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PubMedDate not supplied

A comparative study of clonidine versus a combination of diazepam and atropine for premedication in orthopaedic patients.

Sixty patients in the age group of 18-60 years of A.S.A. Grade I/II risk, scheduled for elective orthopaedic surgeries under general anaesthesia were studied for pre-medication with either oral clonidine or with combination of effects of diazepam & atropine. Patients in Group A (clonidine group) received tablet clonidine 100 mcg (1 tablet) if less than 50 kg in weight and 200 mcg if weighing more than 50 kg two hours before surgery. Patients in Group B (Diazepam-atropine group) received one tablet of Diazepam (10 mg) orally two hours before surgery and injection atropine-sulphate 0.01 mg/kg half an hour preoperatively by intramuscular route. In our study, the sedative and anti-sialogogue effects of clonidine were comparable to those of diazepam-atropine combination, which are commonly used premedicants. The anti-anxiety effect of clonidine was found to be better than that of diazepam-atropine combination. Clonidine also proved to be a better agent for the attenuation of pressor response to laryngoscopy and intubation. Thus, oral clonidine is a better premedicant compared to atropine-diazepam combination. Also, it is a more acceptable agent because of its oral route of administration.

Adjuvants, Anesthesia↗
PubMed1988

Comparative cardiac effects of intravenous bolus of ipratropium bromide (itrop) and atropine sulfate in 22 patients.

At the present time, there is no satisfactory pharmacological treatment for arrhythmia or conduction disorders induced by or aggravated by vagal hypertonia. The limited duration of action of the atropine derivatives currently available justifies the development of new compounds with expected longer acting duration. The aim of this study was to compare the effects of a single blind intravenous injection of ipratropium bromide to those of atropine sulfate in 22 patients. These patients were studied with continuous Holter recordings for three days. During the second and the third nights (patient sleeping), boluses of atropine (0.03 mg/kg) and of ipratropium bromide (0.03 mg/kg), respectively, were added to a continuous saline intravenous infusion. Accurate ECG analysis allowed determination of maximal heart rate peak, timing of maximal heart rate, variations in sinus cycle length, atrioventricular conduction, and durations of drug action. A nonsuggestive questionnaire was presented to patients to detect possible occurrence of side effects. The mean maximal heart rate rose significantly (p less than 0.001) for atropine (+46.2%) and for ipratropium bromide (+57.4%). The effects obtained with ipratropium bromide on the heart rate lasted nearly twice as long as those obtained with atropine (respectively, 120 +/- 38.4 min and 70 +/- 30 min- for the pharmacological half-life). Common minor muscarinic side effects (dryness of the mouth) were noted with the two drugs. In conclusion, this comparative intraindividual study confirmed the prolonged vagolytic effects of intravenous ipratropium bromide, which may be valuable in the treatment of patients with vagally mediated automaticity and conduction disturbances.

Adult↗
PubMed1994

Effect of atropine injected into the nucleus tractus solitarius on the regulation of blood pressure.

Previous experiments have demonstrated that stimulation of muscarinic cholinergic receptors in the nucleus tractus solitarius (NTS) of the rat decreases arterial blood pressure and heart rate. The present studies were designed to examine the role of cholinergic mechanisms in the NTS in the tonic regulation of arterial pressure and the baroreceptor reflex. Atropine injected into the NTS of chloralose-anesthetized rats produced a dose-dependent inhibition of cardiovascular responses elicited by injection of acetylcholine into the same site; 240 pmol atropine eliminated acetylcholine-evoked responses. Atropine also increased arterial blood pressure but only at higher doses. Even larger doses of atropine were required to alter cardiovascular responses elicited by electrical stimulation of the aortic depressor nerve. Methylatropine injected into the NTS also blocked acetylcholine-evoked responses but, in contrast to the actions of atropine, did not increase arterial pressure in the dose range required to block acetylcholine-evoked responses. Furthermore, a dose of methylatropine (1 nmol) capable of blocking acetylcholine-evoked cardiovascular responses did not alter aortic depressor nerve-evoked cardiovascular responses. This lack of an effect of methylatropine on arterial pressure and aortic depressor nerve-evoked responses was not due to limited diffusion of the drug within the NTS since 1 nmol methylatropine completely blocked acetylcholine-evoked responses even when injected 0.5 mm distant from the site of acetylcholine injection. These results suggest that cholinergic mechanisms in the NTS are not involved in the tonic regulation of cardiovascular function or the baroreceptor reflex. Furthermore, these results highlight the importance of characterizing doses of drugs used in microinjection studies.

