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At least 235 records · Page 13Linked to original sources
PubMed1991

Oral clonidine blunts the heart rate response to intravenous atropine in humans.

Clonidine, recently introduced into anesthesia practice, may cause bradycardia. Whether this bradycardia is reversible with atropine is not known. Accordingly, we studied heart rate (HR) responses to intravenous atropine in 80 patients assigned randomly to either a control group, who received no medication (n = 20), or a clonidine group, who received oral clonidine of approximately 1.2 micrograms.kg-1 (n = 20), 2.5 micrograms.kg-1 (n = 20), or 5 micrograms.kg-1 (n = 20). All patients received incremental doses of atropine, 2.5, 2.5, and 5 micrograms.kg-1, at 2-min intervals (total dose 10 micrograms.kg-1). Positive chronotropic response to the cumulative atropine dose of 10 micrograms.kg-1 was attenuated significantly only in patients given clonidine 5 micrograms.kg-1 (7 +/- 1 beats per min, mean +/- standard error) when compared with those given smaller doses of clonidine (15 +/- 2, 16 +/- 2 beats per min) or no clonidine (19 +/- 2 beats per min) (P less than 0.05). To determine whether HR hyporesponsiveness to atropine induced by clonidine can be overcome by a larger dose of atropine, the authors studied 30 additional patients given clonidine 5 micrograms.kg-1 or no medication. In all patients not receiving clonidine (n = 15), HR increased by more than 20 beats per min when atropine of 15 micrograms.kg-1 was administered, whereas in only 5 patients (33%) receiving clonidine did the HR increase by 20 beats per min after atropine 15 micrograms.kg-1 (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1995

Oral clonidine premedication blunts the heart rate response to intravenous atropine in awake children.

BACKGROUND: Clonidine, which is known to have analgesic and sedative properties, has recently been shown to be an effective preanesthetic medication in children. The drug may cause side effects, including bradycardia and hypotension. This study was conducted to evaluate the ability of intravenous atropine to increase the heart rate (HR) in awake children receiving clonidine preanesthetic medication. METHODS: We studied 96 otherwise healthy children, 8-13 yr old, undergoing minor surgery. They received, at random, oral clonidine 2 or 4 micrograms.kg-1 or placebo 105 min before scheduled induction of anesthesia. Part I (n = 48, 16 per group): When hemodynamic parameters after insertion of a venous catheter had been confirmed to be stable, atropine was administered in incremental doses of 2.5, 2.5, and 5 micrograms.kg-1 every 2 min. The HR and blood pressure were recorded at 1-min intervals. Part II (n = 48, 16 per group): After the recording of baseline hemodynamic values, successive doses of atropine (5 micrograms.kg-1 every 2 min, to 40 micrograms.kg-1), were administered until HR increased by 20 beats.min-1. The HR and blood pressure were recorded at 1-min intervals. RESULTS: Part I: The increases in HR in response to a cumulative dose of atropine 10 micrograms.kg-1 were 33 +/- 3%, 16 +/- 3%, and 8 +/- 2% (mean +/- SEM) in children receiving placebo, clonidine 2 micrograms.kg-1, and clonidine 4 micrograms.kg-1, respectively (P < 0.05). Part II: The HR in the control group increased by more than 20 beats.min-1 in response to atropine 20 micrograms.kg-1 or less. In two patients in the clonidine 4 micrograms.kg-1 group, HR did not increase by 20 beats.min-1 even after 40 micrograms.kg-1 of atropine. CONCLUSIONS: Oral clonidine premedication (4 micrograms.kg-1) blunted the increase in HR after intravenous atropine in awake children, although clonidine 2 micrograms.kg-1 did not. A larger dose of atropine was required to increase the HR by 20 beats.min-1 in children receiving the premedicant in the larger dose.

Administration, Oral↗
PubMed1999

Comparison of anti-M2-muscarinic effect of AF-DX 116 on atrioventricular nodal conduction with those of pirenzepine and atropine as antibradyarrhythmic drugs.

