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PubMed1976

[Cardiovascular changes caused by atropine in normo- and hypothermic methoxyflurane anaesthesia (author's transl)].

The authors examined in 25 patients, of which 15 were normo- and 10 in hypothermic, the cardiovascular effects of 1 mg atropine i.v. In normothermia the heart rate increased significantly from 100 to 110 beats/min after atropine. At the same time the stroke index and stroke work decreased significantly. The mean arterial pressure, the heart index, the left ventricular minute- and stroke work and the total peripheral resistance did not change. In two patients with an arteriovenous fistula and hypervolaemia, the atropine injection caused an increased of heart- and stroke index. Arrhythmias did not occur after atropine. In hypothermia on the other hand atropine was shown to have no effect on heart frequency and all other examined parameters. In one patient in which the P-R interval was shortened, the atropine injection was followed by an total atrio-ventricular block. The authors cannot recommend atropine therapy in cases of hypothermic bradycardia, because of its lack of effect on the heart rate in hypothermia.

Adult↗
PubMed1998

Effects of atropine, isoproterenol and propranolol on the rabbit bladder contraction induced by intra-arterial administration of acetylcholine and ATP.

INTRODUCTION: In the rabbit, both cholinergic and purinergic nerves mediate bladder contraction. Acetylcholine is the neurohumoral transmitter for the cholinergic nerves, and ATP is the neurohumoral transmitter for purinergic innervation. Beta-adrenergic stimulation mediates relaxation of the bladder. In the current study, we investigated the effects of atropine, isoproterenol and propranolol on the bladder contraction induced by intra-arterial administration of acetylcholine and ATP. METHODS: Mature male New Zealand White rabbits were used in this study. A polyethylene catheter with an outer diameter of 0.043 inches was inserted through the rabbit's right femoral artery until it reached the lower abdominal aorta. An 8 F catheter was inserted through the urethral orifice into the bladder and secured by tying a 2-0 silk ligature around the bladder neck. The catheter was connected to an infusion pump and a pressure transducer by a 3-way valve. After 15 ml. of saline was infused into the bladder, an intra-arterial administration of acetylcholine and ATP was infused and the change of intravesical pressure was quantitated and recorded with a Grass model 7D polygraph. The procedure was repeated after a 5-minute pretreatment with atropine, isoproterenol or propranolol. RESULTS: The results are summarized as follows: 1) Baseline intravesical pressure was not altered by pretreatment with atropine. Pretreatment with atropine shifted the dose-response curve of acetylcholine to the right and the maximal response was reduced by 9%, 49% and 77% respectively with pretreatment with atropine 10(-8), 10(-7) and 10(-6) mole/kg. The dose-response curve of ATP was not significantly affected by pretreatment with atropine. 2) Baseline intravesical pressure was lowered by pretreatment with isoproterenol. Pretreatment with isoproterenol shifted both dose-response curves of acetylcholine and ATP rightward. The maximal response of acetylcholine was reduced by 10%, 26% and 37% respectively, and the maximal response of ATP was reduced by 6%, 31% and 43% respectively by pretreatment with isoproterenol 10(-8), 10(-7) and 10(-6) mole/kg. 3) Baseline intravesical pressure was not changed by pretreatment with propranolol. Both dose-response curves of acetylcholine and ATP were not significantly affected by pretreatment with propranolol. SUMMARY: In conclusion, pretreatment with atropine inhibited acetylcholine-induced bladder contraction, but had no effect on ATP-induced contraction. Pretreatment with isoproterenol significantly inhibited both contractile stimulation by acetylcholine and ATP. Pretreatment with beta-adrenergic antagonist had no effect on the bladder contraction induced either by acetylcholine or by ATP. Thus, although beta-adrenergic stimulation is capable of significantly inhibiting the contractile responses to both cholinergic and purinergic stimulation, under normal conditions, sympathetic nerves do not modulate either cholinergic or purinergic stimulation.

Acetylcholine↗
PubMed1976

[Eosphagomanometric finding in man after intravenous administration of a new cholinolytic (pramiverine), atropine and scopolamine butylbromide].

