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PubMed1994

Effect of atropine, HLö 7 and HI 6 on respiratory and circulatory function in guinea-pigs poisoned by O-ethyl S-[2-(diisopropylamino) ethyl] methylphosponothioate (VX).

In a guinea-pig model with on-line respiratory and circulatory monitoring the therapeutic efficacy of atropine, HLö 7 and HI 6 in VX poisoning was compared. In female urethane-anaesthetized Pirbright-white guinea-pigs the a. carotis, v. jugularis and trachea were cannulated. After base line measurements the animals received VX (22.5, 45 or 90 micrograms/kg = 5, 10 or 20 x LD50) intravenously and 2 min. later the antidotes: HLö 7 or HI 6 (30 mumol/kg, each) or atropine 10 mg/kg or a combination of atropine and one of the oximes (all intravenously). Respiratory and circulatory parameters were recorded for 60 min. or until death of the animal. Erythrocyte, brain and diaphragm acetylcholinesterase (AChE) activity was determined after the experiment. VX poisoning caused a rapid respiratory arrest within 4-5 min. Atropine treatment was effective in improving the respiratory function after VX, 22.5 micrograms/kg, but had only a small effect after the higher VX doses. The treatment of VX (10 or 20 x LD50) poisoned animals with oxime plus atropine improved respiration to various extents, restored circulation and prolonged the survival time, HLö 7 being more effective than HI 6 after VX 90 micrograms/kg. Oximes alone were completely ineffective. Erythrocyte and diaphragm AChE was reactivated by HLö 7 and, less effectively, by HI 6, while brain AChE remained almost completely inhibited in all groups. The results of this investigation demonstrate a reasonable efficacy of atropine after lower VX doses and of HLö 7 and HI 6 (plus atropine) after high-dose VX poisoning, HLö 7 being slightly more effective than HI 6.

Acetylcholinesterase↗
PubMed1980

Atropine does not abolish cephalic vagal stimulation of gastrin release in dogs.

1. The effect of atropine was studied on serum gastrin responses to feeding in conscious gastric fistula dogs. Intragastric pH was monitored and could be maintained at pH 6.0 by infusion of sodium bicarbonate into the gastric fistula.2. A standard liquid meal was consumed by the dogs in less than a minute. Serum gastrin increased from a basal concentration of 8 pmol/l to a peak of 27 pmol/1 at 4-7 min, and intragastric pH fell to less than 3.0 after 20 min. Since vagotomy abolished the early gastrin response to feeding, and instillation of the meal directly into the fistula produced only a modest and delayed increase in serum gastrin, we conclude that cephalic vagal stimulation played a major part in mediating the gastrin responses. When intragastric pH was maintained at 6.0 serum gastrin was significantly higher at all times from 4 to 50 min after feeding, indicating the importance of acid inhibition in the control of gastrin secretion.3. After atropine (25 or 100 mug/kg), acid secretion was abolished and intragastric pH was about 6.0 at all times. The low dose of atropine enhanced the gastrin response to feeding, but the time course and magnitude of the response closely resembled that to normal meals pH-stated to 6.0. The high dose of atropine decreased, but did not abolish serum gastrin responses to feeding.4. When the meal was allowed to drain freely from the gastric fistula (virtually eliminating stimulation of gastrin release by luminal mechanisms) serum gastrin again reached a peak after 4-7 min, and neither dose of atropine significantly changed the response.5. It is concluded that cephalic vagal stimulation of gastrin release is atropine resistant and so unlikely to be mediated by muscarinic receptors. The enhanced gastrin response to feeding caused by moderate doses of atropine can be attributed to the loss of acid inhibition of gastrin release. The neuropeptide bombesin is a candidate neurotransmitter for the action of post-ganglionic vagal nerves on gastrin cells.

Animals↗
PubMed1969

Timing of atropine and neostigmine in the reversal of muscle relaxants.