Selectivity of antimuscarinic actions of AF-DX 116 (AF-DX) on the atrioventricular (AV) nodal conduction was compared with those of pirenzepine and atropine by using the canine isolated, blood-perfused AV node preparation and the open-chest in situ dog heart. In the isolated AV node preparation, dose-response curves for negative dromotropic effects (prolongation of Atrio-His interval) of carbachol (CCh) injected into the posterior septal artery were shifted to the right in parallel by AF-DX, pirenzepine, and atropine with apparent pA2-values of 13, 27.5, and 0.45 microg, respectively, and slopes of the modified Schild plot of nearly unity. Meanwhile, dose-response curves for coronary vasodilator effects of CCh were shifted to the right by AF-DX, pirenzepine, and atropine with the apparent pA2 values of 68, 12.5, and 0.55 microg, respectively, but the slopes were far from unity. In the in situ open-chest heart, dose-response curves for negative dromotropic effects (prolongation of AV conduction time) of CCh given intravenously were shifted to the right in parallel by AF-DX, pirenzepine, and atropine with apparent pA2 values of 36, 32, and 1.25 microg/kg, respectively, and the slope of nearly unity, whereas dose-response curves for hypotensive effects of CCh were shifted to the right by AF-DX, pirenzepine, and atropine with apparent pA2 values of 105, 15, and 0.65 microg/kg, respectively, but the slopes of AF-DX and pirenzepine were far from unity. In addition, prolongations of AV conduction time by electrical stimulation of the left vagus nerve in the in situ heart were suppressed by AF-DX, pirenzepine, and atropine with the ID50, dose for 50% suppression, of 40, 35, and 1.9 microg/kg, respectively. These results suggest that (a) the potency of antimuscarinic actions of AF-DX on the CCh-induced negative dromotropic effects was almost equal to that of pirenzepine, and approximately 30 times less potent than atropine; (b) the M2-subtype selectivity of AF-DX was considerably higher in comparison with pirenzepine and atropine; and (c) the muscarinic receptor subtype on the canine AV node is entirely of the M2-type, but only sparsely developed in the coronary vascular beds.

Animals↗
PubMed1990

Effect of intravenous atropine on gastric emptying, paracetamol absorption, salivary flow and heart rate in young and fit elderly volunteers.

1. The effects of atropine on gastric emptying, paracetamol absorption, salivary flow and heart rate were examined in young and elderly subjects. 2. Seven healthy young male subjects of age 23 +/- 1.3 years (mean +/- s.e. mean) and seven fit elderly subjects of age 70 +/- 1.6 years received placebo (P), 300 micrograms atropine (A300) or 600 micrograms atropine (A600) in randomized order at weekly intervals. After 10 min they ingested a 500 ml orange drink containing 1 g paracetamol. Gastric emptying was measured by ultrasound, blood samples were taken to measure plasma paracetamol concentration by h.p.l.c., salivary flow was measured by dental cotton wool cylinder technique and pulse rate was recorded. 3. In young subjects, the gastric 5 min volumes were 260.1 +/- 17.9 ml (s.e. mean) with P, 310.6 +/- 10.5 ml with A300 and 317.9 +/- 8.9 ml with A600. In elderly subjects, the gastric 5 min volumes were 166.7 +/- 10.1 ml with P, 252.6 +/- 13.7 ml with A300 and 266.0 +/- 14.8 ml with A600. Thus the early adaptive phase of gastric emptying was more rapid in the elderly than the young with all treatments (P less than 0.05). The gastric emptying half-lives were 18.8 +/- 2.5 min with P, 30.0 +/- 2.7 min with A300 and 34.5 +/- 3.3 min with A600 in young subjects (P less than 0.01). In elderly subjects, the gastric emptying half-lives were 16.1 +/- 2.5 min with P, 23.7 +/- 2.4 min with A300 and 30.0 +/- 2.9 min with A600 (P less than 0.01). Thus atropine intravenously in therapeutic dose (300 and 600 micrograms) delayed gastric emptying in both young and elderly subjects. The inhibitory effect of atropine on the early adaptive phase of gastric emptying appeared to be greater in the elderly. The maximum plasma concentration (Cmax) of paracetamol was greater in the elderly than young with all treatments (P less than 0.05). There was a close relationship between the early adaptive phase of gastric emptying and paracetamol absorption (P less than 0.05). Atropine reduced salivary flow and increased resting heart rate in both young and old subjects. The effect of atropine on salivary flow was greater in the elderly. 4. The dose-response relationship varied in the three systems (stomach, salivary glands and heart rate) studied. Age had an effect on the magnitude of the response, but not on the slope of the dose-response curve for the two doses of atropine studied.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetaminophen↗
PubMed1982

Atropine before enflurane anaesthesia: effects on cardiac rhythm, pulse rate, blood pressure and airway secretion.

