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PubMedDate not supplied

Identification and estimation of the levo isomer in raw materials and finished products containing atropine and/or hyoscyamine.

The belladonna alkaloids atropine sulfate and hyoscyamine sulfate, occasionally used as anticholinergic and antimuscarinic agents, have identical molecular formulas but different stereo configurations. Hyoscyamine sulfate contains almost 100% of the levo isomer, whereas atropine sulfate is composed of equal parts of dextro and levo isomers. It is believed that the therapeutic properties of these alkaloids are due exclusively or primarily to the levo isomer. Currently available methods determine only the total amount of atropine (hyoscyamine) sulfate. A method has been developed and is reported for the identification and estimation of the levo and dextro isomers of atropine and hyoscyamine. Reference solutions are prepared in methanol at the following weights per 100 mL: 8.0 mg atropine sulfate; 4.0 mg hyoscyamine sulfate; 7.0 mg scopolamine hydrobromide; and 10.0 mg homatropine methylbromide. Samples of raw materials are similarly prepared in methanol, commercial products are also extracted or diluted with methanol, and solutions are filtered. Liquid chromatography is used for separations on a 25 cm Chirobiotic T2 column. The mobile phase is prepared by mixing 3.0 mL acetic acid and 2.0 mL triethylamine with 1000 mL methanol. The injection volume is 100 or 200 microL; the flow rate is about 0.35 mL/min. Fluorescence detection is at 255 nm excitation and 285 nm emission. Scopolamine hydrobromide and hyoscyamine eluted after 20 and 60 min, respectively. Atropine sulfate generated 2 peaks after 60 and 65 min. Homatropine methylbromide also produced 2 peaks after 70 and 85 min. Samples tested in this study included raw materials and commercial tablets or injections containing belladonna alkaloids. In all cases, the percentage calculated was that of the levo isomer relative to the total amount of atropine (hyoscyamine) present.

Atropine↗
PubMed1991

Modulation of acetylcholine release from rat striatal slices: interaction between 4-aminopyridine and atropine.

The objective of these studies was to determine whether the muscarinic receptor-mediated autoregulation of the basal release of acetylcholine (ACh), like the modulation of evoked release, involves 4-aminopyridine (4-AP)-sensitive potassium channels. To accomplish this, striatal and hippocampal slices were incubated with 4-AP in the absence or presence of atropine, and the release of ACh was measured. 4-AP increased the release of ACh in a concentration-dependent manner; a maximal effect (280% of control release) was achieved in the presence of 100 microM. The maximal release of ACh from hippocampal slices was approximately 150% of control release and was achieved in the presence of a broad range of concentrations (33-333 microM 4-AP). Tetrodotoxin (1 microM) totally abolished the 4-AP-induced release of ACh from hippocampal slices, but only attenuated the 4-AP-induced release from striatal slices, i.e., in the presence of tetrodotoxin, the 4-AP-induced release of ACh from the latter was significantly greater than control release by 54%. Atropine (0.1 microM) increased significantly the basal release of ACh from striatal slices by 61%. When striatal slices were incubated with 4-AP in the presence of this maximally effective concentration of atropine, ACh release was significantly greater than release from slices incubated with either atropine or 4-AP alone, suggesting that atropine and 4-AP increase neurotransmitter release by independent mechanisms. Although oxotremorine did not alter either the 4-AP- or atropine-induced release of ACh, it prevented the potentiated response exhibited by slices incubated with both atropine and 4-AP.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminopyridine↗
PubMed1990

Comparison of central nervous system and peripheral pharmacodynamics to atropine pharmacokinetics.

Two experiments were designed to examine the pharmacokinetic-pharmacodynamic relationship for the central nervous system and peripheral effects of atropine. According to a random Latin square design, healthy young male volunteers were given i.m. injections containing single doses of placebo or 0.5, 1.0, 2.0 or 4.0 mg of atropine. The central nervous system tests included wheel tracking, a coordination task, and digit symbol substitution, a memory-psychomotor speed task; the physiological variable was heart rate. The pharmacokinetics of atropine were best described by a two-compartment model with very rapid first order absorption. Changes in plasma atropine levels and heart rate closely overlapped for all four doses throughout most of the time course. In contrast, the differential time course of changes in atropine levels and behavioral impairment indicates that pharmacokinetics is not the primary rate-limiting mechanism for the central nervous system effects of atropine. Alternative explanations are discussed, including differential atropine effects on peripheral M2 receptors mediating a heart rate effect and on CNS M1 receptors mediating the memory-psychomotor effect.

