Atropine decreased the QRS duration of pattern W in 11 of 13 cases showing pattern W or WN both before and after atropine. Since the QRS duration showing pattern W correlated with P-H interval and (see article) and had the negative correlation with H-d interval (p less than 0.001), fusion mechanism was considered as the genesis of electrocardiographic pattern in most cases with WPW syndrome. Atropine influence was negative on QRS complex of pattern W i2 cases showing the co-existence of Kent bundle and James fibers or exclusive Kent bundle conduction. In the latter case the selection of antiarrhythmic agents should be made with caution. A-V dissociation with junctional rhythm developed in 9 cases (4 in group II) within 2 and a half minutes after atropine. The duration was as short as 15 seconds or less in 6 cases. The continuous tracing is necessary not to miss the AV dissociation. The disappearance of delta wave after atropine was observed during the change to pattern WN and the occurrence of A-V junctional rhythm or beat in 5 of 12 cases showing pattern W prior to the drug administration, and right bundle branch block was disclosed in 2 cases. The normalization of QRS complex also made it possible to measure His-Purkinje conduction time. In this point atropine is superior to the other antiarrhythmic agents which prolong H-V interval. Paroxysmal supraventricular tachycardia induced after atropine revealed shorter A-H with fixed H-V and V-A intervals, compared with the tachycardia before atropine in one case. The administration of atropine serves as an aid to evaluate the participation of anomalous A-V pathway in the tachycardia circuit.

Adolescent↗
PubMed1999

The action mechanism of relaxation effect of atropine on the isolated rabbit corpus cavernosum.

PURPOSE: Atropine has been used to block cholinergic neurotransmission in basic research and has received recent interest clinically in the intracavernosal pharmacotherapy of erectile dysfunction. It has been suggested that at a low dose (10(-8) M), atropine blocks muscarinic receptors, and that at a large dose (10(-3) M), it induces the release of EDRF. However, no report has supported this idea experimentally. We tried to confirm the action of atropine in cavernosal tissue and define its mechanism. MATERIALS AND METHODS: Strips of rabbit corpus cavernosum were mounted in organ chambers. On the precontracted muscle strips with phenylephrine (PHE; 5 x 10(-6) M), atropine was treated with increasing concentration from 10(-11) M. The relaxing activity of atropine was observed in deendothelialized tissue and preparation with treatment with methylene blue (10(-4) M), pyrogallol (10(-4) M), NW-nitro-L-arginine (L-NNA; 3 x 10(-4) M) and indomethacin (10(-4) M). To evaluate the relationship of atropine to Ca++, the muscle strip was incubated in Ca++ free solution, and Ca++ induced contraction by addition of CaCl2 (10(-3) M) was recorded with atropine. Depolarization by KCl was observed with atropine to investigate the relationship of atropine relaxation to K+. RESULTS: On the precontracted muscle strip with PHE, atropine induced a dose-related contraction up to 10(-8) M and began to exert a relaxing effect at the concentration of 10(-7) M and reached the 93.6% relaxation effect at the concentration of 10(-4) M, causing dose-dependent relaxation. The relaxing effect of atropine was partially inhibited by endothelial disruption, and by pretreatment with methylene blue, pyrogallol, L-NNA, and indomethacin, although they were not statistically significant. At the basal state of muscle strips in Ca++ free solution, atropine decreased basal tension as well as inhibited the contraction induced by CaCl2 dose-dependently. However, atropine did not influence depolarization by KCl. CONCLUSIONS: Atropine has both a contraction effect at lower concentrations and a relaxation effect at higher concentrations on cavernosal smooth muscle. It is presumed that the relaxation at higher concentrations is mediated via increasing intracellular calcium sequestration, not by hyperpolarization or secretion of EDRF.

Animals↗
PubMed1992

Atropine poisoning in children during the Persian Gulf crisis. A national survey in Israel.

