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PubMed2000

Systemic effects of topical and subconjunctival ophthalmic atropine in the horse.

OBJECTIVE: To identify any systemic effects of topical and subconjunctival administration of atropine sulfate in the horse. Animals studied Six mature grade horses were treated hourly in one eye with topical ophthalmic atropine drops for 24 h. Five horses were treated subconjunctivally in one eye with 3 mg of atropine sulfate. Procedures Pupillary light reflexes, pupil size, electrocardiographic parameters, girth measurements, intestinal motility, and clinical signs of abdominal pain were monitored. RESULTS: Alteration in auscultated gut motility and clinical signs of abdominal pain were the most sensitive indicators of the systemic manifestations of the topically applied atropine. Gut motility was absent in all horses for periods of 2-18 h in all four abdominal quadrants in horses given topically administered atropine. Signs of abdominal pain were observed in four of six horses that received topical atropine. In the subconjunctival test study, gut motility was absent in three horses for periods of 3-7 h. Uniocular subconjunctival injection of 3 mg atropine sulfate produced signs of abdominal pain in one of six horses. Conclusion The ophthalmic administration of atropine can affect gut motility and induce signs of colic in selected horses.

Journal Article↗
PubMed2002

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

OBJECTIVE: To compare patching and atropine as treatments for moderate amblyopia in children younger than 7 years. METHODS: In a randomized clinical trial, 419 children younger than 7 years with amblyopia and visual acuity in the range of 20/40 to 20/100 were assigned to receive either patching or atropine at 47 clinical sites. MAIN OUTCOME MEASURE: Visual acuity in the amblyopic eye and sound eye after 6 months. RESULTS: Visual acuity in the amblyopic eye improved in both groups (improvement from baseline to 6 months was 3.16 lines in the patching group and 2.84 lines in the atropine group). Improvement was initially faster in the patching group, but after 6 months, the difference in visual acuity between treatment groups was small and clinically inconsequential (mean difference at 6 months, 0.034 logMAR units; 95% confidence interval, 0.005-0.064 logMAR units). The 6-month acuity was 20/30 or better in the amblyopic eye and/or improved from baseline by 3 or more lines in 79% of the patching group and 74% of the atropine group. Both treatments were well tolerated, although atropine had a slightly higher degree of acceptability on a parental questionnaire. More patients in the atropine group than in the patching group had reduced acuity in the sound eye at 6 months, but this did not persist with further follow-up. CONCLUSION: Atropine and patching produce improvement of similar magnitude, and both are appropriate modalities for the initial treatment of moderate amblyopia in children aged 3 to less than 7 years.

Amblyopia↗
PubMed1975

Cardiac rate and rhythm changes with atropine and methscopolamine.

The effects of methscopolamine bromide (MSB) and atropine were compared in patients prior to elective surgery. After administration of the second dose of MSB (total dose 1.5 mug/kg) all patients exhibited at least 20% increase in heart rate. In contrast, three doses of atropine (total dose 5.3 mug/kg) were required for most patients to attain a 20% increase in heart rate while 2 patients did not attain this heart rate with a dose of 10.6 mug/kg of atropine. Comparison if single injections of MSB and atropine in normal subjects also demonstrated a more reliable dose-response relationship with MSB. Electrocardiographic changes recorded were typical of those reported with anticholinergic agents. Sinus and atrial arrhythmias were more common with atropine and nodal arrhythmias and conduction disturbances were more common with MSB. This study demonstrated that MSB can be reliably substituted for atropine when an anticholinergic drug is needed to increase heart rate. Since MSB has a limited ability to cross the blood-brain barrier, it may be the more desirable drug in patients in whom the central nervous system effects of atropine may be deleterious.

Adult↗
PubMed1985

Integrated pharmacokinetics and pharmacodynamics of atropine in healthy humans. I: Pharmacokinetics.

