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PubMed1987

Effects of atropine and 2-PAM chloride on vision and performance in humans.

These experiments assessed the time course and severity of effects of atropine and 2-PAM chloride on selected visual functions, physiological measures, and a tracking performance task. Atropine up to 4 mg X 70 kg-1 body weight and 2-PAM Cl in doses up to 1200 mg X 70 kg-1 body weight were administered intramuscularly in a double-blind Latin square design. A long lasting and dose-related increase in pupillary diameter and decrease in accommodative amplitude with accompanying loss of near visual acuity was found following atropine administration. These functions returned to baseline 2 d after injection. Distance acuity, contrast sensitivity, color vision, and intraocular pressure showed no changes after atropine. Tracking performance was significantly decreased by 4 mg of atropine. The changes in vision function cannot readily explain the tracking performance loss, since the tracking involved a distant visual target while the atropine produced degradation of near vision. Most of the physiological tests, tracking performance and all visual functions were unaffected by 2-PAM Cl.

Accommodation, Ocular↗
PubMedDate not supplied

Determination of small quantities of atropine in commercial preparations by liquid chromatography with fluorescence detection.

A method is presented for the determination of small quantities of atropine in commercial preparations by liquid chromatography (LC) with fluorescence detection. The sample is extracted with CHCl3 from basic suspension, the CHCl3 is evaporated on the steam bath, and the dry residue is dissolved in a small volume of CH3OH. A reverse phase column is used for the LC analysis; the eluting solvent is prepared by mixing 950 mL CH3OH with 50 mL water containing 1 g of the sodium salt of 1-pentanesulfonic acid. The fluorescence detector is set at an excitation wavelength of 255 nm and an emission wavelength of 285 nm. Several commercial tablets and injections containing atropine in combination with other ingredients and a commercial sample of belladonna extract were analyzed by the proposed method. Recoveries of atropine sulfate from aqueous solutions averaged 100.7% with a relative standard deviation (RSD) of 3.35% for atropine sulfate levels of 0.12 mg. Recoveries of atropine sulfate from synthetic injection formulations were 99.8 and 100.0% with RSDs of 2.03 and 2.35%, respectively; the atropine sulfate concentrations of commercial injections with the same formulations were found to be 97.0 and 100.0% of the labeled amounts with RSDs of 0.53 and 1.46%, respectively.

Atropine↗
PubMed1985

[Diagnostic value of the atropine test in the sick sinus syndrome].

Altogether 63 patients with clinical signs of the SNWS (the 1st group), 16 patients with coronary heart disease and the latent SNWS (the 2nd group), 26 patients with heart coronary disease without disorder of sinus node function (the 3rd conventionally control group) and 60 healthy persons (the 4th control group) were examined. Atropine was administered i. v. to them all at a a dose of 0.02 mg/kg of the body mass. The heart beat rate (HBR) was measured before atropine injection as well as its increment after atropine injection. The HBR after atropine injection in the patients of the 1st group was significantly higher than that in the 2nd-4th groups; in the patients of the 2nd group the HBR was significantly less than that in the 3rd-4th groups. In the 3rd group the HBR was significantly less than that in the 4th group. An increased percentage of the HBR in the patients with clinical signs of the SNWS and in the healthy persons did not differ significantly (46.6 +/- 3.7% and 51 +/- 2.4% P greater than 0.2). The sensitivity of the atropine test in the patients of the 1st group was 76.3%. The test specificity was 93.3%. Among the patients with coronary heart disease the atropine test specificity was much less (65.4%).

Atropine↗
PubMed1983

Membrane-bound ATP-dependent energy systems and gastric cytoprotection by prostacyclin, atropine and cimetidine in the rat.