The antimuscarinic effects of atropine were studied in 46 patients to whom neostigmine had been given after operation to reverse the action of a muscle relaxant. Neostigmine was given to alternate patients three minutes after, or together with, atropine, and the effects of the two procedures were compared by measuring the secretions which collected in the buccal and oropharyngeal cavities and observing the heart rate.It was found that the glands of the oral cavity were stimulated to a greater extent when neostigmine was given with atropine than after atropine. Any dose of atropine sufficient to inhibit peristaltic movements of the bowel is more than enough to block completely secretion by the salivary glands, and the appearance of some secretion in all cases after the administration of neostigmine suggests that the bowel was at liberty to react to the neostigmine in every case, but perhaps particularly so when atropine and neostigmine were given mixed. The integrity of an anastomosis of the bowel could be endangered by vigorous peristalsis in the early postoperative period.Electrocardiograms in about half the patients from each group confirmed earlier work that the muscarinic effects of neostigmine on the heart can be prevented by giving the atropine either before or together with the neostigmine.

Adult↗
PubMed2006

Is atropine needed with ketamine sedation? A prospective, randomised, double blind study.

OBJECTIVE: To compare atropine with placebo as an adjunct to ketamine sedation in children undergoing minor painful procedures. Outcome measures included hypersalivation, side effect profile, parental/patient satisfaction, and procedural success rate. METHODS: Children aged between 1 and 16 years of age requiring ketamine procedural sedation in a tertiary emergency department were randomised to receive 0.01 mg/kg of atropine or placebo. All received 4 mg/kg of intramuscular ketamine. Tolerance and sedation scores were recorded throughout the procedure. Side effects were recorded from the start of sedation until discharge. Parental and patient satisfaction scores were obtained at discharge and three to five days after the procedure, with the opportunity to report side effects encountered at home. RESULTS: A total of 83 patients aged 13 months to 14.5 years (median age 3.4 years) were enrolled over a 16 month period. Hypersalivation occurred in 11.4% of patients given atropine compared with 30.8% given placebo (odds ratio (OR) 0.29, 95% confidence interval (CI) 0.09 to 0.91). A transient rash was observed in 22.7% of the atropine group compared with 5.1% of the placebo group (OR 5.44, 95% CI 1.11 to 26.6). Vomiting during recovery occurred in 9.1% of atropine patients compared with 25.6% of placebo patients (OR 0.29, 95% CI 0.09 to 1.02). There was a trend towards better tolerance in the placebo group. No patient experienced serious side effects. CONCLUSION: Ketamine sedation was successful and well tolerated in all cases. The use of atropine as an adjunct for intramuscular ketamine sedation in children significantly reduces hypersalivation and may lower the incidence of post-procedural vomiting. Atropine is associated with a higher incidence of a transient rash. No serious adverse events were noted.

Adjuvants, Anesthesia↗
PubMed1981

Effect of atropine on esophageal motor function in humans.

In this study, we used a high-fidelity manometric recording system to quantitate the effects of atropine on lower esophageal sphincter (LES) pressure and primary peristalsis (1 degree P). A sleeve sensor recorded LES pressure, and seven recording orifices spaced at 3-cm intervals registered motor activity in the esophageal body. Five randomized manometric studies were done in each of five normal subjects. LES pressure and 1 degree P with wet swallows were recorded for 30 min before and 70 min after intravenous injection of saline or atropine, 3, 6, 12, and 24 micrograms/kg. We also studied the effect of atropine on LES pressure in five additional subjects, four dogs, four opossums, and six monkeys. In humans, saline and 3 micrograms/kg atropine caused no significant change in pulse rate, LES pressure, or the incidence of complete peristaltic sequences. The 6, 12, and 24 micrograms/kg atropine doses caused significant inhibition of LES pressure and the incidence of intact 1 degree P. Only the 12 and 24 micrograms/kg doses increased pulse rate. When 1 degree P occurred in the smooth muscle portion of the esophagus its appearance in the proximal portion of the smooth muscle segment was delayed for several seconds. The amplitude of 1 degree P was decreased 30-60% in the smooth muscle segment, but 1 degree P was not affected in the proximal striated muscle esophageal segment. Atropine reduced canine LES pressure substantially but caused no change in opossums or monkeys. We conclude that 1) basal LES tone in humans and dogs, unlike that of the opossum and monkey, is partially generated by cholinergic neural input, 2) cholinergic nerves elicit 1 degree P in human esophageal smooth muscle, and 3) species variation exists in esophageal responses to atropine.

Animals↗
PubMed1986

Dose-response effects of atropine on pancreatic secretory response to intestinal tryptophan in dogs.