The occurrence of cardiac arrhythmias and changes in pulse rate and blood pressure during mask anaesthesia with enflurane was investigated in 92 patients with special reference to the influence of atropine (0.01 mg kg-1 5 min before anaesthesia) and thiopental. The average duration of anaesthesia was a little less than 1 h in all four groups. More than five ventricular extrasystoles occurred in one patient (38 min after atropine). Supraventricular (mainly nodal) arrhythmias were significantly (P less than 0.005) more common in the atropine groups (15/45) than in the non-atropine groups (4/47). Following atropine, heart rate increased by about 25 beats min-1, whereas only very slight increases were seen in the non-atropine groups. Blood pressure fell at the induction but was almost back to normal at the end of anaesthesia. Blood pressure was unaffected by atropine. Slightly lower values of blood pressure were suggested in the thiopental groups, whereas thiopental did not modify cardiac rhythm or pulse rate. Suction of the pharynx was necessary in only one patient. In conclusion, the present study does not support the routine administration of atropine before enflurane anaesthesia with or without thiopental induction.

Adolescent↗
PubMed1995

Induction of insulin resistance by cholinergic blockade with atropine in the cat.

1. Insulin sensitivity was quantified using a modified euglycaemic technique after hepatic cholinergic blockade with atropine and compared with that after surgical denervation. 2. Intraportal administration of atropine produced dose-dependent inhibition of insulin sensitivity in glucose metabolism. ED50 of atropine was 0.99 mg kg-1 (1 mg = 1.5 microM) with maximum inhibition of 40.3 +/- 11.6%. 3. Atropine (3 mg kg-1) reduced insulin sensitivity by a similar amount (33.6 +/- 3.4%) to that produced by hepatic surgical denervation (37.8 +/- 9.8%). Doses greater than 3 mg kg-1 failed to further alter the insulin resistance produced by surgical denervation or atropine (3 mg kg-1) administration, suggesting that activation of hepatic parasympathetic nerves is necessary to fully express the insulin effect. 4. Atropine reduced insulin sensitivity without changes in plasma concentrations of glucagon or insulin. The temporal response to insulin in this euglycaemic study was not changed after atropine administration or after surgical hepatic denervation. 5. It is suggested that hepatic parasympathetic nerves show a synergistic effect with insulin. Disease states that result in hepatic parasympathetic neuropathy would be expected to produce an insulin resistant liver. 6. The modified euglycaemic clamp method for assessing insulin responses was shown to be reproducible up to four times in the same animal and was sufficiently sensitive and quantitative to be able to generate a dose-response curve in each animal for atropine-induced insulin resistance.

Animals↗
PubMedDate not supplied

The effects of atropine and glycopyrrolate on heart rates in conscious mature goats.

The effects of intravenously administered atropine (0.2 mg/kg) and glycopyrrolate (0.01 mg/kg) on heart rate were studied in 10 conscious mature goats. In a drug cross-over fashion, either atropine, glycopyrrolate, or 0.9% saline solution was administered using the same volume (0.05 mL/kg). Atropine and glycopyrrolate caused a significant increase in heart rate (P < .05), whereas saline solution (0.09%) did not. The mean percent changes in heart rate from baseline were similar for atropine and glycopyrrolate up to 14 minutes after administration. Thereafter, glycopyrrolate had a significantly greater mean change in heart rate than atropine, ie, up to 29 minutes (P < .05). Within the atropine group, the mean percentage changes in heart rate became significantly lower compared with the initial increase (1 minute) starting at 11 minutes. For the glycopyrrolate group, the mean percent changes became significantly lower starting at 27 minutes. Glycopyrrolate and atropine had a mean percentage change in heart rate of greater than 1.0%, up to 31 and 22 minutes, respectively. At the doses used, glycopyrrolate had longer duration of action than atropine but the magnitude of increase was similar.

