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At least 19 recordsLinked to original sources
PubMed1990

Relative effects of xylazine-atropine, xylazine-atropine-ketamine, and xylazine-atropine-pentobarbital combinations and time-course effects of the latter two combinations on brain stem auditory-evoked potentials in dogs.

Brain stem auditory-evoked potentials (BAEP) were recorded in 4 dogs to analyze the relationship between acoustic stimulus intensities and peak latencies of each wave, and to investigate the relative effects of xylazine-atropine, xylazine-atropine-ketamine, and xylazine-atropine-pentobarbital combinations and the time-course effects of the latter 2 drug combinations on BAEP. Click stimulations fixed at a stimulus rate of 10/s and a frequency of 4 kHz were delivered at intensities ranging from 10- to 110-dB sound pressure level (SPL) in 10-dB steps for analyzing the relationship between the acoustic stimulus intensities and the peak latencies and at an intensity of 110-dB SPL for investigating the effects of the sedative and anesthetic drug combinations and their time-course effects on BAEP. Waves I to VI were identified with stimulus intensity of greater than or equal to 50-dB SPL. Wave VII was observed in some records, but was excluded from statistical analysis. As stimulus intensity was increased from 50- to 110-dB SPL, the latency decreased for all waves during xylazine-atropine-ketamine anesthesia. There were no statistically significant differences in the peak latencies of each wave in BAEP among xylazine-atropine, xylazine-atropine-ketamine, and xylazine-atropine-pentobarbital combinations 20 minutes after drug administration, except that the latency of wave VI during xylazine-atropine sedation was significantly (P less than 0.01) shorter than that detected during xylazine-atropine-ketamine or xylazine-atropine-pentobarbital anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acoustic Stimulation↗
PubMed1983

Effect of the combinations atropine + cyproheptadine and atropine + carbenoxolone in duodenal ulcer therapy.

Prospective randomized studies were carried out in 136 endoscopically verified duodenal ulcer patients to evaluate the healing effects of the following four-week courses of treatment: placebo, atropine (3 X 0.66 mg), carbenoxolone (3 X 100-3 X 50 mg), atropine + cyproheptadine (3 X 4 mg), atropine + carbenoxolone. Antacid powder was also supplied for relief of symptoms as required. Ulcer healing (incidence and planimetrically calculated surface), changes in complaints, antacid consumption and subjective and objective side-effects were evaluated during each type of treatment. The effectiveness of the different treatments were compared according to these points. The results showed: (i) that atropine, atropine + cyproheptadine and carbenoxolone all had good ulcer healing effects (75%, 74%, 62% respectively), according to incidence; (ii) that the atropine + carbenoxolone combination did not have a better healing effect (44%) than placebo (41%); (iii) that there were no significant differences among the planimetrically calculated ulcer healing effects during the different types of treatment; (iv) that the earliest diminution in complaints the greatest increase in body weight were found in the atropine + cyproheptadine group; (v) that there were no objective side-effects during the four-week treatment periods; and (vi) that definite subjective side-effects were observable only in the two atropine-treated groups. The findings led to the conclusion that the atropine + cyproheptadine combination is of value for the treatment of duodenal ulcer, while the atropine + carbenoxolone combination presents no practical advantages.

Adult↗
PubMed2003

Atropine availability as an antidote for nerve agent casualties: validated rapid reformulation of high-concentration atropine from bulk powder.