In dogs with gastric and pancreatic fistulas, we studied the effect of intravenous infusion of atropine in doses of 0.9, 1.8, 7, and 29 nmol X kg-1 X h-1 on the pancreatic secretory response to graded loads of intraduodenal infusions of tryptophan, given with a secretin background. Infusions of 1.8, 7, and 29, but not 0.9 nmol X kg-1 X h-1 of atropine sulfate significantly (P less than 0.05) decreased the incremental protein response to all loads of tryptophan. The cumulative incremental protein output was reduced by 44, 37, and 52%, respectively. Infusions of 1.8, 7, and 29 nmol X kg-1 X h-1 of atropine significantly decreased by approximately 50% the incremental bicarbonate response to low (0.12 and 0.37 mmol/h) but not high loads (1.1, 3.3, and 10 mmol/h) of tryptophan. The inhibitory potency of the effective doses of atropine did not differ significantly. Only the highest dose of atropine significantly increased heart rate by 76%. These findings indicate that 1) in the intact animal, the minimal dose of atropine required for inhibition of pancreatic bicarbonate and protein response to intraduodenal tryptophan seems to be 1.8 nmol X kg-1 X h-1, a dose that causes probably few systemic effects, since it does not increase heart rate; and 2) the inhibitory action of atropine on the pancreatic response to tryptophan appears to be an "all-or-none" effect.

Animals↗
PubMed1991

Effects of atropine on pancreatic response to bethanechol, cholecystokinin, and food intake in rats.

Atropine was used to examine the role of cholinergic mechanisms in the pancreatic secretory response to food intake. Unanesthetized rats with gastric, jugular vein, bile-pancreatic, and duodenal cannulas were used; bile-pancreatic juice was recirculated. The maximal response to bethanechol (4 mg.kg-1.h-1) was similar to cholecystokinin (CCK)-8-induced maximal secretion. Atropine (25-200 micrograms.kg-1.h-1) markedly inhibited basal amylase output and caused dose-related inhibition of the incremental response to a maximal dose of bethanechol. Atropine (50 micrograms.kg-1.h-1) shifted the dose-response curve to bethanechol (1-32 mg.kg-1.h-1) to the right but did not alter maximal amylase output. L 364718 (0.5 mg/kg), a CCK receptor antagonist, had no effect on bethanechol-stimulated pancreatic secretion. Atropine (50 micrograms.kg-1.h-1) did not affect the incremental responses to low doses of CCK-8; the maximal response occurred at a higher CCK-8 dose because atropine decreased basal secretion. Atropine (50 or 200 micrograms.kg-1.h-1) did not decrease the amylase response to ingestion of a liquid meal. We conclude that 1) bethanechol is a full agonist for stimulation of pancreatic enzyme secretion and its effects are not mediated by CCK release; 2) atropine is a competitive antagonist of bethanechol-induced pancreatic secretion in vivo but does not directly affect responses to CCK-8; 3) cholinergic mechanisms do not mediate the pancreatic enzyme response to a liquid meal in rats.

Animals↗
PubMed1982

Atropine does not attenuate cerebral vasodilatation during hypercapnia.

To study the contribution of cholinergic nerves to cerebral vasodilation during hypercapnia, we blocked muscarinic cholinergic receptors with atropine. We used two new approaches. First, total and regional cerebral blood flow (CBF) were measured with microspheres. Second, efficacy and specificity of muscarinic blockade by atropine were examined using the cranial window method. In anesthetized cats we measured CBF with 15-micrometers microspheres six times during each experiment: during normocapnia (PCO2 = 32-34 Torr), moderate hypercapnia (PCO2 = 48-50 Torr), and severe hypercapnia (PCO2 = 61-64 Torr), before and after intravenous administration of vehicle or atropine (0.5 mg/kg). Hypercapnia produced graded increases in blood flow in all areas of the brain. Atropine did not attenuate increases in CBF during hypercapnia. We examined efficacy and specificity of muscarinic blockade by atropine using the cranial window method. Acetylcholine (10(-7) and 10(-6) M) and adenosine (10(-7) and 10(-5) M), dissolved in artificial cerebrospinal fluid, dilated pial arteries in a dose-dependent fashion. Intravenous administration of atropine attenuated vasodilation produced by acetylcholine but did not affect the response to adenosine. Thus atropine, at a dose that effectively blocked muscarinic receptors, did not attenuate the increase in CBF during hypercapnia. The study suggests that cholinergic nerves are not involved in steady-state cerebral vasodilatation during hypercapnia.

Acetylcholine↗
PubMed1988

Effect of exercise in sheep on the absorption of intramuscular atropine sulfate.