The pharmacokinetics of atropine in three healthy male volunteers after intravenous administration of 1.35 and 2.15 mg of the drug was determined. Pharmacodynamic effects of atropine were measured simultaneously. All the data were fitted to a novel integrated kinetic-dynamic model. Plasma concentrations of atropine and the amounts of atropine and its primary metabolite, tropine, excreted in the urine were measured by a sensitive gas chromatographic-mass spectrometric assay. The kinetics of elimination of atropine was first order. There was evidence that the kinetics of distribution of the drug was dose dependent. Two phases with apparent half-lives of 1 and 140 min were distinguishable in accordance with a linear two-compartment disposition model for atropine. The urinary excretion of unchanged drug was 57% of the dose. The steady-state volume of distribution was 210 L, implying extensive tissue binding and/or partitioning. Renal plasma clearance was 660 mL/min, suggesting significant tubular secretion. The renal clearance of atropine depended on urine flow. Urinary excretion of tropine amounted to 29% of the dose. The kinetics of the metabolite was first order.

Adult↗
PubMed1988

Effect of atropine on feedback regulation of pancreatic enzyme secretion in rats.

The effect of atropine on the feedback regulatory mechanism of pancreatic enzyme secretion exerted by intraluminal trypsin was investigated in conscious rats. Intravenous atropine infusion (50 micrograms/kg/h) suppressed pancreatic enzyme secretion to the same extent in both the presence and the absence of pancreatic juice in the intestine. However, with or without atropine infusion, pancreatic secretory rate was higher throughout diversion of pancreatic juice than during intraduodenal return of the juice. Atropine also inhibited the stimulatory response to intraduodenal trypsin inhibitor and intravenous caerulein. The atropine-induced inhibitory effect was not significantly different between the two experimental conditions. Regardless of atropine administration, both trypsin inhibitor and caerulein caused a significant increase in pancreatic secretion. The results suggest that cholinergic mechanisms have little influence on the feedback regulation. Cholinergic mechanisms may play an important role in maintaining the physiologically basal secretion because the basal secretion is atropine-sensitive.

Amylases↗
PubMed2001

Increase of peak expiratory flow by atropine is dependent on circadian rhythm.

PURPOSE: To examine whether the bronchodilatory effect of atropine differs in the evening from the morning. METHODS: Thirteen adult healthy volunteers with no oral medication intake were studied. At 1600, peak expiratory flow (PEF) was measured three times, and the highest value recorded. Subsequently, the volunteer received 0.01 mg(-1) x kg(-1) atropine im, and the PEF was measured every 30 min for 180 min. On a different day, at 0400, the effect of atropine on the PEF was measured again in the same way. RESULTS: The PEF values before atropine at 1600 and 0400 were 485 +/- 92 (350-730) and 458 +/- 76 (340-600) 1 min(-1),(P < 0.05). There was no difference in PEF values between the 1600 and 0400 time courses after atropine. The PEF value was increased only at 90 min at 1600 (P = 0.0012), but at 30, 60, 90 and 120 min at 0400 (P = 0.0001). CONCLUSION: Atropine administration has a weak bronchodilatory effect in the evening, but a stronger effect in the morning. Airways are narrower in the morning than in the evening, and this change is inhibited by atropine such that the PEF values are restored to those observed in the evening.

Adult↗
PubMed2000

Efficacy of biperiden and atropine as anticonvulsant treatment for organophosphorus nerve agent intoxication.