Adult↗
PubMed1989

[Study and application of atropine field-effect transistor].

Atropine-H2SO4 is widely used in clinic. The atropine sensitive electrode has been prepared, but Atropine field-effect transistor (Atropine-FET) has not been reported. In this communication, electro-active material is atropine tetraphenylboron. The sensor was fabricated by coating solution composed of electro-active material, dibutyl phthalate (DBP) and 5% PVC in tetrahydrofuran (THF) on Pt wire of gate electrode of MOSFET. The sensor showed linear response to atropine within concentration range 2.0 x 10(-2)-6.3 x 10(-5) mol/L. The slope of the sensor was 55 mV/decade and the limit of detection was 1.6 x 10(-5) mol/L. The sensor response was not affected by pH in the range 3.2-8.2, and the sensor can be used for the determination of atropine sulphate in drug-substances by direct potentiometry. The results of determination were in agreement with the data obtained by the official method in Chinese Pharmacopoeia. The method appears to be a rapid, simple and precise one.

Atropine↗
PubMed1987

Comparison of inhaled metaproterenol, inhaled atropine sulfate, and their combination in treatment of children with acute asthma.

The separate and combined effects of inhaled metaproterenol and atropine sulfate were evaluated in the treatment of 44 episodes of acute asthma occurring in 35 children ranging in age from 13 months to 13 years. Peak expiratory flow rate and pulmonary index were measured before and after each of up to three inhalation treatments. Significant improvement in peak flow rate (P less than .04) was noted after the second inhalation of metaproterenol both with and without the combination of atropine sulfate compared with the effects of atropine alone. Patients treated with metaproterenol and metaproterenol combined with atropine also experienced fewer therapeutic failures (2/15 and 2/16, respectively) compared with those treated with atropine (6/13, P less than .02). Pulmonary index scores did not differ among the treatment groups. Inhaled metaproterenol appears to be more effective than inhaled atropine sulfate in the treatment of children with acute asthma. The addition of inhaled atropine sulfate appears to offer no advantage over treatment with inhaled metaproterenol alone.

Acute Disease↗
PubMed1988

Atropine-edrophonium mixture: a dose-response study.

The dose-response and the doses required to prevent bradycardia in 50% (ED50) and 95% (ED95) of patients were determined for atropine after antagonism of pancuronium-induced neuromuscular blockade in 72 patients with edrophonium-atropine mixtures. Edrophonium 0.67 mg/kg (group A, n = 37) or 1.0 mg/kg (group B, n = 35) was randomly mixed with one of seven doses of atropine (ranging from 0.0125 to 0.0215 mg/kg in group A and from 0.02 to 0.04 mg/kg in group B); with dose-response curves for atropine being constructed for both groups 5 and 10 minutes after the injection of the mixture. These dose-response curves were found to be parallel in both groups. The calculated ED50 values of atropine were 1.6-2 times greater in group B, compared with those in group A. The estimated ED50 doses of atropine in groups A and B at 5 minutes were 0.018 and 0.029 mg/kg, respectively, and at 10 minutes, the ED50 doses were similar, being 0.016 and 0.032 mg/kg, respectively. The calculated ED95 doses of atropine in groups A and B at 5 minutes were 0.024 and 0.055 mg/kg, and at 10 minutes, the ED95 doses were also similar, being 0.027 and 0.05 mg/kg, respectively.

Adult↗
PubMed1986

An atropinized heat-stressed rat model: dose response effects and pharmacokinetics.