Animals↗
PubMed2003

Impact of patching and atropine treatment on the child and family in the amblyopia treatment study.

OBJECTIVE: To assess the psychosocial impact on the child and family of patching and atropine as treatments for moderate amblyopia in children younger than 7 years. METHODS: In a randomized, controlled clinical trial, 419 children younger than 7 years with amblyopic eye visual acuity in the range of 20/40 to 20/100 were assigned to receive treatment with either patching or atropine at 47 clinical sites. After 5 weeks of treatment, a parental quality-of-life questionnaire was completed for 364 (87%) of the 419 patients. Main Outcome Measure Overall and subscale scores on the Amblyopia Treatment Index. RESULTS: High internal validity and reliability were demonstrated for the Amblyopia Treatment Index questionnaire. The overall Amblyopia Treatment Index scores and the 3 subscale scores were consistently higher (worse) in the patching group compared with the atropine-treated group (overall mean, 2.52 vs 2.02, P<.001; adverse effects of treatment: mean, 2.35 vs 2.11, P =.002; difficulty with compliance: mean, 2.46 vs 1.99, P<.001; and social stigma: mean, 3.09 vs 1.84, P<.001, respectively). CONCLUSION: Although the Amblyopia Treatment Index questionnaire results indicated that both atropine and patching treatments were well tolerated by the child and family, atropine received more favorable scores overall and on all 3 questionnaire subscales.

Adult↗
PubMed1977

Atropine inhibition of echothiophate cataractogenesis in monkeys.

One cynomolgus and three vervet monkeys were treated topicall twice daily in one eye with 63 microgram of echothiophate iodide and 750 microgram of atropine sulfate. The opposite eyes were treated with echothiophate alone. The eyes treated with echothiophate alone all developed posterior and/or anterior subcapsular cataracts within 26 to 66 days. The echothiophate plus atropine-treated cynomolgus eye developed a cataracts of much delayed onset and lesser severity compared to its echothiophate-only-treated fellow. None of the echothiophate plus atropine-treated vervet eyes developed cataracts during the 121 (two eyes) or 231 (one eye) days of treatment. After 121 days of echothiophate plus atropine treatment, two vervet eyes were switched to echothiophate alone. Both eyes developed unequivocal posterior and anterior subcapsular lens opacities, one within 51 and one within 71 days after the switch. We conclude that atropine inhibits echothiophate cataracto-genesis in vervet and cynomolgus monkeys.

Administration, Topical↗
PubMed1996

Duration of action of intranasal atropine on methacholine-induced nasal secretions.

OBJECTIVE: To evaluate the duration of the inhibitory action of intranasal atropine on the secretory response to nasal challenge with methacholine. DESIGN: Double-blind, placebo-controlled, four-way crossover trial. SUBJECTS: Twelve volunteers with perennial allergic rhinitis. INTERVENTIONS: Subjects were treated intranasally with placebo or 100, 200, and 400 micrograms of atropine in each nostril. They were then challenged 30 minutes after administration of the nasal spray and hourly for 6 hours with 0.19 mg of methacholine. The weight of nasal secretions generated by methacholine challenge served as an indicator of the secretory response. The nasal challenges and the collection of nasal secretions were performed using filter paper disks. RESULTS: After placebo treatment, the response to methacholine was similar at each time point. In contrast, all doses of atropine significantly reduced the response to methacholine stimulation at the 30-minute, 1-hour, and 2-hour time points. CONCLUSIONS: Our data show that the anticholinergic activity of intranasal atropine lasts at least 2 hours with no significant difference in the duration of inhibitory action between the doses used. The results suggest that intranasal atropine could become a therapeutic modality for patients in whom glandular hypersecretion is a major symptom.