The effects were studied of different doses of prostacyclin (PG12), atropine and cimetidine on the gastric secretory responses of four-hour pylorus-ligated rats and on the gastric mucosal damage produced by intragastric administration of 0.6 M HCl, to determine the cytoprotective doses of PG12, atropine and cimetidine. In another series of observations, gastric mucosal damage was produced by intragastric administration of 0.6 M HCl and the effects were studied of cytoprotective doses of PG12, atropine and cimetidine on the number and severity of gastric lesions, in connection with the biochemical changes of the rat gastric fundic mucosa. The drugs were given intraperitoneally 30 min before the application of the necrotizing agent, and the animals were killed one hour later. During the experiments, the tissue levels of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP) and lactate were measured enzymatically, and the tissue content of cyclic adenosine monophosphate (cAMP) was determined by radioimmunoassay. The specimens were taken from the gastric fundic mucosa of groups of animals treated with saline solution (absolute control), with 0.6 M HCl (pathological control) and with 0.6 M HCl plus PG12, atropine and cimetidine (given in cytoprotective doses). The ratio of ATP.ADP-1, adenylate pool (ATP + ADP + AMP) and energy charge (ATP + 0.5 ADP.ATP + ADP + AMP-1) were calculated in all groups of animals. It was found that: (i) PG12 (in a dose of 5 micrograms.kg-1) atropine (in a dose of 0.025 mg.kg-1) and cimetidine (in a dose of 2.5 micrograms.kg-1) have cytoprotective effects; (ii) the gastric fundic mucosal damage produced by intragastric administration of 0.6 M HCl appears as a result of a positive metabolic adaptation of the gastric fundic mucosa; (iii) the development of gastric cytoprotection by PG12, atropine and cimetidine give rise to very different changes in the tissue levels of ATP, ADP, AMP and cAMP.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1984

Interrelationships between the development of the gastric cytoprotective effects of prostacyclin, atropine, cimetidine and the gastric mucosal superoxide dismutase activity in rats.

Gastric mucosal damage was produced by the intragastric administration of 96% ethanol or 0.6 M HCl. The cytoprotective doses of prostacyclin (PGI2) (5 micrograms/kg), atropine (0.025 mg/kg) or cimetidine (2.5 mg/kg) were given intraperitoneally 30 min before the administration of the necrotizing agents. The animals were killed 1 hr later. The number and severity of gastric mucosal lesions (ulcer) were recorded. At the time of the sacrifice of the animals, superoxide dismutase (SOD) was prepared from the gastric fundic mucosa and its activity was measured. It was found that PGI2 (5 micrograms/kg), atropine (0.025 mg/kg) and cimetidine (2.5 mg/kg) significantly decreased the number and severity of gastric mucosal lesions (ulcers) produced by the intragastric administration of 96% ethanol a 0.6 M HCl, PGI2, atropine, cimetidine, given in cytoprotective doses, significantly mounted the ethanol-induced increase of gastric mucosal SOD activity; PGI2, atropine, cimetidine, given them in cytoprotective doses significantly shunted the HCl-induced decrease of gastric mucosal SOD activity. It has been concluded that; chemically different cytoprotective agents (PGI2, atropine, cimetidine) give rise to similar tendencies in the changes of gastric mucosal SOD activity; both the significant decrease (in the ethanol-model) and the significant increase (in the HCl-model) of this enzyme seem to be involved in the development of gastric mucosal protection by PGI2, atropine and cimetidine.

Animals↗
PubMed1984

Evidence for the existence of gastric cytoprotective effect of atropine and cimetidine in humans.

The effects of cimetidine (12.5 mg i.m.) and atropine (0.125 mg i.m.) were studied on the basal (BAO) and pentagastrin (6 micrograms X kg-1 s.c.)-stimulated (MAO) gastric acid secretion; the gastric mucosal microbleeding provoked by one-day treatment with indomethacin (4 X 25 mg orally) in patients with chronic disorders of the joints. The extent of the gastric microbleeding was measured by spectrophotometric determination of haemoglobin in gastric lavage fluid. The aims of this study were to determine the doses of cimetidine and atropine in humans without any significant inhibitory effects either on the basal or on the maximal gastric acid output to evaluate the cytoprotective action of these doses of cimetidine and atropine on the indomethacin-induced gastric microbleeding in the man. It was found that cimetidine (12.5 mg i.m.) and atropine (0.125 mg i.m.) did not cause any significant inhibition either of the BAO or of the MAO; indomethacin (4 X 25 mg orally) significantly increased gastric microbleeding in the patients; cimetidine and atropine, in the above doses, were able to prevent significantly indomethacin-induced gastric microbleeding in the patients. These results provide evidence for the existence of gastric cytoprotective effects of cimetidine and atropine in humans.