Atropine and other anticholinergic drugs are widely used in common medications and in the treatment of organophosphate poisoning. Man dissipates heat by the evaporation of sweat. Analogously, rats spread saliva over their bodies for evaporative cooling. Atropine inhibits both sweating and salivation. Therefore, we sought to quantitate the effects of atropine in our rat heatstroke model. While heat-stressing adult male rats of 500 or 250 g at 41.5 degrees C, we measured the effects of i.v. atropine (10-4000 micrograms X kg-1) on the following: heating rate (HR), % wt loss (saliva production), and fecal loss (intestinal motility). HR (degree C X min-1) was the most sensitive index of drug activity with a 200 micrograms X kg-1 dose (equivalent to 2 mg in man for organophosphate poisoning) eliciting an increased HR from 0.022 degrees C (saline) to 0.087 degrees C X min-1 (atropine). Atropine (200 micrograms X kg-1) increased HR even if administered 3 h prior to heat exposure. Large (500 g) rats showed an increase in HR with 25 micrograms X kg-1 of atropine, but 250 g rats required 50 micrograms X kg-1. This model could be used to assess the relative effects of other anticholinergic drugs and as a non-dehydrated heatstroke model.

Animals↗
PubMedDate not supplied

Beneficial and adverse effects of atropine in patients with acute myocardial infarction.

The action of atropine on heart rate, prevention of arrhythmias, electrical activity and heart contractility was studied in 35 patients with acute myocardial infarction. Atropine had a favourable effect in 24 out of 27 patients with sinus bradycardia, and hypotension present in some cases was improved. Ventricular extrasystoles observed in 12 patients were suppressed within one hour after atropine administration. A--V block was well influenced in 9 of 16 cases. Nine patients with A--V block, of whom 8 with pump failure, presented arrhythmias after atropine. In 12 patients atropine determined a transient enhancing of the ST segment elevation, caused a persistent increase of the Q wave and altered the systolic time intervals by reducing contractility, with subsequent partial return to initial values. The data obtained justify the use of atropine for the improvement of sinus bradycardia, of arterial hypotension and of A--V block. During the effect of the drug there occurred electrical and contractility changes and, in some patients with pump failure, arrhythmias appeared. These observations demonstrate the necessity of monitoring the patients under atropine treatment and of using small doses, repeated if necessary.

Arrhythmia, Sinus↗
PubMed1984

Effects of heat acclimation on atropine-impaired thermoregulation.

The effects of saline or atropine injection (2 mg, im) on eccrine sweating and performance time in seven healthy male subjects were evaluated during treadmill walking (1.34 m X s-1) in a hot-dry environment (Ta = 49 degrees C, Tdp = 20.5 degrees C) before and after heat acclimation (HA). Mean skin temperature (Tsk), rectal temperature (Tre), and heart rate (HR) were continuously measured. Sweat loss from the skin (Msw) was calculated by changes in body weight. HA resulted in decreased (p less than 0.05) Tre (0.4 degrees C) and HR (17 b X min-1), and increased (p less than 0.05) Msw (16 g X m-2 X h-1) during the saline experiments. Pre-acclimation, Msw was reduced (p less than 0.01) 65% (151 g X m-2 X h-1) with atropine, which resulted in higher (p less than 0.01) Tre (0.4 degrees C) and Tsk (2.8 degrees C). HR was increased 48% (53 b X min-1) by atropine pre-acclimation (p less than 0.01). Post-acclimation, atropine reduced (p less than 0.01) Msw 33% (100 g X m-2 X h-1) and increased (p less than 0.01) HR 63% (62 b X min-1) compared to saline exposures. The change in Tre X min-1 (delta Tre/delta t) was lower (p less than 0.05) in atropine-injected subjects following heat acclimation, and their worktime was improved by an average of 23.5 min (p = 0.08). These data demonstrate that heat acclimation improves the endurance time of atropine-treated subjects in a hot-dry environment. This improvement was, in part, due to the potentiation of sweat gland activity enabling greater evaporative cooling for the same dose of atropine.

Acclimatization↗
PubMed1983

New aspects in the use of atropine.