In normal female sheep, we investigated effects of exercise on the absorption of atropine sulfate (0.02 mg/kg) given intramuscularly. The exercise regime consisted of treadmill running (20 min at 3-4 mph at 0 degrees grade) starting immediately after intramuscular atropine injection into the biceps femoris. Six normal female sheep received intramuscular atropine and 7-14 days later an identical intramuscular dose of atropine with exercise. Serum levels of atropine measured by radioimmunoassay were monitored over a 6-hour period. The time to peak concentration was significantly less with exercise than without, 2.9 +/- 2.1 and 13.7 +/- 5.4 min, respectively (p less than 0.005). In addition, peak serum atropine concentrations tended to be higher, 9.7 +/- 1.3 ng/ml with exercise versus 7.1 +/- 2.9 ng/ml without exercise; however, the difference did not attain statistical significance (p less than 0.08). This study demonstrates that exercise increases the early absorption of intramuscularly administered atropine sulfate.

Absorption↗
PubMed1979

Presynaptic muscarinic and alpha-adrenergic receptor blocking effect of atropine on the noradrenergic neurones of the rabbit pulmonary artery.

The effect of atropine on the electrical-field stimulation-evoked overflow of tritium from isolated rabbit pulmonary arteries preincubated with 3H-noradrenaline was studied. Atropine (10(-4) M) and phentolamine (10(-6) M) increased stimulation-induced overfoow of tritium. Clonidine (10(-6) to 10(-5) M) and acetylcholine (10(-6) M) diminished the stimulation-evoked overflow of tritium. After the overflow had been raised by either atropine (10(-4) M) or phentolamine (10(-6) M), clonidine (10(-6) M) decreased the overflow below control values. Clonidine (10(-5) M) prevented the enhancement of tritium overflow evoked by atropine (10(-4) M). A lower concentration of clonidine (10(-6) M) only caused a partial prevention. Enhancement of the overflow by phentolamine (10(-6) and 3 X 10(-5) M) was not altered by atropine (10(-4) M). Atropine (10(-7) M), in a concentration which was without any effect on the stimulation-induced tritium overflow, prevented the reduction evoked by acetylcholine (10(-6) M). It is concluded that atropine in a low concentration blocks presynaptic inhibitory muscarinic receptors; at higher concentrations it blocks in addition presynaptic alpha-adrenoceptors.

Acetylcholine↗
PubMed1975

Atropine dose in acute myocardial infarction in man.

Heart rate response to intravenous atropine therapy in acute myocardial infarction (MI) was assessed from detailed studies performed on 18 of 492 consecutively admitted coronary care unit patients. Atropine was given for extreme bradycardia (less than 40/min) or bradycardia (less than 60/min) coincident with hypotension or ventricular premature beats. 14 patients had posterior and 4 anterior infarction. Degree of cardioacceleration evoked by atropine depended upon drug dose and route of administration. Atropine, 0.0053-0.0088 mg/kg, given within 15 sec increased heart rate by 20-72/min but never beyond a peak rate of 120. Larger atropine doses, 0.120-0.148 mg/kg, increased heart rate by 51-92/min and, in four to five instances to a peak rate exceeding 120/min. Intramuscular atropine was associated with paradoxical slowing of heart rate in one case. Multiple neural, hormonal, and circulatory factors can modify heart rate response to fixed amounts of intravenous atropine but 0.008 mg/kg represents a safe and suitable initial drug dose for use in acute MI.

Acute Disease↗
PubMed1981

Inhaled atropine sulfate in acute asthma.

We administered inhaled atropine sulfate to acute asthmatics already receiving therapeutic doses of adrenergic agonists, theophylline, and corticosteroids. Following atropine, hyperinflation diminished whereas vital capacity and expiratory flow rates breathing air and helium-oxygen increased (p less than 0.025 - p less than 0.005). Initial density dependence correlated inversely with changes in density dependence after atropine (r = -0.69, p less than 0.001). We conclude that: (1) inhaled atropine sulfate was effective therapy for acutely ill asthmatics already being treated with multiple antiasthmatic agents; (2) atropine caused large and peripheral airways bronchodilatation, and (3) the predominant site of bronchodilatation after atropine was related to the site of flow limitation before atropine.

Acute Disease↗
PubMed1982

Atropine methonitrate and salbutamol in chronic airways obstruction: peak effect and duration of action.