OBJECTIVE: To evaluate the effects of high doses of atropine in children accidentally injected with automatic atropine injectors. These were distributed in Israel during the Persian Gulf Crisis as an antidote for chemical warfare agents. DESIGN AND SETTING: A national survey in pediatric emergency departments in Israel, involving 22 medical centers, with prospective data collection in 14 centers. PATIENTS: Children (n = 268) presenting to emergency departments following misuse of automatic atropine injectors. MAIN OUTCOME MEASURES: Documentation of atropine dose and clinical manifestations; determination of a clinical severity score and its correlation with atropine dose; measurements of serum atropine levels in six patients. RESULTS: Over a period of 4 months, 268 cases were reported, of which 240 were clinically evaluated. The most common site of injection (75%) was the finger or palm. Doses were up to 17-fold higher than standard doses for age. In 116 children (48%), systemic effects of atropine were observed, and 20 (8%) had severe atropinization. Seizures and life-threatening arrhythmias were not reported, and there were no fatalities. The severity of atropinization was correlated with the dose following a classic nonlinear, dose-response relationship. Serum atropine levels (6.2 to 61.0 ng/mL) were much higher than those observed after administration of therapeutic doses. CONCLUSIONS: The high incidence of injection in the hand implies accidental use of automatic atropine injectors among children. The lack of mortality or life-threatening complications from injection of large doses of atropine attests to its relative safety in children. The low risk from atropine injections weighed against expected benefit as a lifesaving antidote justifies the distribution of personal atropine injectors to children at risk of organophosphorus nerve agent attack.

Accidents↗
PubMed1996

The atropine factor in pharmacologic stress echocardiography. Echo Persantine (EPIC) and Echo Dobutamine International Cooperative (EDIC) Study Groups.

OBJECTIVES: This study sought to compare, head to head, the two most popular pharmacologic stress echocardiographic tests--dipyridamole and dobutamine--with state of the art protocols in a large multicenter prospective study. BACKGROUND: In the continuing quest for ideal diagnostic accuracy, pharmacologic stress echocardiography has quickly moved over the years from low to high dose regimens and is currently performed with atropine coadministration. METHODS: Dobutamine (up to 40 microgram/kg body weight per min) plus atropine (up to 1 mg over 4 h) and dipyridamole (up to 0.84 mg/kg per min over 10 h) plus atropine (up to 1 mg over 4 h) stress echocardiography was performed on different days, in random order and within 1 week in 360 patients with chest pain syndrome. Thirteen different echocardiographic laboratories, all fulfilling quality control criteria for stress echocardiographic reading, contributed to the study. RESULTS: No major complications occurred during either test. The test was interrupted before achievement of predetermined end points for limiting side effects in 37 dobutamine-atropine and 7 dipyridamole-atropine stress echocardiographic studies (feasibility 90% vs. 98%, p < 0.01). Diagnostic accuracy was assessed in a subset of 110 patients with no obvious rest dyssynergy (akinesia or dyskinesia) who underwent coronary angiography independently of test results and within 1 week of testing. Significant coronary artery disease (> or = 50% diameter reduction in at least one major coronary vessel by quantitative coronary angiography) was found in 92 patients. Sensitivity for detection of coronary artery disease was 84% (77 of 92) for dobutamine-atropine and 82% (75 of 92) for dipyridamole-atropine stress echocardiography (p = NS), with a specificity of 89% (16 of 18) for dobutamine-atropine and 94% (17 of 18) for dipyridamole-atropine stress echocardiography (p = NS). A significant correlation was present between peak wall motion score index during dipyridamole-atropine and dobutamine-atropine stress echocardiography (r = 0.83, p < 0.0001). CONCLUSIONS: Dobutamine-atropine and dipyridamole-atropine stress echocardiography are safe and feasible, although submaximal studies are more frequent with dobutamine. The two stresses have comparable accuracy in the detection of angiographically assessed coronary artery disease, although dobutamine is marginally more sensitive and dipyridamole marginally more specific. Stratification of the ischemic response in the space domain is also comparable with the two stresses.

Angina Pectoris↗
PubMed1996

Atropine augmentation in dobutamine stress echocardiography: role and incremental value in a clinical practice setting.