Several new factors have recently been shown to influence the pharmacokinetics of atropine. Age appears to have a clear effect on the elimination of atropine: for example, prolonged elimination has been found in children under 2 years of age and in the elderly. The higher sensitivity of these patients to the effects of atropine can be explained, at least partly, by this phenomenon. Due to the fast placental transfer of atropine, i.v. administration before cesarean section can have strong effects on the newborn. Most important, however, it decreases the barrier pressure of the lower cardioesophageal sphincter (pulmonary aspiration). Thus, routine atropine premedication is contraindicated before cesarean section. On the other hand, children appear to need a routine anticholinergic premedicant. Without it profuse salivary secretion may interfere with anesthesia. The use of atropine in premedication of healthy adult patients is controversial. Because peroral premedication (benzodiazepines) is nowadays increasing in the adult patient, especially in the elderly, routine use of atropine should be avoided.

Aging↗
PubMed1982

Decrease of basal plasma histamine levels by application of atropine in man.

The influence of atropine sulfate on plasma histamine levels was studied in 28 oral surgery patients with no history of allergy. 11 patients were given atropine sulfate for premedication (atropine group), and 17 patients were not (non-atropine group). The measurement of histamine in blood plasma was made using high speed liquid chromatography which was available for quantifying the trace elements. The concentration of histamine of the atropine group was 0.32 +/- 0.17 ng.ml-1 and that of the non-atropine group was 0.68 +/- 0.20 ng.ml-1, showing that atropine sulfate can suppress the release of histamine into human blood.

Adolescent↗
PubMed1982

Edrophonium: duration of action and atropine requirement in humans during halothane anesthesia.

Edrophonium's onset and duration of antagonism (n = 26) and atropine requirement (n = 24) were determined under conditions of d-tubocurarine (dTc) neuromuscular blockade and halothane, nitrous oxide anesthesia. Results are compared with previous work in our laboratory on neostigmine and pyridostigmine under similar conditions. dTc was administered by continuous infusion to maintain a 90% depression of muscle twitch tension. Edrophonium (0.03-1.0 mg/kg) was injected as an iv bolus in combination with atropine (0.5 mg). dTc infusion was continued until a stable 90% depression of muscle twitch tension was reestablished. Time-to-peak effect (onset of action), duration, and magnitude of antagonism were recorded. The atropine requirement was determined during spontaneous recovery from dTc (0.3 mg/kg) and stable halothane, nitrous oxide anesthesia. Edrophonium (0.5 mg/kg) was mixed with 7, 15, or 30 micrograms/kg of atropine and compared to neostigmine (0.043 mg/kg) and atropine (15 micrograms/kg). Blood pressure, heart rate, and rhythm were recorded for 60 min following edrophonium administration. The time-to-peak antagonism for edrophonium (0.8-2.0 min) was far more rapid than neostigmine (7-11 min) or pyridostigmine (12-16 min). The ED50 for edrophonium was 0.125 mg/kg, however, the dose-response curve was not parallel to those for neostigmine or pyridostigmine. In equiantagonistic doses, the duration of antagonism by edrophonium (66 min) did not differ from neostigmine (76 min), but was shorter than pyridostigmine. Edrophonium required one-half the amount of atropine as did neostigmine to prevent bradycardia. The authors concluded that edrophonium has a more rapid onset than neostigmine and an equivalent duration of antagonism, and requires less atropine to prevent bradycardia.

Anesthesia, General↗
PubMed1981

Atropine and glycopyrrolate: hemodynamic effects and placental transfer in the pregnant ewe.

Atropine administration in pregnant women may cause fetal tachycardia and a decrease in beat-to-beat variability of the fetal heart rate. In the present study, placental transfer and maternal and fetal hemodynamic effects of atropine and glycopyrrolate were compared in chronically and in acutely instrumented, unanesthetized pregnant ewes. Administration of either atropine (0.05 mg/kg) or glycopyrrolate (0.025 mg/kg) increased maternal heart rate by 25% without changing maternal arterial pressure, fetal arterial pressure, fetal heart rate, or beat-to-beat variability. Maternal and fetal blood gas tensions also did not change. Placental transfer or atropine was significantly greater than that of glycopyrrolate throughout the entire experimental period. The peak fetal/maternal ratios observed 4 hours after injection were 1.0 for atropine and 0.13 for glycopyrrolate. On the basis of placental transfer data only, it is possible to postulate that the use of glycopyrrolate may be preferable to atropine. However, in view of the absence of circulatory effects in the fetal lamb after either atropine or glycopyrrolate, it was concluded that neither agent is preferable to the other insofar as fetal effects are concerned during ovine pregnancy. Whether these conclusions can be applied to human pregnancy remains to be determined.