Administration, Intranasal↗
PubMed1995

Pharmacokinetics of HI-6 and atropine in anaesthetized pigs after administration by a new autoinjector.

A newly developed autoinjector (Astra Tech, Sweden) containing 500 mg HI-6 and 2 mg atropine sulphate was tested in anaesthetized normal pigs. The pharmacokinetics and pharmacodynamics of the drugs after administration by the autoinjector were compared with those after conventional needle and syringe delivery intramuscularly and intravenously. Cardiopulmonary parameters were monitored and serum concentrations of oxime, atropine, and acetylcholinesterase were determined in blood samples taken at intervals over a 6 h period postinjection. After injection in anaesthetized pigs, both HI-6 and atropine were absorbed rapidly and completely from the injection site. Therapeutic serum concentrations of HI-6, arbitrarily taken as 4 micrograms mL-1, were reached within 1 min of intravenous and autoinjector administration, and within 5 min of intramuscular injection. The concentrations remained above this level for 3-4 h. There were no significant changes in acetylcholinesterase activity, mean arterial blood pressure, or respiration frequency after injection of HI-6 and atropine sulphate. The heart rates increased significantly after administration of the two drugs (cardioacceleration defined as > or = 5% increase in heart rate), regardless of the technique employed. Our results show that HI-6 and atropine sulphate can be given intramuscularly by the new autoinjector with the same effectiveness and speed as when given intravenously. Irrespective of the injection technique, no overt signs of toxicity were observed at the drug concentrations used.

Acetylcholinesterase↗
PubMed1999

The use of atropine for facilitation of direct current cardioversion from atrial fibrillation--results of a pilot study.

BACKGROUND: The importance of the role of the autonomic nervous system (ANS) in the initiation and propagation of atrial fibrillation has been demonstrated in the condition of paroxysmal atrial fibrillation. However, the role of the ANS in patients with chronic atrial fibrillation is less clear. Some patients with chronic atrial fibrillation are resistant to the standard techniques of direct current (DC) cardioversion. HYPOTHESIS: We sought to investigate whether excessive vagal tone might prevent the restoration of sinus rhythm and to establish that the abolition of vagal tone using intravenous atropine will facilitate DC cardioversion in patients with atrial fibrillation who are resistant to the standard cardioversion techniques. METHODS: Beginning in August 1994, a change in the protocol for elective DC cardioversion of atrial fibrillation was made to include the use of intravenous atropine for patients resistant to the standard techniques of DC cardioversion. RESULTS: Over a 2-year period, 140 elective cardioversions were performed for atrial fibrillation. Sinus rhythm could not be restored on 31 occasions. Intravenous atropine prior to a further 360 J shock with paddles in the anteroposterior position allowed sinus rhythm to be restored on nine occasions. Patients with successful cardioversion after atropine had significantly better left ventricular function than those who remained in atrial fibrillation (p = 0.001) as well as a tendency toward a smaller left atrium. CONCLUSION: This study suggests that high vagal tone, which is dominant in patients with structurally normal hearts, may prevent the termination of atrial fibrillation by standard techniques of DC cardioversion, and that the abolition of high vagal tone by atropine facilitates the restoration of sinus rhythm.

Adult↗
PubMed1995

The effect of atropine on parasympathetic control of respiratory sinus arrhythmia in two ethnic groups.