STUDY OBJECTIVE: Atropine is the preferred antidote for immediate management of toxicity associated with nerve agents or other cholinergic syndromes. A large-scale exposure to a nerve agent or organophosphate insecticide might result in many victims presenting for care within a short period of time. This situation would require the prompt availability of a large amount of atropine to provide treatment. Antidote stocks at many hospitals are inadequate to meet this demand. Atropine that is commercially available comes supplied at concentrations of either 0.4 mg/mL or 1 mg/mL, thereby requiring intravenous administration because of the volume necessary to administer the commonly recommended initial dose of 2 to 6 mg. Moderately ill victims may not require an intravenous line for other care, and in the setting of overwhelmed resources, intramuscular administration is faster and easier to perform. METHODS: To facilitate the delivery of larger atropine doses, we developed a method of fortifying existing injectable atropine with bulk pharmaceutical-grade atropine powder to a concentration of 2 mg/mL, thereby increasing the amount available and facilitating its intramuscular administration. An independent analysis of the resulting formulation was undertaken to assess its potency, absence of pyrogens, and stability. RESULTS: The amount of atropine initially present varied by less than +/-5%, within the range allowed by the US Pharmacopeia for the original product. The product was pyrogen free and maintained its potency at refrigeration temperature for at least 8 weeks after preparation and at room temperature for 4 weeks. Once all materials were available, the compounding of this preparation required about 1 hour to complete. CONCLUSION: Existing atropine stocks can be readily augmented by fortification with powdered atropine accurately and inexpensively. Common pharmaceutical guidelines recommend refrigeration for compounded products such as this if not completely used within 28 days.

Adult↗
PubMed1983

Comparative effect of atropine on the adrenergic and muscarinic stimulation of phospholipid 32P labelling in isolated parotid cells: atropine, a possible blocker of alpha-adrenergic receptors.

The inhibitory effect of atropine on phospholipid 32P labelling stimulated by muscarinic or alpha-adrenergic agonists was studied in isolated parotid cells. Atropine (10(-11) to 10(-4) M) had no effect on phospholipid 32P labelling in unstimulated cells. In contrast, 10(-8) to 10(-7) M atropine provoked a competitive inhibition of the cholinergic stimulation (i.e. this effect was completely wiped out at high agonist concentration). The atropine app. KD for the muscarinic receptor was 5 X 10(-9) M. Moreover, atropine inhibits the adrenergic stimulation of phospholipid 32P labelling by decreasing the efficacity and potency of the adrenergic agonists. The atropine app. KD for the alpha-adrenergic receptor can be estimated at 10(-5) M. This inhibition of alpha-adrenergic stimulation appears to be specific since atropine was without effect on the substance P or beta-adrenergic stimulation. At very low concentration (10(-10) - 10(-9) M) atropine seems to be a modulator (activator) of the muscarinic or adrenergic agonist-receptor complex. From the present data, it is suggested that atropine, besides its classical blocker effect at the muscarinic receptor, at high concentration is a specific alpha-adrenergic antagonist.

Animals↗
PubMed1992

Cycloplegic refraction in children: single-dose-atropinization versus three-day-atropinization.

A new scheme for refractive measurements under atropine cycloplegia was tested in 90 strabismic children aged two to several years. Refraction was determined by an autorefractor (CANON R 10) 90 minutes after application of two drops of atropine (0.5% atropine children < 2 1/2 years; 1.0% atropine children > 2 1/2 years) and compared with the results after 3 days of receiving 1 atropine eyedrop 3 times daily. In 86.5% the spherical equivalents differ not more than 1.0 diopter (p = 0.05); the correlation was 0.99. Astigmatic corrections were in agreement in 95.5%, the axis of cylinders in 93.0% (p = 0.05); the correlations were 0.95 and 0.97. The residual accommodation 90 minutes after 2 drops of atropine was not more than 1 diopter in all children. The additional cycloplegic effect of the three-day-atropinization was only 0.5 diopters. This new type of application allows a more rapid and less toxic assessment of refraction than the usual three-day-atropinization.

Accommodation, Ocular↗
PubMed1985

Effects of substance P antagonists on the atropine-sensitive and atropine-resistant responses of guinea-pig ileum to substance P.