Animals↗
PubMed1980

Experimental evidence for cytoprotective effect of atropine on the rat gastric mucosa.

The inhibitory effect of atropine on the gastric mucosal damage produced by topical aspirin has been studied in the rat, in the presence and in the absence of intragastrically applied 160 mmole/l HCl. The gastric mucosal damage was produced by aspirin given intragastrically in doses of 192 mg/kg. The topical application was done alone or in the presence of 160 mmole/l HCl. The ulcer incidence, the number and size of gastric mucosal damage were studied during 4 h. The aspirin solutions were administered with or without atropine (in doses of 4 and 10 mg/kg). The atropine was added immediately after the administration of aspirin. The results were as follows 1. A dose-dependent inhibition of ulcer incidence, number and size of gastric mucosal damage was produced by atropine in both groups of animals, when the aspirin was given alone or together with 160 mmole/l HCl; 2. The inhibitory effect of atropine was significantly weaker in the group treated with aspirin plus 160 mmole/l HCl than in th aspirin-treated group. It has been concluded the ulcer-preventing effect of atropine is mediated partly through the inhibition of gastric H+ secretion, and partly some "cytoprotective effect"; the extent of the "cytoprotective effect" of atropine was about half that on gastric H+ secretion.

Animals↗
PubMed1994

[Stress echocardiography with dobutamine: the importance of adding atropine in inconclusive tests].

OBJECTIVES: To study the feasibility of adding atropine after dobutamine infusion in patients with known or suspected coronary artery disease not achieving 85% of predicted maximal heart rate. PATIENTS: We studied with dobutamine stress echocardiography 219 patients (174 men e 45 women; mean age +/- SD: 58 +/- 11 years), 126 patients with a previous myocardial infarction and 93 with angor. One hundred and thirty three (61%) also performed coronariography. METHODS: Dobutamine stress echocardiography protocol consisted of a step-wise infusion of dobutamine from 5 micrograms/kg/min to a maximal dose of 40 micrograms/kg/min or until a new or a worsening wall motion abnormality, 85% of predicted maximal heart rate or any indication for interruption. In patients not achieving any of these end points, intravenous atropine was administered up to 1 mg. Patients were divided in two groups: Group A: infusion of dobutamine alone and Group B: dobutamine plus atropine. RESULTS: With this protocol the test was interrupted in 41 patients (19%) because of adverse effects that were mild and short lived and resolved with discontinuation of the test. After dobutamine infusion 46% of the tests were nonconclusive, the majority were on beta blocker therapy. After atropine administration there was a significant reduction of the nonconclusive studies to 20% (p < 0.001). In patients with a normal rest echocardiogram the sensitivity and specificity of the test to diagnose significant coronary artery disease was respectively 89% e 100% after atropine. The capacity of the test to detect multivessel disease was also increased after atropine, allowing to reach a sensitivity of 85% and a specificity of 90%. CONCLUSIONS: Dobutamine stress echocardiogram supplemented with atropine is a safe and accurate method to diagnose significant coronary artery disease and to detect multivessel disease in patients with a previous myocardial infarction with rest wall motion abnormalities.

Aged↗
PubMed1994

[Effects of intravenous and intramuscular atropine on bradycardia during spinal anesthesia].

The effects of intravenous and intramuscular atropine on pulse rate have been studied in 40 patients undergoing gynecological surgery. Intramuscular atropine 0.5 mg was administered 30 min before induction of spinal anesthesia in 20 patients (i.m. group). Intravenous atropine 0.5 mg was administered immediately after induction of spinal anesthesia in 20 patients (i.v. group). Decrease in heart rate after spinal block was significantly less in i.v. group than in i.m. group. Although no one in i.v. group was given an additional atropine, 10% of the patients in i.m. group was given an additional atropine for bradycardia. Authors conclude that intravenous atropine has more significant effect on prevention of bradycardia during spinal anesthesia compared with intramuscular atropine.