The effects of atropine methonitrate and salbutamol delivered by wet nebulisation, separately and in combination, were studied in 22 patients with chronic airways obstruction. Atropine methonitrate 1.5 mg, 3.0 mg and 6.0 mg, salbutamol 2.5 mg, 5.0 mg and 10.0 mg and the intermediate dose of each agent in combination were used. Peak expiratory flow rat (PEFR), forced expiratory volume in 1 S (FEV1.0) and forced vital capacity (FVC) were measured. Improvement in the measured variables were greater after salbutamol, alone or with atropine, up to 3 h after inhalation, after salbutamol with atropine 4 and 6 h after inhalation, and after atropine, alone or with salbutamol, 12 h after inhalation. For all patients together there were no significant differences in the mean maximum PEFR, FEV1.0 or FVC that were achieved following atropine, salbutamol or both together. Salbutamol, 5.0 or 10.0 mg, and atropine methonitrate, 1.5 or 3.0 mg, were maximally effective in most patients and at these doses serious side effects were unusual.

Adult↗
PubMed1984

Effect of atropine on the plasma cholecystokinin response to intraduodenal fat in man.

The present study was undertaken to determine whether atropine inhibits the plasma cholecystokinin (CCK) response to intraduodenal fat. Plasma CCK concentrations were measured by radioimmunoassay using two sequence-specific antibodies. Antibody 1703 bound to all COOH-terminal CCK peptides containing at least 14 amino acid residues, while antibody T204 was specific for the sulphated tyrosine region of CCK. Intraduodenal instillation of 60 ml corn oil in 6 normal subjects induced significant increases in plasma CCK. Intravenous administration of atropine (0.015 mg/kg as bolus followed by 0.005 mg/kg X h over 3 h) resulted in significant inhibition of plasma CCK concentrations at 10, 20 and 30 min (antibody 1703) and at 20 and 30 min (antibody T204 ) after instillation of fat. However, the peak increments in plasma CCK during atropine (8.6 +/- 1.9 pmol/l, antibody 1703; 5.4 +/- 1.1 pmol/l, antibody T204 ) were not different from those found without atropine (6.3 +/- 0.8 pmol/l, antibody 1703; 3.9 +/- 0.9 pmol/l, antibody T204 ). Similarly, the integrated plasma CCK secretion after intraduodenal fat was not significantly different when measured during atropine (461 +/- 119 pmol/l X 3 h, antibody 1703; 269 +/- 97 pmol/l X 3 h, antibody T204 ) and without atropine (428 +/- 62 pmol/l X 3 h, antibody 1703; 188 +/- 66 pmol/l X 3 h). It is concluded that administration of atropine delays but does not inhibit the CCK response to intraduodenal corn oil in man.

Adult↗
PubMed1998

Central vagotonic effects of atropine modulate spectral oscillations of sympathetic nerve activity.

BACKGROUND: Low-dose atropine causes bradycardia either by acting on the sinoatrial node or by its effects on central muscarinic receptors increasing vagal activity. Any central muscarinic effects of high-dose atropine on RR interval are masked by peripheral muscarinic blockade at the sinoatrial node, which causes tachycardia. Effects of central parasympathetic activation on sympathetic activity are not known. METHODS AND RESULTS: Using power spectral analysis of RR interval, intra-arterial blood pressure, respiration, and muscle sympathetic nerve activity (MSNA), we examined the effects of both low (2 microgram/kg IV) and high (15 microgram/kg IV) doses of atropine. After low-dose atropine, RR increased by 9+/-1% (P<0.0001), the low-frequency (LF) component (in normalized units, NU) of RR variability decreased by -32+/-8%, and the high-frequency (HF)NU component increased (+74+/-19%); hence, LF/HF of RR variability fell by 52+/-10% (all P<0.01). Although overall MSNA did not change, LFNU of MSNA decreased (-15+/-5%), HFNU of MSNA increased (+31+/-3%), and LF/HF of MSNA fell (-41+/-8%) (all P<0.01). After high-dose atropine, LFNU of MSNA decreased (-17+/-12%), HFNU of MSNA increased (+22+/-3%), and LF/HF of MSNA fell (-51+/-21%) (all P<0.02). CONCLUSIONS: Increasing central parasympathetic activity with low-dose atropine is associated with an increase in the HF and a decrease in the LF oscillations of both RR interval and MSNA variability. High-dose atropine similarly induces an increase in the HF and a decrease in the LF components of MSNA variability. Thus, central parasympathetic activation is able to modulate the oscillatory characteristics of sympathetic nerve traffic to peripheral blood vessels.