The ability of the nerve agents tabun, sarin, soman, GF, VR, and VX to produce brain seizures and the effectiveness of the anticholinergics biperiden HCl or atropine SO4 as an anticonvulsant treatment were studied in a guinea-pig model. All animals were implanted a week prior to the experiment with cortical electrodes for electroencephalogram (EEG) recordings. On the day of exposure, the animals were pretreated with pyridostigmine (0.026 mg/kg, i.m.) 30 min prior to challenge with a 2 x LD50 dose (s.c.) of a given agent. In separate experiments, animals were challenged with 5 x LD50 (s.c.) of soman. One minute after agent challenge, the animals were treated intramuscularly (i.m.) with 2 mg/kg atropine SO4 admixed with 25 mg/kg 2-PAM Cl and then observed for the onset of seizure activity. Five minutes after the start of nerve agent-induced EEG seizures, animals were treated i.m. with different doses of biperiden HCl or atropine SO4 and observed for seizure termination. The anticonvulsant ED50 of biperiden HCl and atropine SO4 for termination of seizures induced by each nerve agent was calculated and compared. With equally toxic doses (2 x LD50) of these agents, continuous EEG seizures (status epilepticus) developed in all animals challenged with soman, tabun, or VR, and in more than 90% of the animals challenged with GF or sarin. In contrast, only 50% of the animals developed seizures when challenged with VX. The times to onset of seizures for soman, tabun, GF, and sarin were very similar (5-8 min) while for VR, it was about 10 min. In the case of VX, not only was the time to seizure development longer (20.7 min), but the seizure activity in 19% of the animals terminated spontaneously within 5 min after onset and did not return. Under these conditions, the anticonvulsant ED50s of biperiden HCl for soman, GF, VR, tabun, sarin, and VX were 0.57, 0.51, 0.41, 0.2, 0.1, and 0.09 mg/kg, respectively, while those of atropine SO4 for soman, VR, tabun, GF, sarin, and VX were 12.2, 11.9, 10.4, 10.3, 5.1, and 4.1 mg/kg, respectively. In separate experiments, the anticonvulsant ED50 doses of biperiden for animals challenged with 2 or 5 x LD50 of soman were 0.48 (95% confidence limits 0.25-0.73) or 0.57 (95% CI 0.38-0.84) mg/kg, respectively, while the anticonvulsant ED50s for atropine (12.2 mg/kg, i.m.) were identical under these same two challenge conditions. The present study demonstrates that all nerve agents can produce status epilepticus and that the therapeutic effectiveness of atropine and biperiden roughly paralleled the seizurogenic potential of these agents.

Animals↗
PubMed1987

Bedside evaluation of sinus bradycardia: usefulness of atropine test in discriminating organic from autonomic involvement of sinus automaticity.

In 55 patients with persistent sinus bradycardia who underwent an electrophysiologic study of sinus node, both in the basal state and after autonomic blockade (propranolol, 0.2 mg/kg, and atropine, 0.04 mg/kg), an atropine test (0.02 mg/kg) was performed the following day. The 49 patients in whom sinus rate could be evaluated after atropine were subdivided into two groups--group I, 24 patients (age: 54 +/- 13 years) with normal intrinsic sinus automaticity (normal intrinsic heart rate and intrinsic corrected sinus node recovery time) and group II, 25 patients (age: 62 +/- 9 years) with abnormal intrinsic sinus automaticity. In group I, atropine increased sinus rate from 53.7 +/- 4 to 87.9 +/- 17 bpm (delta %: 65.5 +/- 33) and in group II from 51.6 +/- 5 to 73.9 +/- 14 bpm (delta %: 43.1 +/- 26). The discriminant threshold of sinus rate after atropine and its percent increase, obtained by discriminant analysis, was 80 bpm and +52%, respectively, with a misleading classification of 32% and 36%, respectively. The overall predictive accuracy of sinus rate after atropine was higher than the percent change in sinus rate (73% and 65%, respectively). These data evidence that the atropine test is not very helpful in discriminating between an organic and an autonomic involvement of sinus automaticity in patients with sinus bradycardia.

Adult↗
PubMed1975

New observations on the effects of atropine on the sinoatrial and atrioventricular nodes in man.

Previous observations of slowing of the heart rate after administration of atropine in doses smaller than 0.4 mg and recent reports of development of rhythm disorders in patients with acute myocardial infarction given atropine prompted us to evaluate systematically the effects of various doses of atropine (0.1 to 0.8 mg) on the response of the sinoatrial (S-A) and atrioventricular (A-V) nodes in healthy volunteers. The response of the S-A node to atropine was characteristically bimodal, slowing at smaller doses and accelerating at larger doses. In contrast, the A-V node showed acceleration of conduction in response to all doses of atropine used. A hypothesis based on current understanding of the electrophysiologic parameters governing impulse formation and impulse conduction is advanced to explain the apparent paradox in the S-A and A-V nodal responses to small doses of atropine. The results suggest the need for caution and continuous rhythm monitoring when giving atropine to patients with acute myocardial infarction.