Adult↗
PubMed1978

[Effect of atropine on fetal heart rate].

The effect of atropine on the foetal heart rate (FHR) was examined in 56 normal pregnancies. 40 mcg/kg atropine was administered. According to the results of the examinations the FHR was not effected by atropine in the 8.--13. weeks of gestation. The FHR was effected by the applied dose of atropine only after the 17th week increasing over the physiological oscillation. In the course of pregnancy FHR was increased by atropine in every case it nearly raised to FHR values observed in the 8.--13 weeks still not effected by atropine.

Atropine↗
PubMed1984

Use of atropine in connection with oral midazolam premedication.

The clinical significance of intramuscular premedication with 0.01 mg/kg of atropine in a procedure involving oral benzodiazepine premedication (15 mg midazolam the evening before surgery and on the morning of surgery) was investigated in a double-blind study. As far as sedation, apprehension, excitement, dizziness, emesis, and headache were concerned, there were no significant differences between group 1 (atropine) and group 2 (placebo) patients; however, both during and after anesthesia patients in group 1 had less excessive salivary secretion (especially during extubation). As a result of sympathetic overactivity, patients in group 1 had an increased heart rate and an increased incidence of supraventricular tachycardia. In group 1 intravenous infusion proved more difficult, and in addition, the patients complained more of subjective side effects (dry mouth). There was no significant correlation between the radioimmunologically measured serum concentrations and the clinical effects of atropine measured just before the induction of anesthesia. Substantial interindividual differences were found in these serum levels. From the anesthetist's viewpoint, atropine has both beneficial effects (antisecretory) and unwanted effects (cardiovascular effects). For the patient atropine caused only subjective unwanted effects. Midazolam, a new short-acting, sedative benzodiazepine derivatives, can be used without atropine as an oral premedicant.

Administration, Oral↗
PubMed1983

[Changes in the automatically analyzed features of fetal heart rate patterns and fetal movements as influenced by atropine sulfate].

The influence of atropine sulphate (0.01 mg/kg body weight of pregnant women i.v.) on several parameters of fetal heart rate was investigated with automatic analysis of FHR. Fetal movements were counted, too. After administration of atropine, there was a first period with an "inverse" effect of atropine in all fetuses: decrease in baseline FHR (5.1%, minimum after 4.5 min) and increase in the amplitude of FHR fluctuation (44.6%). Thereafter, in a second period the "true" atropine effect appeared: increase in baseline FHR (15.5% above the level before atropine maximum after 25.1 min) and decrease in the amplitude of fluctuation (64.5%). In the third period baseline FHR returned to normal values but the amplitude of FHR fluctuation as well as the beat-to-beat irregularity remained small in 12 from 14 fetuses. Fetal movements registered by the mothers decreased significantly in this time. The results demonstrate a dualistic effect of atropine in the fetus. Moreover, the amplitude of FHR fluctuation (amplitude of macrofluctuation) and the beat-to-beat irregularity (microfluctuation) changed in an equal manner and appear to be influenced by similar regulatory processes. The divergence in the reaction of the baseline FHR and the amplitude of fluctuation together with a decrease in fetal movements might be caused by a central nervous effect with a change in the behaviour of the fetus.

Atropine↗
PubMed1980

The effect of metoclopramide and atropine on the absorption of orally administered mexiletine.