The effects of low and high doses of atropine on respiratory sinus arrhythmia were assessed to ascertain whether any differences exist in the degree of parasympathetic control on cardiac rhythm between two ethnic groups. The standard deviation of the R-R interval (the R peak-to-peak interval of two QRS complexes of an electrocardiogram) has been used as a noninvasive parameter to measure the degree of parasympathetic cardiac control. Nine black and nine white healthy male volunteers took part in study after approval by the Research and Ethics Committee of the Medical University of South Africa. Thirty consecutive electrocardiographic complex were recorded during each of the following: 3 deep inspirations and expirations, incremental cumulative atropine injections of 0.001 mg/kg until 0.005 mg/kg, followed by two injections of 0.01 mg/kg and 0.015 mg/kg of atropine each. After each of the last two injections the deep inspiration and expiration procedure was repeated. No significant differences could be found at any stage for any parameter between the groups. In both groups the R-R interval variation increased threefold during voluntary induced respiratory sinus arrhythmia. This effect was blocked after 0.01 mg/kg of atropine. The degree of parasympathetic control was not affected by any respiratory maneuver, but was affected by atropine. A significant inverse quadratic relationship was found between parasympathetic control and heart rate change (R = .984 for whites, and R = .905 for blacks). A poor correlation was found between the R-R interval variation and heart rate changes. In conclusion, ethnicity does not affect parasympathetic activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2002

Distinction between atropine-sensitive control of microvascular and cardiac oscillatory activity.

This study tested whether "high frequency" oscillations (HF; >0.12 cycles/s) in microvascular flow during a vasoconstrictive challenge constitute a homeostatic cholinergic response at the level of the microvasculature or simply represent oscillations that originate at the heart and are transmitted to passive microvascular beds. Heart rate, blood pressure, respiratory rate, and laser Doppler flowmetry of the forehead and finger were monitored in healthy volunteers at baseline, during systemic infusion of phenylephrine (0.4-0.6 microg/kg/min), and during subsequent addition of intravenous atropine (< or = 2.0 mg/70 kg). Spectral-domain analysis documented that atropine-sensitive oscillatory power of the R-wave to R-wave intervals of the electrocardiogram was predominant at the respiratory frequency (0.20 Hz) at baseline and during phenylephrine infusion. In contrast, arteriolar-capillary networks of the forehead developed a prominent atropine-sensitive oscillatory peak at 0.14 +/- 0.02 Hz during phenylephrine infusion (P < 0.05 for differences in oscillatory magnitude and frequency between forehead flow and R-R intervals). The cross-power spectral density confirmed the lack of common power between forehead flow and R-R oscillations. Post hoc assessments showed that---similar to heart rate---systemic pressure and systemic flow also had persistent power at 0.20 Hz and did not develop a peak at the forehead oscillatory frequency; phenylephrine likewise did not induce atropine-sensitive oscillations in the finger, a finding attributable to adrenergic predominance in this region. We conclude that atropine-sensitive oscillatory activity in the forehead microvasculature in response to a vasoconstrictive challenge constitutes a local response that is not due to, nor associated with, mechanical transmission from the heart and proximal vasculature.

Atropine↗
PubMed1991

Atropine and verapamil interactions in healthy volunteers.

The calcium antagonist falipamil, a chemical congener of verapamil, has anticholinergic properties. It was decided to study the interaction of verapamil with the anticholinergic drugs, atropine and pirenzepine, using healthy male volunteers. After atropine alone a significant tachycardia developed at 2 min and remained significant up to 90 min. Verapamil pretreatment followed by atropine administration resulted in a significantly greater tachycardia. Pirenzepine alone caused a bradycardic response which was accentuated after verapamil pretreatment. It is postulated that short term verapamil administration is accompanied by reflex activation of the sympathetic nervous system which does not manifest with a tachycardia owing to combined influence of verapamil and vagus on the sino-atrial node. Reduction of vagal tone with atropine treatment results in sympathetic overriding of the sino-atrial suppression, thus causing an additive tachycardia. The clinical use of atropine for prolonged verapamil-induced atrio-ventricular conduction is supported by these results.