Adult↗
PubMed1985

Pathways through cingulate, neo- and entorhinal cortices mediate atropine-resistant hippocampal rhythmical slow activity.

Rats prepared with a lesion separating the entorhinal cortex from the neocortex and cingulate cortex displayed apparently normal hippocampal rhythmical slow activity (RSA) with a frequency of 6-12 Hz in both CA1 and dentate gyrus during Type 1 behavior (locomotion, head movements, changes in posture). Variations in the commissural average evoked potential (AEP) and increased power in the 30-100 Hz range (fast waves) also correlated with Type 1 behavior. Urethane did not abolish the RSA. However, systemic administration of atropinic drugs eliminated all RSA and eliminated or attenuated the Type 1 behavior-related variations in the AEP and fast waves. Thus, the normally present atropine-resistant RSA was eliminated by the cortical lesion while atropine-sensitive RSA remained intact. Removal of cingulate cortex alone was partially effective in suppressing atropine-resistant RSA but a lesion of the neocortex only, sparing cingulate cortex, had a minimal effect on it. Lesions of the amygdala, the anterior or medial thalamus or the cerebellum had little or no effect on atropine-resistant RSA. Previous work has shown that lesions of the entorhinal cortex or lateral hypothalamus eliminate atropine-resistant RSA. We suggest that atropine-resistant RSA is mediated by a somewhat diffuse pathway which traverses the hypothalamus, cingulate cortex, and neocortex before reaching the hippocampus via the entorhinal cortex.

Animals↗
PubMed1995

Glucose attenuation of atropine-induced deficits in paradoxical sleep and memory.

When administered systemically, glucose attenuates deficits in memory produced by several classes of drugs, including cholinergic antagonists and opiate agonists. Glucose also enhances memory in aged rats, mice, and humans. In addition, glucose ameliorates age-related reductions in paradoxical sleep. Because deficits in paradoxical sleep are most marked in those individual aged rats that also have deficits in memory, treatments which improve one of these functions may similarly improve the other. The present experiments show that glucose attenuates deficits in paradoxical sleep and memory after atropine administration, with similar dose-response curves for both actions. In the first experiment, rats received saline, atropine (1 mg/kg), glucose (100 mg/kg) or combinations of atropine + glucose (10, 100, 250, and 500 mg/kg) 30 min before assessment on a spontaneous alternation task. In the second experiment, 3-h EEGs were assessed for spontaneous daytime sleep in rats administered saline, atropine (1 mg/kg), glucose (100 mg/kg) or combinations of atropine + glucose (10, 100 and 250 mg/kg). In both experiments, glucose significantly attenuated deficits at an optimal dose of 100 mg/kg. A third experiment assessed blood glucose levels after injections of atropine + glucose (100 mg/kg) and determined that blood glucose levels were similar to those produced by other treatments which enhance memory. These results are consistent with the view that paradoxical sleep and at least one test of memory are similarly influenced by atropine and glucose.

Animals↗
PubMed1985

Effects of morphine and atropine on motility and transit in the human ileum.

We examined motility of the ileocecal region, pressures at the ileocecal sphincter, and ileal flow after therapeutic doses of morphine and atropine. Using a factorial design in two cells of 8 (2(3] subjects, drugs were given during fasting and postcibally. Morphine (100 micrograms/kg body wt as a bolus intravenously) and atropine (7 micrograms/kg body wt as a bolus) stimulated migrating bursts of phasic activity (similar to phase III of the migrating motor complex). Morphine initially stimulated ileal flow, but atropine could not be shown to have this effect. Atropine reduced markedly the occurrence of sporadic pressure waves in the ileum, but morphine did not. Whereas atropine delayed mouth-to-ileum transit of polyethylene glycol, given in a mixed meal, morphine did not. Naloxone, in the dosage used (40 micrograms/kg body wt as a bolus, followed by 10 micrograms/kg body wt X h) had no independent effects on motility or flow, but did blunt the stimulatory effects of morphine and atropine on migrating motor complexes. We could not demonstrate an effect of any drug on the transit of lactulose from terminal ileum to cecum. Neither morphine nor atropine had impressive effects on tone at the ileocecal sphincter. These observations, while not specifying the mechanisms for constipation after opiates or anticholinergics, highlight the complexities of small bowel transit in humans and point out that the antidiarrheal effects of drugs are probably multifactorial.