The effect of pretreatment with intravenous metoclopramide (10 mg) and atropine (0.6 mg), both separately and combined, on the absorption rate and relative oral bioavailability of the antiarrhythmic drug, mexiletinee (400 mg) was studied in eight fasting healthy males using a Latin Square design for order of pretreatment administration. The time (Tmax) of the maximum mexiletin plasma concentration (Cpmax) was reduced by metoclopramide (P < 0.001) and was increased by atropine (P < 0.01) compared with saline control. Tmax was not significantly altered by combined metoclopramide and atropine pretreatment. Atropine pretreatment was associated with a significant reduction of Cpmax (P < 0.05) and of elimination half-life (P < 0.05). The area under the mexiletine plasma concentration-time curve was not affected by any of the pretreatments. The results suggested that metoclopramide enhanced and atropine decreased the rate of mexiletine absorption without altering the relative oral bioavailability. When the pretreatments were administered in combination, metoclopramide reversed the delay in mexiletine absorption produced by atropine.

Administration, Oral↗
PubMed1980

Domperidone antagonizes the relaxant effect atropine on the lower esophageal sphincter.

A zone of increased intraluminal pressure exists at the gastroesophageal junction in man and is believed to act as a physiologic sphincter. Increasing this lower esophageal sphincter (LES) tone is an accepted and useful method in preventing gastroesophageal reflux. The effects of LES tone were studied in 10 healthy volunteers receiving sequential intravenous injections of atropine, 0.6 mg, or domperidone, 10 mg, followed by domperidone, 10 mg, or atropine, 0.6 mg. The order of drug administration was randomized during the first study. Each volunteer was studied a second time, 1 week later, when the order of drug administration was reversed from the first. Administration of atropine decreased mean LES pressure by 12.6 cm H2O (p < 0.001). Subsequent injection of domperidone restored LES tone to near normal. In contrast, initial injection of domperidone approximately 1 week later in the same subjects, mean LES pressure increased by 18.5 cm H2O (p < 0.001). Intravenous injection of atropine, thereafter, failed to decrease mean LES pressure significantly, LES pressure being sustained at a mean of 14.8 cm H2O above basal control levels (p < 0.005). Results of this study suggest that domperidone given prior to atropine, before induction of general anesthesia, may counteract the potentially deleterious effect of atropine on LES tone, and thereby reduce the chances of regurgitation and pulmonary aspiration of acid gastric contents.

Adult↗
PubMed1993

[Heart rate response to intravenous atropine during cervical and lumbar epidural anesthesia].

The authors evaluated the effect of cervical and lumbar epidural anesthesia on the heart rate response to intravenous atropine 0.01 mg.kg-1 in conscious humans with cervical epidural anesthesia (n = 40), with lumbar epidural anesthesia (n = 15) and without epidural anesthesia (n = 25). During cervical and lumbar epidural anesthesia using 1.5% lidocaine, levels of loss of cold sensation were C3-T7 and T7-S1, respectively. Heart rate increased by 14 +/- 10% (mean +/- SD) and 20 +/- 14% after intravenous atropine 0.01 mg.kg-1 in the patients with cervical and lumbar epidural anesthesia, respectively. These magnitudes of positive chronotropic effects were significantly less as compared with those in the patients without epidural anesthesia (32 +/- 11%). Nine of 40 patients (23%) with cervical epidural anesthesia showed heart rate increases of less than 3 beats.min-1 following atropine 0.01 mg.kg-1. And 30 of 40 patients (75%) required supplementary atropine 0.01 mg.kg-1 to increase heart rate for more than 20 beats.min-1 from baseline values. The present study suggests that the heart rate response to intravenous atropine is blunted in patients during cervical and lumbar epidural anesthesia, and that a larger dose of intravenous atropine may be required to accelerate the heart rate in most patients during cervical epidural anesthesia.

Adult↗
PubMedDate not supplied

Arrhythmias in organophosphate poisoning: effect of atropine and bispyridinium oximes.