The tone depressing effect on deglutition peristaltic processes in the esophagus by i.v. application of 4,4-diphenyl-N-isopropyl-cyclohexylamine hydrochloride (pramiverine, Sistalgin) (0.03 and 0.045 mg/kg body weight), atropine (0.5 mg) and hyoscine-N-butylbromide (scopolamine-butylbromide, SBB) (20 mg) was tested on trained subjects. During the first 30 min following the larger dose of pramiverine, the effect is not quite so pronounced as it is seen after the usual atropine dose; from the 30th to the 60th min, however, the tone depressing effect of pramiverine is superior to that of atropine, 1 h after application of pyramiverine the pressure amplitude is still reduced to 54.3% of the initial value, while after atropine the effect has returned to 70.9% of the initial value by this time. Neither atropine nor pramiverine were able to exert a tone depressing effect as pronounced as that of SSB. But 30 min after application of the effect of SBB was not statistically significant any longer and after 40 min it could not be measured at all. Following atropine and SBB, the side effect of tachycardia was correlated exactly to the main effect tested. Further side effects, such as dryness of mouth and disturbed accomodation, were most pronounced after atropine. With pramiverine at the effective doses of 0.03 and 0.045 mg/kg, the side effects were not appreciable; neither objective measuring nor subjective reports of the subjects indicated any conspicuous deviations.

Atropine↗
PubMed2002

Comparison of heart rate changes after neostigmine-atropine administration during recovery from propofol-N2O and isoflurane-N2O anesthesia.

PURPOSE: Propofol augments the reduction of heart rate (HR) in combination with cholinergic agents and attenuates the HR response to atropine. We examined whether propofol anesthesia was associated with an increased incidence and extent of bradycardia after neostigmine-atropine administration compared with the effects of isoflurane anesthesia. METHODS: Thirty-six adult patients were randomly assigned to two groups ( n = 18 each): the propofol group patients were anesthetized with propofol (5-10 mg.kg(-1).h(-1))-(2)O-fentanyl, and the isoflurane group patients were anesthetized with isoflurane (0.5%-1.0%)-(2)O-fentanyl. When surgery was completed, anesthetics were discontinued, and then a mixture of neostigmine 0.05 mg.kg(-1) and atropine 0.02 mg.kg(-1) was injected intravenously over 20 s. Blood pressure (BP) and HR were measured noninvasively at 1-min intervals for 10 min. RESULTS: At the completion of the surgery, the average infusion rate of propofol was 6.2 +/- 1.7 mg.kg(-1).h(-1), and the average inspired concentration of isoflurane was 0.73 +/- 0.15%. Immediately before the neostigmine-atropine injections, HR and mean BP were similar in the two groups. The maximum increase in HR after the neostigmine-atropine injections was significantly less in the propofol group than in the isoflurane group (16 +/- 9 and 34 +/- 6 beats.min(-1), respectively, P < 0.01). The subsequent maximum decrease in HR was greater in the propofol group than in the isoflurane group (-9 +/- 4 and -5 +/- 4 beats.min(-1), respectively; P < 0.01). The incidence of bradycardia (HR < 50 beats.min(-1)) after neostigmine-atropine injection was greater in the propofol group than in the isoflurane group (61% and 28%, respectively; P < 0.01). CONCLUSION: We conclude that propofol anesthesia attenuates the initial increases in HR, enhances the subsequent decreases in HR, and increases the incidence of bradycardia after neostigmine-atropine injections compared with the effects of isoflurane anesthesia.

Clinical Trial↗
PubMed1999

Effect of topical atropine on intraocular pressure and pupil diameter in the normal horse eye.

The objective was to determine whether topically administered 1% atropine would alter intraocular pressure. The animals studied were four healthy adult horses. Intraocular pressure and pupil diameter were measured prior to and during a 2-day period of treatment with 1% atropine sulfate. No significant changes in intraocular pressure occurred as a result of the treatment with atropine. Pupil diameter increased significantly after atropine was applied. Available information on the outflow of aqueous humor from the horse eye suggests that atropine might reduce intraocular pressure in the horse by increasing uveoscleral outflow. This could prove beneficial in the treatment of equine glaucoma. We could not confirm a significant pressure-lowering effect of atropine. It is possible, however, that a longer treatment period may be required or that atropine may have a more profound effect on glaucomatous globes.

Journal Article↗
PubMed1975

Atropine modification of the pulmonary effects of chemical mediators in the guinea pig.