Adult↗
PubMed1991

The synergism of atropine and the cholinesterase reactivator HI-6 in counteracting lethality by organophosphate intoxication in the rat.

Rats were intoxicated with two different S-aminoalkyl-phosphonothioate cholinesterase inhibitors, viz. I-1 (S-diethylaminoethyl-O-cyclohexyl-methyl-phosphonothioate), which has a mixed central/peripheral mode of action, and I-2, the methiodide derivative of I-1, which acts almost solely peripherally. It was found that atropine did not have any beneficial effect on lethality in the case of an I-2 intoxication but did so, although only slightly, in the case of I-1. Therefore, the effect of atropine against I-1 intoxications must be mediated through central mechanisms, the peripheral parasympatholytic effect being negligible in counteracting lethality. Furthermore atropine antagonized the convulsions caused by intoxication with I-1. The oxime used as a reactivator of inhibited acetylcholinesterase, HI-6, was more effective than atropine against either organophosphate. In the case of an I-2 intoxication HI-6 proved extremely active. It is, therefore, concluded that HI-6 acts mainly peripherally. It was also found that HI-6 has a slight anticonvulsive action. The combination of HI-6 and atropine had a large synergistic effect in the case of I-1, but in the case of I-2 hardly any synergism was observed. Obviously, the combination of the oxime and atropine is particularly effective when the toxicant has a mixed central/peripheral action. In such intoxications the acetylcholinesterase reactivation in the respiratory neuromuscular synapse by the oxime is supplemented by the central action of atropine, which improves respiratory control at the level of the central nervous system.

Animals↗
PubMed1982

A comparison of the central and peripheral effects of atropine on force lever performance.

The central and peripheral effects of atropine, a muscarinic antagonist, on motor control were tested in a force lever apparatus. Three rhesus monkeys were trained to extend their arms through a tube and press a manipulandum with between 25 and 40 grams of force for 3 continuous seconds. Responding was maintained by the delivery of 1.5 ml of water. Single injections of atropine sulfate or atropine methylnitrate (a quaternary derivative) of atropine which does not cross the blood brain barrier) were given 30 min prior to the session. Atropine sulfate disrupted force lever performance in a dose related fashion. Atropine methylnitrate had little or no effect on responding. The effects of atropine on motor control as measured in this procedure, therefore, appear to be centrally mediated.

Animals↗
PubMed1986

Psychoactivity of atropine in normal volunteers.

Subjective effects of atropine sulfate injections were assessed in normal volunteers (n = 10), as one portion of a 3-part study (behavioral, subjective and physiologic effects of atropine). Each volunteer was given 0, 2 or 4 mg/70 kg atropine sulfate intramuscularly according to randomized block sequences on different test days. To assess psychoactivity of atropine, the Single Dose Questionnaire (SDQ) and the Addiction Research Center Inventory (ARCI) were given 1 hr before and 1 hr following drug injections. Data from the SDQ indicated that atropine produced significant discriminable effects but did not elevate scores on a drug liking scale. Data from the ARCI indicated that atropine produced significant sedative-like effects (pentobarbital-chlorpromazine-alcohol scale). Taken together, the data from the psychometric instruments confirms that atropine is a drug of relatively low abuse potential.

Adult↗
PubMed1988

A comparison of the effects of atropine on real-feeding and sham-feeding of sucrose in rats.