The effect of atropine and of the bispyridinium oximes, HI6 and HLö 7, on the electrocardiographic pattern was investigated in acutely nerve agent-poisoned guinea-pigs. The electrocardiographic, circulatory and respiratory parameters were recorded in female urethane-anaesthetized Pirbright-white guinea-pigs. After base line measurements, the animals received pyridostigmine (0.05 mumol/kg) and, 30 min later, tabun (5xLD50), sarin (5xLD50), soman (5xLD50 or 10xLD50) or VX (10xLD50 or 20xLD50), followed by saline or atropine (10 mg/kg) or atropine plus HI 6 or or HLö 7 (30 mumol/kg) 2 minutes later. Nerve agent poisoning resulted in respiratory arrest within 2-3 minutes, followed by circulatory arrest a few minutes later in nontreated animals. Antidote treatment rapidly restored heart rate and mean arterial pressure and improved the respiratory function to various extent. The nerve agent injection caused a marked sinus bradycardia and a subsequent complete atrioventricular block within 1-2 minutes, followed by idioventricular rhythm. No ventricular tachyarrhythmias were observed in these groups just before death. Atropine and atropine plus oxime administration immediately restored sinus rhythm which persisted in animals with sufficient respiration > 50% of base line) throughout the observation period (60 minutes). In guinea-pigs with depressed respiratory function ( < 50%), intermittent ST-T wave alterations and second degree atrioventricular block were observed. In some cases, especially in tabun and soman (10xLD50) poisoning, sinus rhythm converted to deleterious ventricular tachycardia within 1 minute after treatment. These results suggest that atropine-containing antidote combinations may induce lethal arrhythmias in nerve agent poisoning, which may be of clinical importance during intravenous treatment of severe inhalative intoxications.

Animals↗
PubMed1996

Effects of benztropine on behavioral and toxic effects of cocaine: comparison with atropine and the selective dopamine uptake inhibitor 1-[2-(diphenylmethoxy)ethyl]-4-(3-phenyl-propyl)-piperazine.

Behavioral effects of cocaine that are relevant to its abuse have been associated with pharmacological actions at the dopamine uptake carrier. Benztropine (Cogentin) is an antiparkinson agent that has limited abuse despite its ability to block dopamine uptake, and has been suggested as a candidate for the treatment of cocaine dependence. Preclinical studies were conducted to assess the behavioral and toxic effects of benztropine alone and in conjunction with cocaine. Because of the mixed pharmacology of benztropine which includes antimuscarinic as well as dopaminergic actions, results obtained from parallel experiments with atropine and the selective dopamine uptake inhibitor, GBR 12935 (1-[2-(diphenylmethoxy)ethyl]-4-(3-phenyl-propyl)-piperazine), were performed. All of the drugs stimulated locomotor activity of mice, but atropine and benztropine had much lower efficacy. Nonstimulatory doses of GBR 12935 enhanced the locomotor stimulant effects of cocaine, whereas benztropine and atropine did not share this effect. GBR 12935, benztropine and cocaine increased fixed-interval responding, whereas atropine decreased fixed-interval response rates in rats. Only GBR 12935 and cocaine increased responding during timeout periods. GBR 12935, but not benztropine or atropine, fully reproduced the discriminative stimulus effects of cocaine (10 mg/kg). GBR 12935 and atropine augmented the discriminative stimulus effects of lower cocaine doses in rats. Only GBR 12935 and cocaine had convulsant effects and only GBR 12935 significantly enhanced the convulsant effects of cocaine in mice. These results document a behavioral and toxicity profile for benztropine distinct from that of classical dopamine uptake blockers. The data underscore further the potential of benztropine as a candidate for clinical evaluation in the treatment of cocaine dependence.

Animals↗
PubMed1995

Is atropine alone sufficient in acute severe organophosphorus poisoning?: experience of a North West Indian Hospital.

Between January 1990 and December 1992, 18 patients with severe organophosphate poisoning (OPP) were admitted to our respiratory intensive care unit (RICU). Suicidal ingestion was the commonest cause of poisoning (15/18). The treatment comprised of atropine in bolus doses. 2-PAM in conventional dose and mechanical ventilation (MV) with positive end expiratory pressure (PEEP) wherever indicated. The mean dose of atropine on day 1 was 178.9 mg (range 60-480 mg) and then gradually reduced. The mean duration of treatment with atropine was 9.6 days (range 1-24 days). We felt that aggressive atropinization and MV with PEEP is adequate and the role of 2-PAM given in 3 gm dose in 12 h is not clear. There is a need for controlled study to assess the efficacy of atropine and MV alone vs. atropine, 2-PAM in suggested doses and MV in severe OPP patients.