The actions of histamine, slow-reacting substance of anaphylaxis (SRS-A), Bradykinin, and prostaglandin F2alpha on pulmonary mechanics in the unanesthetized guinea pig were separated into direct and secondary cholinergic airway effects on the basis of alteration of their actions by atropine. The effects of SRS-A (500 and 3,000 units/kg) on compliance were not significantly altered by atropine, while the effects of bradykinin (3.0 and 30 mug/kg) on compliance were decreased only at 3.0 mug/kg by atropine. The effects of both of these agents on resistance were decreased by atropine, suggesting that SRS-A and bradykinin act directly on the peripheral airways and by secondary cholinergic mechanisms on both central and peripheral airways. The effects of histamine (3.0 mug/kg) on both compliance and resistance were abolished by atropine, suggesting an action mainly via cholinergic pathways; while at a higher dose, 9.0 mug/kg, there was both a direct and a cholinergic action. The effects observed 20 sec after the administration of prostaglandin F2alpha (PGF2alpha) were not altered by atropine suggesting a direct action on airways, while both the compliance and resistance changes observed 3-8 min after PGF2alpha were abolished by atropine suggesting that the latter effects were mediated solely by cholinergic mechanisms

Airway Resistance↗
PubMed1975

Effect of intravenous atropine and methylatropine on heart rate and secretion of saliva in man.

Intravenous atropine sulphate (0.25, 0.40, 0.75 and 1.50 mg), atropine methylnitrate (0.08, 0.13 and 0.25 mg) and saline were given to 72 healthy medical students. The effects on heart rate and rhythm, systolic and diastolic blood pressure and salivary secretion were studied. Salivation was inhibited by all the doses of the two drugs. There was a clear dose-response relationship and methylatropine was about 3 times as potent as atropine. Heart rate was accelerated by 0.75 and 1.50 mg atropine, and 0.25 mg methylatropine, whereas 0.25 mg atropine and 0.08 and 0.13 mg methylatropine induced bradycardia, which was considered to be due to a peripheral action. It is suggested that the drugs act as partial agonists at muscarinic receptors. No clear effect on blood pressure was seen, except for the highest dose of atropine, after which the diastolic pressure was increased. 20 out of 59 subjects who received anticholinergics developed supra-ventricular arrhythmias; with both drugs periods of nodal rhythm were most common. They appeared shortly after the injection and usually lasted for a few minutes.

Adult↗
PubMed1987

Atropine sulfate increases pituitary responses to stress.

The effects of atropine sulfate pretreatment on pituitary indices of stress response were examined. Pituitary cyclic AMP and plasma prolactin increases following 15 min of acute stress were used as measures of stress response. Over a range of doses (0, 5, 10, 30 and 60 mg/kg), pretreatment with atropine sulfate increased the measured stress responses to footshock but had little or no effect on resting or non-stressed levels of the substances measured. The effects of atropine on response to immobilization were tested only at 5 mg/kg. At this dose, atropine sulfate, but not methylatropine nitrate, increased pituitary cyclic AMP response to immobilization stress demonstrating that the potentiation of the pituitary cyclic AMP stress response was not limited to footshock stress and suggesting that this effect of atropine was central rather than peripheral. Neither atropine nor methylatropine pretreatment at this dose potentiated prolactin response to immobilization stress.

Animals↗
PubMed1989

Comparing the cardiac vagolytic effects of atropine and methylatropine in rhesus macaques.

Atropine and methylatropine (190 nmol/kg) were compared in rhesus monkeys (Macaca mulatta) for their ability to produce a cardiac vagal blockade using a noninvasive estimate of respiratory sinus arrhythmia (RSA). Twelve monkeys received both drugs via intravenous (IV) and intramuscular (IM) routes of administration and were monitored for 3 hr after treatment. Both drugs, regardless of the route of administration, reduced RSA amplitude. At this dose, methylatropine was more effective than atropine in its ability to reduce RSA amplitude, heart period (HP; beat-to-beat interval), and overall heart period variability (HPV). Estimated RSA amplitude and HPV returned to basal levels significantly earlier after IM atropine administration than after IV treatment. Methylatropine did not exhibit any route effects. In addition, the mean decrease in RSA amplitude and HPV for the IM route of atropine sulfate was significantly less than that for the IV route. Serum atropine concentrations correlated significantly with all variables after IM treatment but only with RSA and HPV after IV treatment. Methylatropine may therefore be more useful than atropine as a pharmacologic challenge drug for detecting organophosphorus (OP) exposure because of its longer duration of action, lack of route of administration differences, and less likelihood of crossing the blood-brain barrier. Further studies are needed to fully evaluate methylatropine's potential in the challenge method of OP detection.