OBJECTIVES: This study sought to evaluate the role and incremental value of atropine in a large patient group undergoing dobutamine stress echocardiography. BACKGROUND: The use of atropine to potentiate dobutamine stress is not standard practice. Although the utility of atropine has been described, data on its incremental value remain limited and do not exist for a routine clinical practice setting. METHODS: Dobutamine stress echocardiography was performed in 1,171 patients with use of a standard protocol. Atropine (maximal dose 2.0 mg) was given to 299 patients (26%) who did not attain target heart rate. Coronary angiography was performed in 183 patients (46 received atropine), 148 of whom were found to have significant coronary artery disease (> or = 70% diameter stenosis in a major epicardial vessel, > or = 50% stenosis for left main coronary artery disease). All tests were reviewed independently by experienced observers. RESULTS: There were no major adverse events. Patients receiving atropine had a lower rest heart rate (65 vs. 74 beats/min, p < 0.0001) and more often received beta-adrenergic blocking agents (49% vs. 14%, p < 0.0001). Of 444 patients in whom stress-induced ischemia developed, 70 (16%) required atropine before ischemia became evident. Sensitivity for detection of significant coronary artery disease was 90% with dobutamine alone and 95% after the addition of atropine. In 66 patients with normal wall motion at rest, test sensitivity was 65% before and 84% after atropine was given. Atropine use did not compromise test specificity. New diagnostic information was obtained in 20 (50%) of 40 patients with angiographic coronary artery disease given atropine. Proportionately more patients with single-vessel disease required atropine before an ischemic response was observed; this effect appeared related to the higher ischemic threshold in these patients. CONCLUSIONS: Augmentation of heart rate had a modest influence on the overall diagnostic sensitivity of dobutamine stress echocardiography in our study cohort. However, it was particularly helpful in patients receiving beta-blockers and those with milder coronary disease. Despite the use of > or = 1 mg of atropine in some patients, this incremental value was not achieved at the expense of safety.

Adult↗
PubMed2003

The course of moderate amblyopia treated with atropine in children: experience of the amblyopia treatment study.

PURPOSE: To assess the course of the response to atropine treatment of moderate amblyopia and to assess factors predictive of the treatment response in children 3 years old to younger than 7 years old. DESIGN: Multicenter, randomized clinical trial comparing atropine and patching (one of the amblyopia treatment studies). METHODS: A total of 195 children 3 years old to younger than 7 years of age with amblyopia in the range of 20/40 to 20/100 from the atropine treatment arm of this trial were enrolled and included in this analysis. At baseline, daily topical atropine was prescribed for the sound eye. During follow-up, a plano spectacle lens was prescribed for the sound eye for patients whose amblyopia had not been successfully treated with atropine alone. Follow-up examinations were performed at 5 weeks, 16 weeks, and 6 months. The primary outcome measure was visual acuity in the amblyopic eye at 6 months. RESULTS: Mean visual acuity improved from baseline by 1.3 lines after 5 weeks of treatment, by 2.4 lines after 16 weeks, and by 2.8 lines at 6 months. Visual acuity of 20/30 or better and/or 3 or more lines of improvement from baseline was achieved by 75% of the patients. Improvement occurred over the entire range of baseline acuities (20/40 to 20/100) and was not related to patient age (P =.36). Among the 134 patients improving 3 or more lines from baseline, 7% achieved their maximum improvement by 5 weeks and 46% by 16 weeks. Among the 55 patients who did not respond adequately to atropine alone and were prescribed a plano lens for the sound eye, the mean improvement before the use of the plano lens was 1.0 lines, compared with 1.6 lines after prescribing the plano lens (P =.11). None of the demographic or clinical factors assessed was predictive of the response to treatment. A shift in fixation preference at/near from the atropinized sound eye to the amblyopic eye was not required for the amblyopic eye to improve; amblyopic eye acuity improved 3 or more lines in 29 (60%) of the 48 patients who were found to be using the atropinized sound eye on fixation preference testing. A 2 or more line decrease in sound eye visual acuity occurred more frequently when a plano lens was prescribed in addition to atropine (7 of 43, 16%) compared with treatment with atropine alone (4 of 123, 3%; P =.01). CONCLUSIONS: A beneficial effect of atropine is present throughout the age range of 3 years old to younger than 7 years old, and with an acuity range of 20/40 to 20/100. A shift in near fixation to the amblyopic eye is not essential for atropine to be effective in all cases. Sound eye acuity should be monitored when a plano spectacle lens is prescribed for the sound eye to augment the treatment effect of atropine.