Acute Disease↗
PubMed1996

Atropine versus cyclopentolate plus tropicamide in esodeviations.

BACKGROUND AND OBJECTIVE: The correction of the total hypermetropic refractive error in the management of esodeviations is well accepted. The choice of the appropriate cycloplegic agent is still not settled. Despite evidence that atropine will more effectively uncover the total refractive error, cyclopentolate in combination with other cycloplegic agents continues to be recommended. This study evaluates the use of atropine compared with a combination of cyclopentolate and tropicamide and analyzes age, size of the refractive error, and size of the esodeviation as possible contributing variables in the response. PATIENTS AND METHODS: The records of 74 patients who underwent refraction with atropine 1% on one occasion and a combination of 1% cyclopentolate and 1% tropicamide on another occasion were reviewed. The mean and range of refractive errors for each eye for each group were determined. Comparisons were made for groups depending on age, size of the refractive error, and size of the esodeviation. RESULTS: The amount of hypermetropia determined with atropine was significantly higher than the amount determined with the combination of cyclopentolate and tropicamide. This difference was significant for three age groups of three groups with increasing amounts of hypermetropia, and two groups with differing amounts of esodeviations. In addition, 11% of right eyes and 19% of left eyes showed 1.25 D or more of hypermetropia with atropine. CONCLUSION: Refraction with 1% atropine ointment yields a significantly larger amount of hypermetropia than does refraction with a combination of cyclopentolate and tropicamide. This difference is statistically significant regardless of age, amount of hypermetropia, or size of the esotropia.

Administration, Topical↗
PubMed1977

[New experiences in the diagnosis of the sick sinus syndrome (correlation between clinical symptoms, long-therm ecg monitoring, atropine- and exercise testing and sinusnode recovery time) (author's transl)].

The tests recommended for establishing the diagnosis Sick Sinus Syndrome (SSS) were carried out on 36 patients with non-drug-induced Sinusbradycardia (16 symptomatic, 20 asymptomatic) and their resp. diagnostic value was then analysed. Contrary to previous publications, response of heart frequency to exercise testing was normal in all subjects as well as response to intravenous Atropine administration with the exception of 3 cases. A good correlation was found between typical arrhythmias in long-term Ecg monitoring and clinical symptoms. A pathologically prolonged Sinus Node Recovery Time (SNRT) is found in the same number of symptomatic and asymptomatic subjects, frequency-corrected SNRT shows the same results. Shortening of SNRT after Atropine is the more pronounced, the longer SNRT was before Atropine administration. Non-normalization and paradoxical prolongation of SNRT after Atropine have also been observed. In 8 patients stepwise progressive atrial pacing beginning with pacing-frequencies of 70 p.m. was performed before and after Atropine administration. Observation of the effect of Atropine on SNRT may prove to be more important for prognosis and treatment of the SSS than the finding of a prolonged SNRT for establishing the diagnosis. The diagnosis "SSS" should not be based on a pathologically prolonged SNRT alone. Analysis of long-term Ecg monitoring and clinical symptoms should be the main diagnostic tool.

Adult↗
PubMedDate not supplied

[The effect of a microinjection of atropine into the rat motor cortex on the acquisition of a motor skill].

Atropine is known to impede the acquisition of conditioned responses by neurons of the motor cortex. Does atropine exert influence (and of what kind) on acquisition of local movements controlled by neurons of the motor cortex? In the present study we examined the influence of atropine microinjections on acquisition of reaching movement in freely moving rats. The intracortical pressure injections of atropine (5 mcg and 15 mcg/0,6 mcl/40 s) were made unilaterally into the forearm area of the motor cortex in adult mongrel rats. Hungry rats learned to reach sunflower seeds form a horizontal tube by using the forelimb contralateral to the injected site. Atropine exerted dose-dependent influence of the acquisition of the motor skill. All the tested doses depressed the inhibition of concurrent movements during learning. In addition, the higher dose of atropine inhibited the initiation of the reaching movements. A hypothesis was proposed to explain these differences.

Animals↗