Animals↗
PubMed1977

Comparison of aerosolized atropine sulfate and SCH 1000 on exercise-induced bronchospasm in children.

The new anticholinergic compound Sch 1000 (ipratropium bromide) has been reported to be an effective bronchodilator without significant atropine-like side effects. We evaluated the effectiveness of different doses of nebulized Sch 1000 (40 microgram and 80 microgram) aerosolized atropine sulfate (1 mg) and placebo in the prevention of exercise-induced bronchospasm (EIB) in 20 children with atopic bronchial asthma. A random, crossover double-blind protocol was used. Standard exercise on a cycloergometer was used to induce EIB. Pulmonary function was determined before and after drug administration and exercise. Following no treatment or placebo, exercise resulted in average reductions of 33% to 43% in plethysmographic specific airway conductance (SGaw), of 20% to 25% in forced expiratory volume in 1 sec (FEV1), and of 25% to 32% in maximal midexpiratory flow rate. Exercise following no treatment or placebo resulted in average increases of 23% to 30% in thoracic gas volume (Vtg). Prior to exercise atropine and either dose of Sch 1000 caused significant increases in SGaw (48% to 59%). After pretreatment with Sch 1000 or atropine, exercise caused SGaw to fall to values that were not significantly different from pretreatment medication values, but were significantly higher than values following exercise without pretreatment or after pretreatment with placebo. No significant differences were noted between the effects of atropine and Sch 1000 on EIB. We conclude that at the doses used atropine and Sch 1000 cause equivalent degrees of bronchodilation but neither drug specifically inhibits EIB.

Adolescent↗
PubMed2026

Efficacy, tolerability, and threshold effect of atropine eye drops for myopia control: A systematic review and dose-response meta-analysis.

Atropine is an emerging therapy for myopia, yet the optimal concentration for prescription remains uncertain. We searched PubMed, Embase, Web of Science, Cochrane Library, World Health Organization International Clinical Trials, and ClinicalTrials.gov registry platforms. We included the randomized clinical trials (RCTs) that compared any dose of atropine against a placebo in myopic children. Among 3566 studies assessed, we identified 33 eligible RCTs involving 6301 children aged 4-18 years, with 10 different concentrations and a mean follow-up time of 19.5&#x202f;&#xb1;&#x202f;12.3 months. A nonlinear relationship was observed between atropine dosage and treatment efficacy (P&#x202f;<&#x202f;0.001). Compared to placebo groups, the mean differences in reducing annual spherical equivalent refraction progression for atropine concentrations of 0.01%, 0.02%, 0.03%, 0.04%, and 0.05% were 0.21 diopters (D) (95% CI, 0.13-0.28), 0.35 D (95% CI, 0.23-0.46), 0.42 D (95% CI, 0.28-0.56), 0.45 D (95% CI, 0.30-0.60), and 0.46 D (95% CI, 0.32-0.61) respectively For higher concentrations, the estimates were 0.49 D (95% CI, 0.34-0.63) for 0.1% and 0.99 D (95% CI, 0.66-1.31) for 1%, although these were based on fewer and smaller trials. Higher doses of atropine were associated with decreased amplitude of accommodation (P&#x202f;=&#x202f;0.02), increased pupil diameters (P&#x202f;=&#x202f;0.01) and a higher frequency of photophobia (P&#x202f;=&#x202f;0.02). Our findings suggest that the increase in treatment efficacy with higher concentrations may plateau beyond a certain range, and that the current practice of increasing atropine concentrations for children who show inadequate responses to lower doses should be confined to a specific concentration range. This analysis is limited by the number, design heterogeneity, and sample sizes of available trials for higher concentrations, and by the frequent lack of pre-intervention refractive history in included studies. Therefore, estimates-particularly for doses exceeding 0.1%-should be interpreted with caution.

Humans↗
PubMed1986

Lack of task specificity and absence of posttraining effects of atropine on learning.