Animals↗
PubMed2000

Impact of atropine injection on heart rate response during treadmill exercise echocardiography: a double-blind randomized pilot study.

We evaluated the effect of atropine on the heart rate (HR) response during treadmill exercise echocardiography. A potential limitation of treadmill exercise echocardiography is the requirement for postexercise imaging. Rapid recovery of HR and wall motion abnormalities may decrease test sensitivity. A double-blind randomized study was performed at a tertiary care center. Fifty-two patients (age, 63 +/- 9 years) with known or suspected coronary artery disease were injected with either 0.5 mg of atropine or saline before treadmill exercise echocardiography. HR response during and after exercise was recorded. Atropine resulted in a greater increase in HR before exercise (increase of 15 +/- 9 vs 5 +/- 7 beats per minute, P < 0.0001) and a higher HR rate during the first 5 minutes of exercise (P < 0.05). In recovery, there was an exponential decrease in HR in both atropine and control groups. However, at the end of image acquisition (66 +/- 15 seconds), the HR was higher in the atropine group (128 +/- 21 vs 115 +/- 19 beats per minute, P = 0.02) and remained higher throughout the 10-minute recovery period (P = 0.0015). Dry mouth was more common after atropine injection (P = 0.005); other side effects were similar. The extent and resolution of myocardial ischemia were comparable in both groups. Atropine injection before treadmill exercise echocardiography results in a higher HR during the acquisition of echocardiographic images; whether atropine could affect the diagnostic accuracy of tread mill exercise echocardiography requires further study.

Acetylcholine↗
PubMed1980

Radioimmunoassay for atropine and l-hyoscyamine.

A simple, specific and sensitive radioimmunoassay is described for atropine (dl-hyoscyamine) and l-hyoscyamine. Antiserum was obtained from rabbits immunized with an immunogen prepared by coupling l-hyoscyamine to human serum albumin. By using 3H-atropine as tracer, the assay can detect atropine and l-hyoscyamine concentratins down to 9 nmol/l(2.5 ng/ml) in a 0.1 ml serum or plasma sample. The recovery of atropine was near 100% when the drug was added at different concentrations to normal, pooled human plasma. Atropine and l-hyoscyamine are recognized equally well by the antibodies, but some other structurally related drugs (homatropine scopolamine) and atropine hydrolysis products (tropine, tropic acid) do not interfere. The usefulness of the method in pharmacokinetic studies was shown by assaying atropine concentrations in serial serum samples from two patients, who were given 1.3 mg atropine on connection with anaesthesia. A biexponential serum decay curve was demonstrated in both cases with a very rapid distribution phase (t 1/2 0.63 and 1.38 min.) and a much slower elimination phase (t 1/2 1.86 and 2.09 hrs.).

Adult↗
PubMed1992

Effects of acute and long-term atropine treatment on levels, release and response to VIP and PHI in the submandibular gland of cat and rat.

We have studied the effects of acute and long-term treatment of cats and rats with atropine on the levels, release and effects of two peptides, vasoactive intestinal polypeptide (VIP) and peptide histidine isoleucine (PHI), that probably co-exist with acetylcholine in the parasympathetic nerves supplying the submandibular gland. Atropine treatment (progressively increasing doses from 2 to 15 mg kg-1 injected s.c.) for 14 days did not alter the contents of VIP- or PHI-like immunoreactivity (-IR) in the cat submandibular gland or in three other tissues (nasal mucosa, trachea and tongue). Acute as well as long-term atropine treatment decreased the vasodilation following low-, but not high-, frequency parasympathetic nerve stimulation. During prolonged stimulation (60 min) there was a decreased vasodilatation response following both acute and long-term atropine treatment. The overflow of VIP-IR and PHI-IR following parasympathetic nerve stimulation was markedly increased by acute, but not by long-term atropine treatment. The VIP- or PHI-induced stimulation of cyclic AMP (cAMP) accumulation in the cat submandibular gland was not altered after long-term atropine treatment. Similarly, treatment of male Sprague-Dawley rats with atropine (20 mg kg-1) or imipramine (20 mg kg-1) for 14 days did not alter the sensitivity to VIP or to PHI of cAMP accumulation in the submandibular gland, nor was there any change in VIP-IR or PHI-IR content. In conclusion, although atropine treatment causes an acute increase in the overflow of VIP and PHI evoked by parasympathetic nerve stimulation, there is no depletion of peptide stores upon long-term treatment, nor is there any change in the effect of exogenous VIP and PHI on cAMP-accumulation.