The effects of substance P (SP) antagonists on the atropine-sensitive and atropine-resistant responses to SP of guinea-pig isolated ileum were investigated. The atropine-resistant response to SP was the contractile response on untreated preparations, and the atropine-sensitive response was the response to high concentrations of SP (5 X 10(-7) M) on preparations desensitized to SP with a concentration of SP of 3 X 10(-7) M. The SP antagonists tested, (D-Pro2,D-Phe7,D-Trp9)-SP, (D-Pro2,D-Trp7,9)-SP, (D-Arg1,D-Pro2,D-Trp7,9,Leu11)-SP and (D-Arg1,D-Trp7,9,Leu11)-SP (spantide), did not have similar orders of potency on the atropine-sensitive and atropine-resistant responses to SP, spantide being more potent than the other antagonists on the atropine-resistant response but no more potent on the atropine-sensitive response than (D-Pro2,D-Phe7,D-Trp9)-SP or (D-Arg1,D-Pro2,D-Trp7,9,Leu11)-SP. These findings are consistent with the hypothesis that neuronal receptors for SP differ from those on smooth muscle in guinea-pig ileum.

Acetylcholine↗
PubMed1985

Comparison of pharmacokinetic and pharmacodynamic parameters following oral or intramuscular atropine in children. Atropine overdose in two small children.

Pharmacokinetic and pharmacodynamic parameters of atropine 0.03 mg/kg p.o. or 0.02 mg/kg i.m. were compared in a double-blind study in 20 children with a mean age of 5.1 years undergoing otolaryngological surgery, mostly adenotomy. Outside the study protocol, two small children accidentally received an overdose of atropine 0.3 mg/kg p.o. In addition to atropine, all children received triclofos 70 mg/kg p.o. Following p.o. administration of atropine, the mean maximum serum concentration of 6.7 nmol/l occurred at 2 h. The corresponding result after i.m. administration was 5.7 nmol/l at 0.5 h. Serum concentrations of atropine were 3.5 and 1.3 nmol/l 8 h after p.o. and i.m. administration, respectively. At 70 min the anti-sialogogue effect was clinically satisfactory after both modes of administration. The heart rate increased statistically significantly only after i.m. administration. The mean maximum rise in the rectal temperature before the start of anaesthesia occurred at 1 h and was 0.5 degrees C in the p.o. group and 0.7 degrees C in the i.m. group. The flush phenomenon, mostly on the face and sometimes also on the chest, occurred in both groups, being more intense in the i.m. group than in the p.o. group. The children who developed flush had a statistically significantly higher rise in rectal temperature than the children without flush. There was a positive but weak correlation between the serum concentration of atropine and the heart rate, whereas the correlation between the serum concentration after i.m. atropine and the rectal temperature was weakly negative. On the basis of the present study, there were no decisive differences between the effects and side-effects of the two modes of administration of atropine.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1983

Methyl atropine bromide versus atropine sulphate. A clinical comparison.

In a double blind clinical investigation we compared methyl atropine bromide to atropine sulphate in equivalent doses for their effects on changes in the heart rate and dryness of the mouth. Drugs were administered five minutes before the induction of anesthesia. Methyl atropine bromide appeared to have a stronger positive chronotropic effect on the heart rate and a more pronounced mouth drying action. Less dysrhythmias were observed after the methyl congener. Both drugs failed to alter blood pressure significantly. We concluded that methyl atropine bromide is superior to atropine sulphate because it does not produce side effects which may cause the central anticholinergic syndrome. For clinical use, however, methyl atropine bromide should be administered only in half-equivalent dose of atropine sulphate to prevent excessive tachycardia and dryness of the mouth.

Adult↗
PubMed1997

Full-time atropine, intermittent atropine, and optical penalization and binocular outcome in treatment of strabismic amblyopia.