In Experiment 1 the influence of atropine methyl nitrate on the sham-feeding response of adult female rats to a sucrose solution was determined. Atropine (1 or 5 mg/kg) reliably suppressed the sham-intake of sucrose when the drug was administered 30 or 0 min prior to, or 17 min after the start of the feeding session. The suppressive effect was less, however, when the drug was administered 30 min before testing compared to the other two injection-test conditions. In Experiment 2 atropine failed to reliably decrease the real-feeding of a sucrose solution whether it was injected 30, 15, or 0 min prior to testing. These results were replicated in Experiment 3; atropine (0 min injection-test interval) reduced the sham-intake but not the real-intake of a sucrose solution. However, atropine decreased the rate of feeding under both real- and sham-feeding conditions. The fact that atropine reduced feeding rate but not meal size in the real-feeding condition was attributed to the drug's lack of effect on postingestive satiety. The present findings along with other recent results indicate that (1) the injection-test interval is a potentially important variable in studies involving atropine; (2) results obtained with sham-feeding animals do not always generalize to real-feeding animals; and (3) cholinergically-mediated cephalic responses are of questionable importance in the control of meal size.

Animals↗
PubMed1989

Effect of low-dose atropine on heart rate fluctuations during orthostatic load: a spectral analysis.

Spectral analysis was utilized in order to determine the influence of low (0.7 microgram/kg)-dose atropine sulfate injections on the isolated spectral power components of heart rate fluctuations in contrast to moderate (0.02 mg/dose)-dose atropine and unmedicated states in human subjects during orthostatic load. Low-dose atropine decreased mean heart rate and increased respiration-related spectral power compared with controls in both the supine and standing posture. In supine subjects total power (0.01-0.5 Hz) was unchanged compared with controls due to a decreasing trend of low-frequency (0.01-0.05 Hz) and mid-frequency (0.05-0.15 Hz) heart rate spectral power. Standing upright, there was a distinct increase in total power with significantly higher values than in the controls resulting from an enormous activation of mid-frequency heart rate fluctuations. The peak frequency of the mid-frequency component was increased with a strong tendency compared with controls. Moderate-dose atropine increased mean heart rate and decreased total power, mid-frequency and respiration-related heart rate spectral power and peak frequency compared with controls in both positions. Our results suggest that low-dose atropine affects the interaction between sympathetic and parasympathetic limbs in the autonomic control of cardiac function in a complex manner producing a differentiated pattern of heart rate fluctuations dependent on the body posture. We suggest that low-dose atropine augments and moderate-dose atropine attenuates the vagal cardiac efferent activity in each position.

Adult↗
PubMed1995

Quantitative assessment of the autonomic nervous system activities during atropine-induced bradycardia by heart rate spectral analysis.

Using power spectral analysis of heart rate fluctuation, autonomic nervous system activities in bradycardia appearing in the initial phase of atropine administration were evaluated quantitatively in 16 healthy females. Atropine sulfate (10 micrograms/kg), diluted in 100 ml of 0.9% NaCl solution, was intravenously infused at a rate of 0.5 micrograms/kg per min. Electrocardiograms were sampled for 4 min for later analysis before and 0, 5, 10, 15 and 20 min after initiation of atropine infusion. Powers of low (LFC, 0.05-0.15 Hz) and high-frequency (HFC, 0.15-0.4 Hz) components in the power spectrum of R-R interval variations, and the LFC/HFC ratio were determined at each sampling point. HFC power at 0-4 min increased from 1.11 +/- 0.18 ms2 (mean) of baseline value to 1.37 +/- 0.19 ms2 (P < 0.05). The next 5-9-min value of 1.48 +/- 0.14 ms2 was the maximum, and the amount of atropine infused by 9 min was 4.5 micrograms/kg. The HFC powers following this point decreased. The 20-24-min value after 10 micrograms/kg atropine decreased to 0.21 +/- 0.03 ms2 (P < 0.01), which was lower than the previous 15-19-min value of 0.36 +/- 0.04 ms2 (P < 0.01). The LFC/HFC ratios showed no significant change for the initial 9 min of the atropine infusion. However, these ratios at 15-19 min and 20-24 min were increased from 0.50 +/- 0.04 (mean) of baseline value to 0.75 +/- 0.09 and 0.81 +/- 0.09, respectively (P < 0.01). A transient vagotonic state after atropine administration, followed by the well-known vagolytic state, was quantitatively detected by non-invasive spectral analysis of heart-rate fluctuation.

Adolescent↗