Three experiments are reported whose purpose was to examine the effect of the cholinergic antagonist atropine on the acquisition of different learning tasks known to be sensitive or insensitive to impairment by hippocampal lesions; on the retention of performance acquired in the absence of the drug; and on memory consolidation immediately after daily training trials. In Experiment 1, atropine sulfate (10 or 50 mg/kg, ip), injected 30 min prior to training, severely impaired learning of both spatial and nonspatial discrimination tasks when compared with saline or atropine methylnitrate (50 mg/kg). In Experiment 2, atropine sulfate (50 mg/kg) also impaired spatial discrimination accuracy in rats previously trained to asymptote under drug-free conditions. These deficits were not due to either peripheral drug effects or gross sensorimotor impairments. In Experiment 3, daily posttraining injections of atropine sulfate (50 mg/kg) failed to influence either learning or subsequent retention of place navigation in rats that were trained to find a single hidden escape platform. The data confirm that profound learning deficits occur when training is conducted under atropine but offer no support to the hypothesis that cholinergic neurons play an important role in memory consolidation or other posttraining processes. Furthermore, these results point to dissimilarities between the behavioral impairments induced by cholinergic blockade and hippocampal lesions under appropriate test regimes.

Animals↗
PubMed1986

The metabolism of atropine in man.

A metabolic pattern of atropine in man, based on the detection of radiolabelled products in urine by high performance liquid chromatography after administration of [3H]atropine sulphate to a normal volunteer is proposed. Noratropine (24%), atropine-N-oxide (equatorial isomer) (15%), tropine (2%) and tropic acid (3%) appear to be the major metabolites, while 50% of the administered dose is excreted as apparently unchanged atropine. No conjugates were detectable. Evidence that atropine is present as (+)-hyoscyamine was found, suggesting that stereoselective metabolism of atropine probably occurs.

Atropine↗
PubMed1984

[Hemodynamic effects in antagonism of neuromuscular blockage: atropine-pyridostigmine versus ipratropium bromide-pyridostigmine].

Antagonism of neuromuscular block using cholinesterase inhibitors and atropine is charged with several risks, which are at least partly caused by pharmacological characteristics of the anticholinergic drugs, e.g. short duration of action causing secondary bradycardia. Compared to atropine, ipratropium bromide, a new anticholinergic drug, is--due to its quarternary ammonium compound--characterized by longer duration of action. In contrast to atropine, this substance does not penetrate the blood-brain and placental barrier. Our present study was designed to compare the haemodynamic effects of both substances, using invasive monitoring, during antagonism of neuromuscular block with pyridostigmine. In contrast to atropine, ipratropium bromide induced a higher degree of initial tachycardia but did not allow secondary reduction of heart rate by rebound vagal stimulation. While cardiac output was almost constant, ipratropium bromide caused changes in stroke volume, which were due to alterations in heart rate. There were no clinically relevant changes of the other haemodynamic parameters. Cardiac arrhythmia were observed more often after administration of atropine and were of longer duration. In conclusion, ipratropium bromide is a useful alternative to atropine in patients with pre existing low heart rate and bradyarrhythmia.

Atropine↗
PubMed1989

Effects of inhaled metaproterenol and atropine on the pulmonary mechanics of infants with bronchopulmonary dysplasia.

We evaluated the individual and combined effects of an inhaled beta-adrenergic agent (metaproterenol) and an inhaled anticholinergic agent (atropine) on the pulmonary function of infants with bronchopulmonary dysplasia. In this randomized, double-blind study we studied 15 infants at a mean postnatal age of 15.8 weeks (range 4-28 weeks). On 4 successive days, pulmonary function tests were measured before and after a single treatment with one of the following four aerosols: placebo, metaproterenol, atropine, and combined metaproterenol and atropine. Following treatment with metaproterenol, atropine, and combined metaproterenol and atropine, airway resistance and maximal expiratory flow at functional residual capacity improved significantly when compared with baseline. Pulmonary function values returned toward baseline by 3 hours after the treatments. We found no significant differences between the effects of metaproterenol and atropine and were unable to show any synergy of the two agents.

Administration, Inhalation↗
PubMed1988

Complex dose-response curves of atropine in man explained by different functions of M1- and M2-cholinoceptors.