OBJECTIVE: The purpose of the study is to evaluate the monocular and binocular outcome of three types of "penalization" (blurring of the sound eye) treatment of amblyopia: traditional full-time atropine or optical penalization and a new intermittent atropine regimen involving atropine instillation 1 to 3 days a week. DESIGN: The study design was a retrospective study. PARTICIPANTS: A total of 163 patients with strabismic amblyopia treated by full-time atropine (n = 38), intermittent atropine (n = 73), or optical (n = 52) penalization participated. MAIN OUTCOME MEASURES: Logarithm of the minimum angle of resolution (logMAR) visual acuity, and binocularity index were determined. RESULTS: All three forms of penalization produced statistically significant mean reduction in amblyopia (1.7-2.7 logMAR lines) and mean improvement in binocularity by the end-of-treatment or long-term follow-up visit or both, with minimal mean loss after discontinuation or slight mean improvement on these measures at long-term mean follow-up of 1.9 to 4 years across groups. Few patients achieved high-grade stereoacuity. Compliance was high. Comparable efficacy was found for all three treatment groups after controlling for age, depth of amblyopia, and binocularity at the initial visit. Initial-visit amblyopia depth was strongly and significantly associated with amblyopia depth at both post-treatment visits. Pretreatment and post-treatment binocularity showed a similar strong relationship. Surprisingly, however, there was no consistent or significant association found between depth of amblyopia and binocularity in any visit combination. Post-treatment measures of these two variables also were not associated with initial-visit age or refractive error at any clinically significant level. Mean treatment duration was 1.1 to 2.9 years and was not found to be associated with visual outcome. Amblyopia reversal was found in one (full-time atropine) case at a clinically important level. CONCLUSIONS: The authors confirmed previous reports of penalization's efficacy as a primary treatment of moderate amblyopia (20/100 or better acuity) and, in some cases, relatively severe amblyopia (>20/100) and also confirmed its ability to significantly improve mean binocularity. Amblyopia and binocularity appear to respond to treatment independently and, within the postinfancy age range of the sample studied, the responses appear to be independent of initial-visit age. The high acceptability to patients and parents of atropine penalization, and particularly of the intermittent regimen introduced here, suggests the need for prospective-study-based re-evaluation of the relative merits of penalization and occlusion as the standard of care for mild-to-moderate amblyopia.

Accommodation, Ocular↗
PubMed1987

Influence of atropine and N-methyl atropine pretreatments on behavioral and physiological effects of the irreversible muscarinic agonist, BM123.

The irreversible muscarinic agonist, BM123 (63 mu moles kg-1, IV), was shown to produce central and peripheral physiological signs characteristic of cholinergic agonists. It also induced hypothermia, elevated nociceptive thresholds, reduced locomotor activity and disrupted spontaneous alternation performance in rats. The centrally acting muscarinic antagonist, atropine (50 mu mole kg-1) prevented or reduced all the above effects of BM123 when given SC 40 min prior to the BM123 injection. In contrast, the peripherally acting muscarinic antagonist, N-methyl atropine, prevented only the peripheral effects and the elevated nociceptive thresholds. Habituation of activity during a 20 min session was observed in all groups despite different levels of general activity. These findings are consistent with a model in which atropine and N-methyl atropine compete with BM123 for reversible association with the muscarinic receptor. In the case of BM123 administered alone, the association results, first, in agonist effects and proceeds to form an irreversible complex. Our present results show that by competing with BM123 for mAChR sites during the initial, reversible state of the interaction, atropine blocks the cholinomimetic effects of the agonist during both this state and its otherwise subsequent irreversible state.

Animals↗
PubMed2003

Isometric handgrip exercise during dobutamine-atropine stress echocardiography increases heart rate acceleration and decreases study duration and dobutamine and atropine dosage.