Adult↗
PubMed1980

The inhibiting effect of atropine on growth hormone release during exercise.

The effects of atropine upon changes in the circulating levels of growth hormone (GH), cortisol, lactate, glucose, and free fatty acids (FFA) were studied during exercise using both constant and progressively increasing work loads. At low work loads, atropine had no effect upon the changes in either cortisol or lactate levels, but the normal exercise-induced rise in GH was abolished or markedly reduced. At higher work loads, especially when prolonged, the usual rises in cortisol and lactate were enhanced by atropine, but the rise in GH was diminished and delayed. In no circumstances were the changes in FFA or glucose significantly affected by atropine. We regard the effect of atropine upon changes in cortisol and lactate responses as secondary to its cardiovascular effect, but suggest that the inhibition of Gh release may be evidence of a cholinergic mechanism in the control of Gh release during exercise.

Atropine↗
PubMed1976

Effect of atropine and oxotremorine on the release of acetylcholine from the frog spinal cord.

The in vitro frog spinal cord has been used to study acetylcholine (ACh) release and spinal root potentials. The preparation bathed in an eserine-containing medium spontaneously released ACh into the bathing fluid. This release was enhanced by atropine in a dose-related and long-lasting manner and transiently by oxotremorine. The release rate of ACh was increased by low frequency ventral root stimulation; this increase was found to be proportionally the same after application of atropine. Oxotremorine did not modify the elctrically-evoked ACh release but blocked or reduced the effect of atropine. It is concluded that the stimulatory action of atropine on ACh output cannot be entirely explained by an interaction of atropine with presynaptic cholinergic receptors and that other indirect mechanisms (via interneurones) may play a role in this effect.

Acetylcholine↗
PubMed1982

Effect of sodium concentration and of atropine on the contractile response of the guinea-pig ileum to potassium ions.

The possibility that the guinea-pig ileum's contractile response to K+-rich solutions is partly mediated by acetylcholine release from the intramural nervous tissue was examined by studying the inhibition of that response by atropine at different values of [Na+]o. In a medium in which the NaCl was replaced by iso-osmotic glucose, the response to high [K+]o was not greatly affected, while the responses to acetylcholine and to other agonists were significantly reduced. In control medium (149 mM Na+), atropine (10(-7) M) partly inhibited the responses to K+-rich solutions and to agonists such as histamine, 5-hydroxytryptamine and bradykinin. When [Na+]o was reduced to 12 mM, by iso-osmotic substitution of glucose for NaCl, the response to high K+ was no longer inhibited by atropine, which still partly inhibited the contractions elicited by the three agonists and totally blocked the response of acetylcholine. It is proposed that atropine's inhibition of the response to high K+ and to agonists is not due to its specific anti-muscarinic effect, but to an unspecific action, which in the case of the agonists is independent of [Na+]o. In addition, the inhibition of the response to high K+ would results from a different Na+-dependent mechanisms, possibly involving the stimulation of the Na-K pump by atropine. This is supported by the observation that this drug partly relaxed ileum preparations that were contracted by ouabain.

Acetylcholine↗
PubMed1992

Heart rate responses to deep breathing and 4-seconds of exercise before and after pharmacological blockade with atropine and propranolol.