Adult↗
PubMed1988

Constricting and stiffening action of atropine on aortic response to angiotensin in dogs.

The elasticity of the thoracic aorta was studied in nine dogs instrumented with a pressure microtransducer and two ultrasonic crystals diametrically fixed in the adventitia. Systolic and diastolic changes in pressure and diameter were used to calculate Peterson and incremental elastic moduli. Acute hypertension was induced by infusions of angiotensin performed 1) during the control period, 2) after propranolol (1.5 mg/kg), 3) after atropine (0.2 mg/kg), and 4) after propranolol plus atropine. Absolute and percent variations of mean diameter were correlated to pressure in the control period and after autonomic blockade (p less than 0.01). The slopes of these correlations were not different between propranolol and control groups, but were lower with atropine (p less than 0.01) and with atropine plus propranolol (p less than 0.001) than in the control period. Correlations were also found between Peterson and incremental elastic moduli and mean pressure in the control period and after blockade (p less than 0.001). No differences of slopes existed between propranolol and control groups, but the slope of the correlation relative to the incremental elastic modulus was higher with atropine than in the control period (p less than 0.05), and the slopes of the correlations relative to the Peterson and the incremental elastic moduli were respectively higher with atropine plus propranolol than in the control period (p less than 0.05, p less than 0.05). Thus, atropine decreased the distention and increased the stiffness of the aorta in response to acute angiotensin-mediated hypertension.

Angiotensin II↗
PubMed1992

Enhanced muscarinic receptor blockade with atropine in the asthmatic tracheobronchial tree. Evidence for increased drug delivery.

We measured the competitive antagonistic effect of atropine in bronchi of 8 normal and 15 asthmatic subjects. Classic pharmacologic theory states that the degree of competitive antagonism depends only upon (1) antagonist concentration at the receptor and (2) receptor affinity. Delivery and affinity also influence agonist responsiveness, but measurement of bronchial antagonism allows study of these factors in isolation. Bronchial responsiveness to methacholine was measured as the cumulative dose required to produce a 35% fall in specific airway conductance (PD35). On different days three measurements of control PD35 were made on each subject. On 2 days PD35 was measured after inhalation of 0.14 mg atropine and, on another day, after intravenous injection of 0.32 mg atropine. The antagonist effect of atropine was measured as dose ratio - 1 (DR - 1), where DR = PD35 after atropine/control PD35. Geometric mean DR - 1 with inhaled atropine in asthmatic subjects (11.7) was 6.3 times that of normal subjects (1.9) (p less than 0.001), and DR - 1 with intravenous atropine in asthmatic subjects (8.0) was 5.6 times that of normal subjects (1.4) (p less than 0.001). In conclusion, there is enhanced muscarinic blockade from inhaled and intravenously administered atropine in asthmatic bronchi. We suggest that this is due to increased access of the drug to bronchial muscarinic receptors.

Adult↗
PubMed1983

Antihistaminic versus anticholinergic effects of atropine on canine trachealis muscle.

To determine antihistaminic versus anticholinergic effects of atropine in airway smooth muscle, we used an in vitro preparation of canine trachealis muscle strips and determined atropine's effect on contractile responses induced by histamine or by electrical field stimulation of cholinergic nerves. In the first series of experiments, 53 strips had initial responses to field stimulation determined and were then randomly assigned to a control group or to a group treated with atropine before field stimulation was repeated and histamine was given. Atropine in concentrations of 10(-8), 10(-7), and 10(-6) M decreased the response to field stimulation to 61.4, 10.5, and 0% of the initial response, respectively, but had no effect on the responses to histamine. In the second series of experiments, 24 strips were treated with indomethacin to prevent histamine tachyphylaxis; these strips had initial responses to both field stimulation and histamine determined and were then assigned to a control group or to a group treated with atropine before field stimulation and histamine were repeated. In these experiments, a concentration of atropine (10(-6) M), which again completely blocked the response to field stimulation, still had no effect on histamine-induced contraction. We conclude that atropine in a concentration that completely blocks the response to cholinergic nerve stimulation has no antihistaminic effect.

Animals↗