BACKGROUND: Dobutamine-atropine stress echocardiography (DASE) is an established test for the diagnosis and risk stratification of patients with coronary artery disease. Atropine use to attain target heart rate prolongs test time. HYPOTHESIS: The aim of this study was to assess the utility of isometric handgrip exercise (33% maximal voluntary contraction x 4 min) with DASE. METHODS: We prospectively evaluated 131 patients undergoing DASE randomized to handgrip exercise or no handgrip. Effect of handgrip exercise on endpoints: time to target heart rate (85% maximum predicted), recovery time, total test time, mean dobutamine and atropine dosage, and the number of ischemic responses were assessed. Effect of current beta-blocker medication use was also evaluated. RESULTS: Heart rate rose more quickly in the handgrip group. At 6-10 min (peak handgrip), mean heart rate rose 51 +/- 14 beats/min in the handgrip group compared with 38 +/- 18 beats/min in the no handgrip group (p < 0.0001). With handgrip, overall dobutamine study time was reduced by a mean of 4.3 min (16.4 +/- 6.9 vs. 20.7 +/- 8.4, p = 0.004) in all patients, and by a mean of 5.9 min in patients not on beta-blocker medication (p = 0.001). The handgrip group also had a lower mean dose of dobutamine (25.8 +/- 13.5 vs. 32.4 +/- 16.4 mg, p = 0.025). The mean atropine dose was also lower (0.2 +/- 0.4 vs. 0.4 +/- 0.5 mg, p = 0.04). Handgrip exercise, however, did not decrease endpoints in patients on beta-blocker medication. CONCLUSIONS: Use of isometric handgrip exercise with DASE decreases time to target heart rate, recovery time, overall study time, and mean dosage of dobutamine and atropine. In patients not on beta-blocker medication, handgrip exercise should be routinely incorporated into all DASE protocols.

Adrenergic beta-Antagonists↗
PubMed1979

A comparison of changes in atropine-induced tachycardia and atropine concentration in conscious dogs.

In the conscious dog, after intravenous injection of 0.2 mg/kg 3H-labelled atropine the progressive decrease of the heart rate was well correlated with the disappearance of atropine from the blood. But, with atropine infusion (0.2 mg/kg/h) the tachycardia decreased progressively in spite of an increase in the blood concentration of atropine. Differences appeared between the normal animals or those pretreated with propranolol or reserpine, and the animals which had undergone bilateral thoracic sympathectomy. In the stellectomized animals atropine induced a smaller but much more lasting cardiac acceleration than under the other experimental conditions. It seems that only peripheral factors are involved in the complex interactions between the adrenergic and cholinergic nervous systems at the sinus node level.

Animals↗
PubMed1992

[Cardiovascular effects of a combination of vecuronium and low-dose fentanyl in atropinized and non-atropinized subjects].

The cardiovascular effects of the pharmacologic association of low-dose fentanyl (2 micrograms/kg) and vecuronium (120 micrograms/kg) have been studied in 38 ASA I and II atropinized and non-atropinized patients scheduled for abdominal surgery during induction of anaesthesia with thiopentone or propofol. Whatever the induction agent used, heart rate was consistently reduced in patients not receiving an anticholinergic drug, while it was unchanged in patients treated with atropine intravenously. In non-atropinized patients impressively lower minimum heart rates were observed during induction of anaesthesia with thiopentone. In this last group one patient suffered from a cardiac arrest resolved without sequelae. In patients treated with the association between vecuronium and low doses of fentanyl a pretreatment with atropine is always indicated. Propofol seems to be a better induction agent than thiopentone.

Aged↗
PubMed1985

Atropine serum concentrations after multiple inhaled doses of atropine sulfate.

Atropine may be given by inhalation for bronchodilation. Intravenous atropine at doses of 0.32 to 1 mg yields serum levels of 2 to 6 ng/ml, with an elimination t1/2 of about 4 hours. Efficient inhalation of large single doses leads to similar concentrations in some individuals, but under clinical conditions drug delivery may be less efficient. Of concern is accumulation of the drug in the body with multiple-dose therapy. We measured serum levels of atropine after single inhaled doses and again after 48 to 72 hours of inhalation every 4 to 6 hours in 11 subjects. The drug was administered by therapists at doses and techniques commonly used in the clinical setting. Serum concentrations of atropine were negligible after the first dose in all subjects but were detectable in six of nine subjects who received the drug for more than 48 hours. Three of the subjects had levels greater than 2 ng/ml.