Two autonomic tests which evaluate cardiac vagal activity, the respiratory sinus arrhythmia and the newer 4-second exercise test, have been compared. From electrocardiograph tracings, respiratory sinus arrhythmia was quantified by the ratio between the longest R-R interval during expiration and the shortest one during inspiration (E/I ratio), and the 4-second exercise test by the ratio between the last R-R interval before and the shortest one during exercise (B/C ratio). In 29 healthy subjects there was a correlation (R = 0.60, p less than 0.05) between the responses to the two tests. In a group of six healthy subjects the same tests were performed after autonomic blockade with intravenous atropine and/or propranolol. The heart rate rise during the 4-second exercise test was nearly abolished by atropine (mean +/- SD) (B/C: control = 1.53/0.33; after atropine = 1.04/0.03), whereas RSA was diminished to a lesser extent (E/I: control = 1.59/0.24; after atropine = 1.13/0.07). beta-adrenoceptor blockade did not affect the test ratios (after propranolol: B/C = 1.51/0.33 and E/I = 1.45/0.14). Successive tests during the following hour after atropine infusion showed a somewhat faster recovery of the respiratory sinus arrhythmia than the heart rate acceleration induced by the 4-second exercise test (p less than 0.05). We conclude that there may be some difference in the mechanisms which contribute to the heart rate changes in these two autonomic cardiovascular tests; these remain to be clarified. The 4-second exercise test may be an alternative to the respiratory sinus arrhythmia test in the non-invasive evaluation of cardiac parasympathetic activity.

Adult↗
PubMed1985

Influence of atropine on taste-stimulated parotid secretion.

Elemental taste qualities as "sour" and "sweet" showed different stimulatory effects on the parotid secretion when given in concentrations with comparable gustatory intensity. Sweet (fructose 10%) exerted an adrenergic-like activity, sour (citric acid 1%) a more parasympathetic-like influence on parotid secretion. The vagal pathway of the gustatory stimuli was further investigated by the simultaneous infusion of atropine sulfate (17 micrograms/kg per 30 min). Atropine reduced the flow rate during sour and sweet stimulation in the range of 500% and 300%. In 60% of the test persons parotid flow rate could not be totally depressed in any of three 10-min sampling fractions by atropine when a sour stimulus was applied; in these subjects protein and amylase concentration increased significantly. Following fructose stimulation the flow rate was totally depressed in all subjects by atropine in the 20- and 30-min sampling fractions. In the first 10-min fraction protein and amylase concentration were not influenced by atropine. The cholinergic pathway seems to be responsible primarily for the flow rate and has further different modulating influence on the stimulatory effect of the individual taste qualities.

Adult↗
PubMed1981

Atropine: a sensitive gas chromatography-mass spectrometry assay and prepharmacokinetic studies.

A novel assay method for the determination of atropine in biological fluids is presented. Atropine is extracted and subsequently hydrolyzed. The generated tropine is them derivatized to heptafluorobutyryl-tropine, which is measured by GLC-MS. Base peaks m/z 124 and m/z 127 are simultaneously monitored. Deuterated atropine serves as internal standard. This specific and sensitive assay permits a delineation of the disposition pharmacokinetics in humans after i.v. administration of the drug. Prepharmacokinetic studies determined pKa values for atropine and tropine of 9.56 and 10.35 respectively at 22 degrees C. Solvent partitioning experiments showed that atropine exerts a significantly larger lipophilicity than tropine. This was consistent with tropine (0%, 0.85) at 37 degrees C and pH 7.4. Plasma protein binding and erythrocyte partitioning of both compounds were concentration independent and invariable in the presence or absence of each other.

Atropine↗
PubMed1979

Inhibition of pepsin secretion by metiamide and atropine in the conscious rat.

The inhibition of pepsin secretion by metiamide and atropine has been studied in the gastric fistula rat and the Heidenhain pouch rat. A comparison of the effectiveness of metiamide and atropine in inhibiting pepsin secretion was made by using doses of the antagonists which produced a similar level of inhibition of acid secretion. In the gastric fistula rat both atropine and metiamide inhibited the basal pepsin output, but atropine was more effective than metiamide in this respect. In the Heidenhain pouch rat a large dose of metiamide which inhibited bethanechol-stimulated acid secretion had no significant effect on the corresponding output of pepsin. In this preparation atropine inhibited both acid and pepsin secretion. Possible reasons for the differences in the two preparations are discussed.

Animals↗