Adenylyl Cyclases↗
PubMed1977

Analysis of atropine action at the frog neutromuscular junction.

1. Atropine action on the end-plate currents (e.p.c.s) has been analysed at the macroscopic and elementary levels. 2. The shortening effect of atropine on the e.p.c. and m.e.p.c. level can be fully explained by a reduction of the life time of the elementary current: this effect is markedly increased at more hyperpolarized membrane potentials and at higher concentrations of atropine. 3. It is therefore suggested that atropine binds to the open acetylcholine-receptor complex, leading to a state with a null conductance. According to this model, the forward rate constant of atropine binding could be calculated and was of the order of 10(7) M-1 S-1 AT -90 MV and 20-22 degrees C. 4. Although the conductance at the peak of the e.p.c. is reduced by atropine and becomes voltage sensitive, the elementary conductance is affected neither by voltage nor by atropine. 5. The exclusive binding of atropine to the activated ACh-receptor complex, as proposed above, does not appear to explain this phenomenon. Another binding occurring before the channel is open with a dissociation constant of 60 micrometer could account for this effect.

Animals↗
PubMed1991

Atropine-resistant submandibular responses to stimulation of the parasympathetic innervation in the anaesthetized ferret.

1. Submandibular salivary and vascular responses to stimulation of the peripheral end of the chorda-lingual nerve at 20 Hz continuously for 60 min were investigated in anaesthetized ferrets, in which the sympathetic innervation to the gland was cut, in the presence and absence of atropine (2.0 mg kg-1). 2. Both the increase in submandibular salivary flow and protein output, which occurred in response to nerve stimulation, were substantially reduced following the administration of atropine, the latency was greatly increased thereby, and both responses were more transient but neither was abolished by atropine. The fall in submandibular vascular resistance was not significantly affected by atropine, either in respect of extent or duration. 3. Chorda-lingual stimulation produced an increase in the output of vasoactive intestinal peptide (VIP), substance P (SP) and calcitonin gene-related peptide (CGRP) in the submandibular venous effluent blood. Each of these responses was maximal within the first 10 min after the onset of stimulation and declined thereafter. The time-scales of both the CGRP and SP responses were similar to those of the atropine-resistant secretory responses, both being quite short-lived, whereas the output of VIP (like the atropine-resistant vascular response) was significantly greater than the basal value throughout the whole of the 60 min period of stimulation. 4. The CGRP response was completely abolished by pre-treatment with atropine, whereas the outputs of both VIP and SP were significantly enhanced thereby. Both the submandibular vascular and secretory responses to chorda-lingual stimulation were almost completely suppressed following the administration of hexamethonium, and there was then no detectable release of peptidergic agonists from the gland. 5. The atropine-resistant submandibular salivary secretory responses were completely abolished by pre-treatment with a tachykinin inhibitor [( D-Arg1, D-Cl2 Phe5, Asn6, D-Trp7,9, Nle11]-SP; 0.75 mg kg-1) without affecting the fall in submandibular vascular resistance. 6. Following pre-treatment with hexamethonium, I.V. bolus injections of methacholine, SP and CGRP elicited increases in submandibular blood flow and secretion of saliva. VIP caused an increase in blood flow without overt secretion, although it is known to increase secretion of protein and to potentiate the secretory response to SP. Taken together, all these results are consistent with the contention that VIP contributes to the vasodilator response to stimulation of the para-sympathetic innervation in this gland and that both SP and CGRP are likely to contribute to the secretory response.

Animals↗
PubMed1987

Atropine does not inhibit late asthmatic responses induced by toluene-diisocyanate in sensitized subjects.