Absorption↗
PubMed1991

Comparison of the combined effects of atropine and neostigmine with atropine and edrophonium on the lower oesophageal sphincter.

In two groups (n = 11) of healthy patients, we have measured gastric, lower oesophageal and barrier pressures before and after antagonism of neuromuscular block during anaesthesia with nitrous oxide and isoflurane. In one group, atropine 1.2 mg and neostigmine 2.5 mg were given and in the second group atropine 0.6 mg with edrophonium 1 mg/kg. One minute after administration of the reversal agents, there was a significantly greater reduction in barrier pressures in the neostigmine and atropine group than in the edrophonium and atropine group, but subsequently, there was no significant difference between the two groups. We conclude that there is no clinical difference between the two reversal mixtures in terms of the risk of regurgitation in the immediate period after reversal.

Adult↗
PubMed1981

Serum atropine concentrations after inhalation of atropine sulfate.

Six male subjects with chronic bronchitis were given a single aerosol dose of atropine sulfate (0.05 mg/kg). Spirometry and venous blood samples were obtained before and at 0.25, 0.5, 1.0, 1.5, 2.0, and 4.0 h after inhalation of drug. All subjects had a satisfactory bronchodilator response and detectable serum concentrations of atropine within 15 min. Measurable serum concentrations persisted for 4 h with apparent continued slow absorption occurring throughout the entire time interval. The maximal concentrations achieved ranged from 1.3 to 5.8 ng/ml in five subjects. A sixth subject achieved much higher concentrations (as high as 21 ng/ml) and experienced systemic side effects. This latter concentration is comparable to those achieved with doses of 1.5 to 2.0 mg of parenteral atropine. Significant systemic absorption may occur after inhalation of atropine sulfate, although the degree of absorption is variable.

Aerosols↗
PubMed1979

Inhibition of constrictor responses of dog coronary artery by atropine. A possible effectiveness of atropine on variant form of angina pectoris.

A possible effectiveness of atropine on variant form of angina pectoris was investigated using the left circumflex coronary arterial strips of dogs. Acetylcholine 10(-5)--10(-3) Gm/ml dose-dependently constricted the isolated arterial strips during potassium-contracture in 6 cases, and repetitive applications of acetylcholine could produce the similar contractions to the control. In 18 strips atropine 10(-6) Gm/ml significantly depressed the contractions of coronary arteries induced by acetylcholine 10(-5)--10(-3) Gm/ml. In 5 arterial strips atropine 10(-6) Gm/ml significantly inhibited norepinephrine-induced responses of these arteries, and by 10(-5) Gm/ml further suppression of the responses was obtained. The results suggest that atropine may suppress the contractile responses of the coronary artery induce by acetylcholine and nonrepinephrine through a muscarinic-receptor blocking action and simultaneously partly through an adrenergic alpha-receptor blocking action.

Acetylcholine↗
PubMed1977

Comparison of aerosolized atropine, isoproterenol, atropine plus isoproterenol, disodium cromoglycate and placebo in the prevention of exercise-induced asthma.

In 15 asthmatic children post-exercise bronchospasm was partially inhibited by placebo and by aerosolized atropine sulphate (1 mg) compared with no treatment, not significantly inhibited by atropine alone compared with placebo, partially blocked by disodium cromoglycate (20 mg) and by isoproterenol (0.625 mg) and completely blocked by the combination of isoproterenol and atropine. Pre-treatment with isoproterenol or atropine resulted in post-exercise values for specific conductance which were significantly greater than those following disodium cromoglycate by virtue of the bronchodilator effect of these drugs independent of or in addition to any specific inhibition of exercise-induced asthma. These results suggest that the bronchoconstrictor response to exercise is partially influenced by suggestion but is influenced to a significantly greater degree by mediator release and beta-adrenergic mechanisms and that bronchodilator drugs have therapeutic advantages over an inhibitor of mediator release in the prevention of exercise-induced asthma.

Adolescent↗