In the present study we set out to explain the complex atropine dose-response curves in man in relation to M-cholinoceptor subtype occupancy. In healthy volunteers the effects of atropine on heart rate and salivary flow were quantified. M-cholinoceptor subtype occupancy by antagonist present in plasma samples was detected in an in vitro radioreceptor assay. Atropine effects were studied without and after propranolol (240 mg oral dose) and without and after pirenzepine (1.1 mg i.v.) to differentiate beta-adrenoceptor and M-cholinoceptor subtype mediated effects. 1. In receptor binding studies, M-cholinoceptors in bovine cerebral cortex membranes were labelled with 3H-pirenzepine (pKd = 8.05), M-cholinoceptors in rat salivary gland membranes with 3H-N-methylscopolamine (pKd = 9.02). Atropine competed for binding of these ligands with a small (2.1-fold) preferential selectivity via the cerebral in comparison to the glandular receptors (pKi = 9.18 versus 8.86). Pirenzepine showed a marked selectivity (40-fold) in this respect with pKi-values of 8.05 (M1: cerebral cortex) and 6.45 (M2: salivary glands). 2. At heart rate and at salivary flow, bivalent dose-response curves of atropine were observed with opposite effect vectors. The typical antagonist effects at M-cholinoceptors (i.e. an increase of heart rate and an inhibition of salivary flow) were observed at doses greater than 1 microgram/kg, whereas "paradoxical" cholinomimetic effects of atropine became apparent at lower doses. From a superposition of two isotherms with opposite effect vectors ED50-values were calculated, which were in the range of half-maximal M-cholinoceptor occupancy in the in vitro radioreceptor assay of plasma samples.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Comparison of Bay K 8644, nitrendipine and atropine on spontaneous and pelvic-nerve-induced bladder contractions on rat bladder in vivo.

The effects of the dihydropyridine-type calcium antagonist (nitrendipine) and agonist (Bay K 8644) in comparison to atropine have been studied after intravenous administration on spontaneous and pelvic-nerve-induced contraction of rat urinary bladder. Bay K 8644 increased the basal internal bladder pressure as well as the amplitude of the spontaneous bladder contractions in a dose-dependent manner. In addition, an increase in systemic arterial blood pressure was noted for a period of about 20 min. In the presence of atropine the effects of Bay K 8644 on the urinary bladder were almost completely antagonized. Both nitrendipine and atropine reduced in a dose-dependent manner the amplitude of spontaneous and nerve-induced bladder contraction. The spontaneous and nerve-induced bladder contractions were significantly reduced by atropine or nitrendipine. Only nitrendipine caused a reduction of the spontaneous bladder contraction frequency. The systemic blood pressure was decreased significantly by nitrendipine but not after atropine administration. We suggest that both calcium antagonist and agonist can change the tension of the urinary bladder in vivo. As a side-effect the systemic blood pressure is altered. Atropine can antagonize the effect of BayK 8644 on the urinary bladder and reduces spontaneous and nerve-induced bladder contractions more specifically than nitrendipine.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1990

A preliminary study on the effects of atropine sulphate on bradycardia and heart blocks during romifidine sedation in the horse.

Romifidine (STH 2130-Cl or Sedivet) is an alpha 2-agonistic imino-imidazol sedative for intravenous use in horses recently developed by Boehringer Ingelheim, Vetmedica GmbH. An exploratory study was done in nine warm-blood horses, randomly divided into three groups, which received different dosages of romifidine (0.04, 0.08 and 0.12 mg/kg of body weight (BWT) intravenously (i.v.)) with at least one week's interval between tests. Romifidine induced a marked bradycardia accompanied by second degree atrioventricular (AV) block and some sinus blocks at all tested dosages. A placebo (NaCl 0.9% i.v.) given 5 min before and after romifidine did not affect the cardiac disturbances induced by romifidine. A low dose of atropine sulphate (0.005 mg/kg of BWT i.v.) given 5 min before romifidine counteracted the bradycardia and caused a normal to increased heart rhythm at all romifidine dosages. A higher dose of atropine sulphate (0.01 mg/kg of BWT i.v.) administered 5 min before sedation induced a tachycardia (average 70 beats/min) at all romifidine dosages and completely prevented the bradycardia and the heart blocks. The positive chronotrope effects of atropine sulphate were attenuated by increasing doses of romifidine. The effects of atropine sulphate (low or high doses) given 5 min after romifidine only appeared after 5 min. Both dosages counteracted the bradycardia and suppressed the heart blocks. No atropine-dependent side effects were observed in non-fasted horses. The degree of the romifidine induced sedation was not affected by the use of atropine sulphate given before or after romifidine.

Adrenergic alpha-Agonists↗