To determine whether early and/or late asthmatic responses induced by toluene diisocyanate (TDI) are caused by a reflex mechanism involving stimulation of muscarinic receptors, we studied the effect of the muscarinic antagonist atropine on early and late airway response induced by TDI. A preliminary study was conducted in asthmatics to assess whether the selected dose of atropine provided adequate muscarinic blockade. On different days we measured the provocation dose (in milligrams) of carbachol causing a 15% decrease in FEV1 (PD15FEV1) without and with atropine premedication (0.008 or 0.012 mg/kg subcutaneous atropine 30 or 90 min before carbachol challenge test). We found that 0.008 to 0.012 mg/kg subcutaneous atropine increased the PD15FEV1 carbachol by 6- to 10-fold, inducing a consistent and prolonged decrease in nonspecific bronchial hyperresponsiveness to cholinergic agent. Then we examined 10 subjects with a history of sensitization to TDI in 2 sets of experiments. In the first set of experiments, we studied the subjects before and after exposure to TDI (0.04 ppm; 30 min) after no treatment. In the second set of experiments, carried out 1 to 2 wk later, we repeated the same procedure after treatment with atropine (0.008 to 0.012 mg/kg atropine sulfate administered subcutaneously 30 min before TDI challenge, and then at 90-min intervals after TDI exposure); all patients showed symptoms of atropine effect (dryness of mouth, cycloplegia, increased heart rate).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1985

Prolongation of gastric emptying by aerosolized atropine.

Aerosolized atropine causes anticholinergic side effects. We evaluated gastroparesis, a previously unreported side effect of inhaled atropine, in a double-blind, placebo-controlled, crossover study. Six young asthmatics received atropine (0.05 mg/kg) or placebo at 4-h intervals for 3 dosages, on 2 separate days at least 1 wk apart. Subjective complaints, pulse, visual accommodation, and citric-acid-stimulated salivary flow were recorded 30 min after each dose on each study day. A radionuclide (99mTc) study of gastric emptying time was done 30 min after the final dose on each study day. Atropine prolonged mean gastric half emptying time (112 +/- 59 min) compared with placebo (65 +/- 34 min) (p less than 0.05). However, gastric emptying after atropine was in the abnormal range in only 2 patients. Stimulated salivary flow decreased after atropine (1.97 +/- 1.7 g saliva) compared with flow after placebo (4.1 +/- 1.2 g) (p less than 0.05). No changes in visual accommodation or pulse rate were seen. Dry mouth and decreased salivation correlated with delayed gastric emptying (r = 0.76, p less than 0.05). Anticholinergic side effects of aerosolized atropine include prolonged gastric emptying in some patients. Gastroparesis after inhaled atropine is suggested by the symptom of dry mouth.

Adult↗
PubMed1994

A national survey of atropine use by Australian anaesthetists.

All Fellows of the Faculty of Anaesthetists, Royal Australasian College of Surgeons (now Australian and New Zealand College of Anaesthetists) were surveyed by mail regarding their use of prophylactic atropine. They were asked whether their usual practice was to give atropine for the following indications: premedication, induction of anaesthesia, intubation of the trachea, one dose of suxamethonium, a second dose of suxamethonium, halothane anaesthesia, oropharyngeal surgery, bronchoscopy and eye surgery. For each indication they were asked for details regarding their practice concerning neonates, infants, children and adults. The large response rate of 86% of Fellows returning a survey form ensured that the survey was representative of Australian anaesthetic practice. Results indicate a wide variation in practice regarding the prophylactic use of atropine, with neonates, infants and children more likely to receive prophylactic atropine than adults. The majority do not give prophylactic atropine as premedication, but may give it in the younger age groups at induction, and many (67%) only give it if they are to administer suxamethonium to a child. The only indication for which a convincing majority (> 80%) of anaesthetists agreed that prophylactic atropine should be given was when a repeated dose of suxamethonium was to be given to neonates, infants or children. A large proportion of anaesthetists (> 80%) agreed that atropine is not necessary prior to halothane anaesthesia in all age groups, nor as premedication, at induction, at intubation, prior to oropharyngeal surgery or prior to eye surgery in adults. These results were compared with the practice at a major paediatric hospital where the practice is not to use routine prophylactic atropine.

Administration, Oral↗
PubMed1983

Inhibition of atropine metabolism by organophosphate pesticides.