Amblyopia↗
PubMed2000

Feasibility and prognostic value of dobutamine-atropine stress echocardiography early in unstable angina.

BACKGROUND AND AIM: Because unstable angina has always been considered a contraindication for dobutamine-atropine stress echocardiography (DSE), the role of dobutamine-atropine stress echocardiography in unstable angina is unknown. Our aim was to assess the safety and prognostic value of dobutamine-atropine stress echocardiography in unstable angina. METHODS: One hundred and thirty-two patients were studied (mean age 64+/-12 years, 29 women). Dobutamine-atropine stress echocardiography was performed on the third day after hospital admission. End-points were unstable angina, myocardial infarction or cardiac death at 1 year follow-up. RESULTS: No major complications occurred during dobutamine-atropine stress echocardiography. Ninety-six (78%) patients were on beta-blocker therapy during the test; mean maximum heart rate achieved was 106+/-23 beats x min(-1). Nine of the 21 patients (43%) with a positive dobutamine-atropine stress echocardiography presented cardiac events during follow-up: two patients died, one had a myocardial infarction and six had recurrent class III-IV angina. Among 80 patients with negative dobutamine-atropine stress echocardiography, one (1%) had myocardial infarction and six patients (7.5%) had recurrent angina. Event-free survival after 1 year for patients with a negative dobutamine-atropine stress echocardiography for ischaemia was 91% compared to 57% for those with a positive dobutamine-atropine stress echocardiography (P<0. 0001). Left ventricular dysfunction (P=0.01), prior myocardial infarction (P=0.03) and a positive dobutamine-atropine stress echocardiography (P=0.004) were independent predictors of cardiac events during follow-up. CONCLUSIONS: Dobutamine-atropine stress echocardiography is safe in unstable angina if it is performed when patients remain asymptomatic for at least 48 h. A negative dobutamine-atropine stress echocardiogram for ischaemia predicts a good prognosis in medically treated patients with unstable angina and may allow their early discharge from hospital. Good prognostic information was obtained despite the use of beta-blockers and low heart rates during dobutamine-atropine stress echocardiography.

Adult↗
PubMed2000

Effects of atropine on anterior chamber depth and anterior chamber inflammation after primary trabeculectomy.

PURPOSE: To investigate the effects of postoperative atropine on central and peripheral anterior chamber depth and anterior chamber inflammation in patients undergoing primary trabeculectomy. METHODS: Two separate groups of patients who were phakic without previous intraocular surgery undergoing primary trabeculectomy were prospectively randomized to atropine or no atropine. In the first group of patients, 24 eyes of 21 patients undergoing primary trabeculectomy were prospectively randomized to atropine or no atropine, and their anterior chamber depth was measured. Central and peripheral chamber depths were measured using the EAS-1000 anterior segment analysis system (Nidek, Tokyo, Japan) before surgery and on postoperative days 1, 3, 7, 14, and 30. In the second group, 34 patients undergoing primary trabeculectomy were prospectively randomized to atropine or no atropine, and their anterior chamber reaction was documented. The amount of cells and flare was measured using the Kowa laser flare meter (FM-500) and cell counter (LC-500) (Kowa Electronics and Optics, Tokyo, Japan) preoperatively and on postoperative day 1, 7, and 30. RESULTS: Compared with preoperative measurements, a small (approximately 0.1 mm) but statistically significant deepening of the central and peripheral anterior chamber depth on days 1, 7, 14, and 30 was found in patients who used atropine. In the nonatropine group, no statistically significant change was found in central or peripheral anterior chamber depths at any time as compared with preoperative values. There was no statistically significant difference in the cell or flare counts between the atropine and nonatropine groups at any time. CONCLUSIONS: This study showed a small but statistically significant deepening of the anterior chamber with atropine. No statistically significant differences were observed in the cell or flare counts between atropine and nonatropine groups. Routine atropine use after trabeculectomy may not be necessary to reduce postoperative complications, such as shallowing of the anterior chamber or anterior chamber inflammation. In patients with a shallow anterior chamber, however, atropine would be expected to deepen the chamber.