Anesthesia, Spinal↗
PubMed1996

Characterization of chronotropic and dysrhythmogenic effects of atropine in dogs with bradycardia.

OBJECTIVE: To characterize the magnitude, character, and time course of chronotropic and dysrhythmogenic responses of dogs with vagally mediated bradycardia to atropine sulfate. DESIGN: Latin square design. ANIMALS: Seven clinically normal adult mixed-breed dogs. PROCEDURE: Vagally mediated bradycardia was induced with morphine and fentanyl citrate. Atropine (0.02 mg/kg of body weight) was administered i.v., s.c., or i.m.. Electrocardiograms were recorded continuously for 5 minutes before and for 35 minutes after atropine administration or until a sustained parasympatholytic response was observed. Data were digitized, analyzed independently for changes in atrial and ventricular rate, and compared between different routes of administration. RESULTS: All dogs developed second-degree atrioventricular (AV) block after i.v. administration of atropine, and 71% of dogs developed AV block after s.c. or i.m. administration. The AV block arose and resolved more rapidly with i.v. administration than with s.c. or i.m. administration. The AV block was principally attributable to an increase in the atrial rate prior to increases in the ventricular rate. Atropine, regardless of route of administration, potentiated baseline ventricular bradycardia in 62% of the experiments (mean heart rate decrease of 16 beats/min; decreased to < 20 beats/min in 2 dogs for < or = 10 seconds). Duration of the bradycardic potentiation was longer with s.c. administration (9.1 minutes, s.c., vs 1.4 minutes, i.v., and 4.6 minutes, i.m.). Parasympatholytic rate was higher for i.v. than s.c. or i.m. administration (128 beats/min vs 92 beats/min and 101 beats/min). Two dogs given atropine s.c. failed to resolve the AV block and attain sinus rhythm. CONCLUSIONS: Administration of 0.02 mg of atropine/kg by i.v., i.m., and s.c. routes for vagally mediated bradycardia in dogs consistently induces AV block and occasional brief potentiation of ventricular bradycardia. CLINICAL RELEVANCE: Parasympathomimetic effects occur and resolve most rapidly and consistently, and the stable parasympatholytic effect is of greatest magnitude after i.v. administration. Thus, vagally mediated bradycardia in clinically normal dogs appears to be best abolished by i.v. administration of atropine.

Analysis of Variance↗
PubMedDate not supplied

Double-blind, randomized, placebo-controlled evaluation of atropine to prevent vasovagal reaction during removal of femoral arterial sheaths.

STUDY OBJECTIVE: To evaluate the efficacy and safety of atropine in preventing vasovagal reactions (VVRs) during removal of femoral arterial sheaths after diagnostic left heart catheterization. DESIGN: Prospective, double-blind, randomized, placebo-controlled study. SETTING: University-affiliated, 450-bed teaching hospital. PATIENTS: One hundred sixty-five patients undergoing left heart catheterization. INTERVENTIONS: Eighty-eight patients were assigned to receive atropine 0.5 mg intravenously and 77 received placebo 5 minutes before sheath removal. MEASUREMENTS AND MAIN RESULTS: The frequency of VVRs was significantly reduced in the atropine group compared with the placebo group, 2.3% and 10.4%, respectively (overall relative risk in the atropine group 0.22, 95% CI 0.12-0.41, p=0.03). Significant decreases in systolic (35.2 +/- 5.8 mm Hg, p<0.001) and diastolic blood pressures (12.6 +/- 12.6 mm Hg, p=0.002) occurred in the 10 patients with VVRs compared with those without VVR. No cardiac arrhythmias occurred after atropine administration. Dry mouth was the only side effect reported with atropine (8/88, 9%). CONCLUSION: Atropine significantly reduced the frequency of VVRs associated with removal of femoral arterial sheaths after diagnostic left heart catheterization. The drug should be studied in a larger series of patients to assess its ability to decrease the morbidity and costs associated with VVR.

Atropine↗