Urine specimens of 8 organophosphate-poisoned patients on treatment with large doses of atropine were screened for atropine metabolites using thin-layer chromatography. Only atropine was detected. High performance liquid chromatography of urine specimens of a poisoned patient receiving large doses of atropine likewise detected only 3H-atropine after administration of 30 microCi 3H-atropine-sulphate. In the urine of a normal human volunteer treated with a single dose of 3H-atropine, 5 metabolic products were detected by this method. It is concluded that acute organophosphate-poisoning blocks atropine metabolism by inhibiting the hepatic microsomal enzymes.

Atropine↗
PubMed1976

Irreversible inhibitory effect of atropine on contractile responses to drugs in isolated rabbit ileum.

Effect of atropine sulfate (atropine) on the contractile responses to acetylcholine chloride (ACh), potassium chloride (K) and barium chloride (Ba) was investigated in isolated rabbit ileum. Tension of the strips suspended in the bath medium (Locke solution, 30 degrees C) was isotonically recorded. The K(ED50)- and Ba(ED50)-induced contractions were not affected by atropine at 3.0 X 10(-4) mM, which reversibly abolished the ACh(ED100)-contraction. After washout of 6.0 X 10(-4) mM atropine, the phasic, but not the tonic, component of ACh(ED50)-, K(ED50)- and Ba(ED50)- contractions was to some extent inhibited irreversibly. On the contrary, such irreversible inhibition of the phasic component was not produced by atropine methylbromide even in the high concentration of 3.0 X 10(-3) mM. The irreversible inhibitions by atropine of 6.0 X 10(-4) mM on the phasic component of ACh- and K-contractions were protected by pretreatment with a high concentration of ACh or K. Further, these irreversible inhibitions by atropine were potentiated by the absence of Ca and were abolished by the increase of Ca content in bath media. These results suggest that the irreversible inhibition of the contractile responses to drugs by atropine in high concentration may be due to the interference with the mobilization of Ca in the deep layer of the membrane, rather than by a blockade of muscarinic receptor sites.

Animals↗
PubMed1996

Dipyridamole and dobutamine-atropine stress echocardiography in the diagnosis of coronary artery disease. Comparison with exercise stress test, analysis of agreement, and impact of antianginal treatment.

STUDY OBJECTIVES: To compare the usefulness of dipyridamole echocardiography, dobutamine-atropine echocardiography, and exercise stress testing in the diagnosis of coronary artery disease and to analyze the agreement among the tests. DESIGN: Performance of these three tests in random order on a consecutive cohort of patients. SETTING: A tertiary care and university center. PATIENTS: One hundred two consecutive patients with chest pain and no history of coronary artery disease. INTERVENTIONS: Dipyridamole echocardiography, dobutamine-atropine echocardiography, exercise stress testing, and coronary angiography. MEASUREMENTS AND RESULTS: Dobutamine-atropine test was positive in 49 (77%) of 63 patients with coronary artery disease, dipyridamole test in 49 (77%), and exercise stress test in 44 (68%; p = NS). Both echocardiographic tests showed an overall specificity (dipyridamole, 97%; dobutamine, 95%) higher than exercise stress test (79%; p < 0.05). Sensitivity of dipyridamole testing decreased from 93 to 61% (p = 0.002) if patients were receiving antianginal treatment but sensitivity of dobutamine-atropine testing was not affected (77% in patients receiving and not receiving treatment). When results were considered as positive-negative, agreement between dipyridamole and dobutamine-atropine echocardiography was 85% (kappa = 0.70). With regards to regional analysis, concordance was good (93% for segments, kappa = 0.76; and 95% for coronary arteries, kappa = 0.92). Major complications were more frequent during dobutamine-atropine (n = 7) than during dipyridamole infusion (n = 2) (p = 0.06). CONCLUSIONS: Dobutamine-atropine and dipyridamole echocardiography have a similar sensitivity and a higher specificity than that obtained by exercise ECG for the diagnosis of coronary artery disease. Similar information is obtained with dipyridamole and dobutamine-atropine echocardiography. It is our thought that pharmacologic stress echocardiography should be used as a first-step test to rule out coronary artery disease in patients not capable of exercising.

Adrenergic beta-Antagonists↗