Adolescent↗
PubMed1992

Possible mechanisms of inhibition with atropine against noradrenaline-induced contraction in the rabbit aorta.

1. In the rabbit isolated aorta, atropine (3 x 10(-6) M-10(-4) M) inhibited contractile response to noradrenaline without affecting contraction to KCl. 2. In the presence of contraction to noradrenaline, atropine (3 x 10(-7) M-10(-4) M) caused concentration-dependent relaxation. Pretreatment with theophylline (10(-3) M) potentiated the relaxant action of atropine. Relaxation to atropine was not affected by the specific guanosine 3':5'-cyclic monophosphate phosphodiesterase inhibitor, M & B 22,948 (10(-4) M), tetraethylammonium (10 mM), indomethacin (10(-5) M), propranolol (10(-7) M), nifedipine (10(-6) M) or removal of the endothelium. 3. Relaxation to either atropine or prazosin was not affected by preincubation with prazosin and atropine, respectively. 4. In Ca(2+)-free medium containing EGTA and nifedipine, atropine (10(-7) M-10(-4) M) inhibited the residual noradrenaline response more than the subsequent Ca(2+)-induced contraction. Pretreatment with either theophylline (10(-3) M), forskolin (3 x 10(-7) M) or a low concentration of prazosin (3 x 10(-9) M) also inhibited the residual contraction to noradrenaline and Ca2+. The effect of combined treatment of atropine and any of these agents was much greater than with each individual agent. 5. Atropine (10(-6) M-10(-4) M) also inhibited increases in the level of inositol monophosphates (IP) in response to noradrenaline. Theophylline (10(-3) M) and a low concentration of prazosin (3 x 10(-9) M) also inhibited IP formation. Combined with atropine, the effect was much greater than with each of these agents individually. 6. Atropine did not affect adenosine 3':5'-cyclic monophosphate (cyclic AMP) levels in the aorta and also failed to displace specific [3H]-prazosin binding.7. These results suggest the possibility that smooth muscle relaxation to atropine may be due to the inhibition of phosphoinositide metabolism. The relaxation is not apparently due to an action of atropine on ax-adrenoceptors, or a change in the level of cyclic AMP.

Animals↗
PubMed1977

Effect of atropine on vascular adrenergic neuroeffector transmission.

Atropine, homatropine, scopolamine, procaine, lidocaine and phentolamine inhibited the contractile response of rabbit isolated pulmonary artery elicited by electrical-field stimulation. Methylatropine had no effect. The inhibition induced by atropine (2 x 10(-6)-2 x 10(-4) M) had a rapid onset of action and then remained almost constant. The inhibition was slowly reversible. The potency of atropine as an inhibitor of responses to field stimulation was very much less than the potency of phentolamine. The inhibition was not antagonized by cocaine or (+)-amphetamine. Atropine (3 x 10(-5) and 3 x 10(-4) M) enhanced the electrical-field-stimulation-induced outflow of tritium from the pulmonary artery preloaded with 3H-(-)-noradrenaline. In contrast, atropine in a concentration-dependent manner either had no effect or slightly decreased the tyramine-induced outflow of tritium. Atropine reduced the contractile response of the pulmonary artery evoked by tyramine. Atropine (10(-4) and 3 x 10(-4) M) and phentolamine inhibited the arterial contractions elicited by exogenous (-)-noradrenaline in an apparently competitive manner. The contractions of rabbit isolated aorta elicited by (-)-noradrenaline, serotonin and histamine were inhibited by atropine (10(-5) and 10(-4) M). Atropine was very much less potent in antagonizing noradrenaline, histamine and serotonin than in antagonizing acetylcholine. tthe inhibotory potency of atropine, procaine and lidocaine on the accumulation of 3H-(-)-noradrenaline by rabbit aorta in vitro was much less than that of cocaine. The relationship between the aortic concentration of 3H-atropine and in vitro accumulation was almost linear. The accumulation was slightly higher at 37 degrees C than at 1 degree C. The results suggest that atropine blocks alpha-adrenoceptors, both presynaptically at the adrenergic neurone terminals and postsynaptically at the smooth muscle. In addition, atropine may possibly act in a nonspecific manner at postsynaptic sites.

Amphetamine↗
PubMedDate not supplied

Medical treatment with atropine sulfate for hypertrophic pyloric stenosis.

We investigated whether atropine sulfate was an effective, non-surgical method for treating hypertrophic pyloric stenosis (HPS). The study group consisted of 5 patients, all of the patients presented with projectile vomiting. Hypertrophic pyloric stenosis was diagnosed based on abdominal sonographic findings. The age when symptom arose was 30.8 +/- 15.5 (mean +/- SD) days, the age upon admission was 43.2 +/- 9.6 days. The frequency of vomiting was 5.8 +/- 2.3 times per day. After admission, all patients received 10% atropine sulfate 0.01 mg/kg intravenous (i.v.) for 5 minutes q4H (every four hours) before each feeding. Formular milk was started and increased by 10 ml every feeding until full feeding (120 ml/kg/day) was achieved. When vomiting had ceased for a period of one day, i.v. atropine was changed to 0.02 mg/kg oral q4H before each feeding. The patient was hospitalized until full feeding was maintained for more than 2 days. Then oral atropine was tapered by half a dose every 2 weeks. Oral atropine was continued until the thickness of the pyloric muscle had normalized (< 3.5 mm). All five patients were successfully treated with atropine sulfate. The frequency of vomiting was reduced to less than two times per day (1.8 +/- 1.3 days). i.v. atropine was used for 6.4 +/- 3.4 days, and the oral form was used for 30 +/- 9 days. The total number of days of atropine sulfate treatment was 36.4 +/- 9.58 days. Full feeding was achieved at 8 +/- 5.3 days. The hospitalization was 14.6 +/- 6.2 days. The body weight when admitted was 4000 +/- 760.8 gm and the body weight when discharged was 4282 +/- 901 gm. The body weight one month after treatment was 5210 +/- 772.5 gm. The body weight gain one month after atropine treatment was 1262 +/- 441.4 gm. Body weigh range on admission was from <3rd to 25th percentile, and after one month of atropine treatment, the body weight range was from 10th to 75th percentile. Complications included transiently elevated heart rates (180-200 times/min) in two patients and facial flushing after the first dose of IV atropine in one patient. In conclusion, conservative treatment with initially IV atropine in the initial stages instead of oral atropine sulfate is an effective alternative to pyloromyotomy, particularly in infants with major concurrent disease or when parents are unwilling to let their infants undergo surgery. Surgical intervention is not always necessary.

Administration, Oral↗
PubMed2006

Blockade of nicotinic receptors of bovine adrenal chromaffin cells by nanomolar concentrations of atropine.

Nanomolar concentrations of atropine have been considered up to now to be selective for blockade of muscarinic receptors for acetylcholine. A collateral finding indicated to us that these low concentrations of atropine could also target the neuronal nicotinic receptors. We report here a detailed study on this novel property of atropine. Catecholamine release, measured on-line with amperometry in chromaffin cells stimulated with acetylcholine pulses was blocked by atropine in a competitive manner. To corroborate a direct action of atropine on nicotinic receptors, we have employed N,N-dimethyl-N'-phenyl-piperazinium (DMPP), a pure nicotinic receptor agonist; atropine blocked its secretory responses with an IC50 of 2.04 nM. Nicotinic currents, recorded with the whole cell configuration of the patch-clamp technique were blocked by atropine in a concentration-dependent manner (IC50 of 11 nM), also showing a competitive nature. Nicotinic receptor currents in oocytes expressing bovine alpha7 and alpha3beta4 nicotinic receptors were blocked by atropine with an IC50 of 11.2 and 46.8 nM, respectively. Atropine (30 nM) also decreased the increment of the cytosolic calcium concentrations after stimulation with 30 microM DMPP in bovine chromaffin cells. However, action potentials evoked by DMPP were not modified by atropine. Our results demonstrate that nicotinic currents and their downstream consequences (i.e. cytosolic calcium elevations and catecholamine release) were blocked by nanomolar concentrations of atropine; although the blockade was partial, it must be considered when using atropine to study cholinergic neurotransmission, particularly at synapses where both nicotinic and muscarinic receptors are present i.e., the adrenal medulla and autonomic ganglia.

Acetylcholine↗