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At least 19 recordsLinked to original sources
PubMed1979

A comparison of changes in atropine-induced tachycardia and atropine concentration in conscious dogs.

In the conscious dog, after intravenous injection of 0.2 mg/kg 3H-labelled atropine the progressive decrease of the heart rate was well correlated with the disappearance of atropine from the blood. But, with atropine infusion (0.2 mg/kg/h) the tachycardia decreased progressively in spite of an increase in the blood concentration of atropine. Differences appeared between the normal animals or those pretreated with propranolol or reserpine, and the animals which had undergone bilateral thoracic sympathectomy. In the stellectomized animals atropine induced a smaller but much more lasting cardiac acceleration than under the other experimental conditions. It seems that only peripheral factors are involved in the complex interactions between the adrenergic and cholinergic nervous systems at the sinus node level.

Animals↗
PubMed1979

Inhibition of constrictor responses of dog coronary artery by atropine. A possible effectiveness of atropine on variant form of angina pectoris.

A possible effectiveness of atropine on variant form of angina pectoris was investigated using the left circumflex coronary arterial strips of dogs. Acetylcholine 10(-5)--10(-3) Gm/ml dose-dependently constricted the isolated arterial strips during potassium-contracture in 6 cases, and repetitive applications of acetylcholine could produce the similar contractions to the control. In 18 strips atropine 10(-6) Gm/ml significantly depressed the contractions of coronary arteries induced by acetylcholine 10(-5)--10(-3) Gm/ml. In 5 arterial strips atropine 10(-6) Gm/ml significantly inhibited norepinephrine-induced responses of these arteries, and by 10(-5) Gm/ml further suppression of the responses was obtained. The results suggest that atropine may suppress the contractile responses of the coronary artery induce by acetylcholine and nonrepinephrine through a muscarinic-receptor blocking action and simultaneously partly through an adrenergic alpha-receptor blocking action.

Acetylcholine↗
PubMed1977

Comparison of aerosolized atropine, isoproterenol, atropine plus isoproterenol, disodium cromoglycate and placebo in the prevention of exercise-induced asthma.

In 15 asthmatic children post-exercise bronchospasm was partially inhibited by placebo and by aerosolized atropine sulphate (1 mg) compared with no treatment, not significantly inhibited by atropine alone compared with placebo, partially blocked by disodium cromoglycate (20 mg) and by isoproterenol (0.625 mg) and completely blocked by the combination of isoproterenol and atropine. Pre-treatment with isoproterenol or atropine resulted in post-exercise values for specific conductance which were significantly greater than those following disodium cromoglycate by virtue of the bronchodilator effect of these drugs independent of or in addition to any specific inhibition of exercise-induced asthma. These results suggest that the bronchoconstrictor response to exercise is partially influenced by suggestion but is influenced to a significantly greater degree by mediator release and beta-adrenergic mechanisms and that bronchodilator drugs have therapeutic advantages over an inhibitor of mediator release in the prevention of exercise-induced asthma.

Adolescent↗
PubMed1977

Effect of atropine on vascular adrenergic neuroeffector transmission.

Atropine, homatropine, scopolamine, procaine, lidocaine and phentolamine inhibited the contractile response of rabbit isolated pulmonary artery elicited by electrical-field stimulation. Methylatropine had no effect. The inhibition induced by atropine (2 x 10(-6)-2 x 10(-4) M) had a rapid onset of action and then remained almost constant. The inhibition was slowly reversible. The potency of atropine as an inhibitor of responses to field stimulation was very much less than the potency of phentolamine. The inhibition was not antagonized by cocaine or (+)-amphetamine. Atropine (3 x 10(-5) and 3 x 10(-4) M) enhanced the electrical-field-stimulation-induced outflow of tritium from the pulmonary artery preloaded with 3H-(-)-noradrenaline. In contrast, atropine in a concentration-dependent manner either had no effect or slightly decreased the tyramine-induced outflow of tritium. Atropine reduced the contractile response of the pulmonary artery evoked by tyramine. Atropine (10(-4) and 3 x 10(-4) M) and phentolamine inhibited the arterial contractions elicited by exogenous (-)-noradrenaline in an apparently competitive manner. The contractions of rabbit isolated aorta elicited by (-)-noradrenaline, serotonin and histamine were inhibited by atropine (10(-5) and 10(-4) M). Atropine was very much less potent in antagonizing noradrenaline, histamine and serotonin than in antagonizing acetylcholine. tthe inhibotory potency of atropine, procaine and lidocaine on the accumulation of 3H-(-)-noradrenaline by rabbit aorta in vitro was much less than that of cocaine. The relationship between the aortic concentration of 3H-atropine and in vitro accumulation was almost linear. The accumulation was slightly higher at 37 degrees C than at 1 degree C. The results suggest that atropine blocks alpha-adrenoceptors, both presynaptically at the adrenergic neurone terminals and postsynaptically at the smooth muscle. In addition, atropine may possibly act in a nonspecific manner at postsynaptic sites.

Amphetamine↗
PubMed1979

Effect of atropine on vagal release of gastrin and pancreatic polypeptide.

We studied the effect of several doses of atropine on the serum gastrin and pancreatic polypeptide responses to vagal stimulation in healthy human subjects. Vagal stimulation was induced by sham feeding. To eliminate the effect of gastric acidity on gastrin release, gastric pH was held constant (pH 5) and acid secretion was measured by intragastric titration. Although a small dose of atropine (2.3 mug/kg) significantly inhibited the acid secretory response and completely abolished the pancreatic polypeptide response to sham feeding, this dose of atropine significantly enhanced the gastrin response. Higher atropine doses (7.0 and 21.0 mug/kg) had effects on gastrin and pancreatic polypeptide release which were similar to the 2.3-mug/kg dose. Atropine (0.78 and 2.3 mug/kg) without sham feeding significantly inhibited basal acid secretion and also led to significant increases in serum gastrin above basal levels. The gastrin response to sham feeding with 2.3 mug/kg atropine was significantly greater than the sum of the gastrin responses to sham feeding alone and to 2.3 mug/kg atropine alone, indicating potentiation of vagal gastrin release by atropine. We conclude: (a) Unlike vagally mediated gastric acid secretion and pancreatic polypeptide release which can be blocked by atropine, vagal gastrin release is potentiated by atropine. This observation suggests the existence of a vagal-cholinergic pathway which normally (i.e., in the absence of atropine) inhibits gastrin release. (b) Because atropine (without sham feeding) increased basal gastrin levels, it is likely that the cholinergic pathway which inhibits gastrin release is active even when the vagus nerve is not stimulated by sham feeding.

Adult↗
PubMed1977

Kinetics of atropine inhibition of pentagastrin-stimulated H+, electrolyte, and pepsin secretion in the dog.

The effects of atropine on pentagastrin-stimulated gastric secretion of water, H, Cl, Na, K, and pepsin were determined by kinetic analysis of dose-response studies in 5 dogs with esophagostomy and gastric cannula. First a dose-response study was done using 7 doses of pentagastrin (1-6 mug/kg hr), each dose given by I.V. infusion for 4 hr at a separate time. The same series of doses was used with atropine sulfate 10 mug/kg hr as background. Atropine inhibited pentagastrin-stimulated secretion competively with a dose ratio change of 20. In a third set of studies pentagastrin was infused alone for 4 hrs in the dose of 1.5 mug/kg hr and then with each of 7 doses of atropine (0.625-40 mug/kg hr), each dose used separately. Atropine competitively inhibited water, H, Cl, and K secretion, with Ki (dose of atropine giving 50% inhibition) of 1.0 mug/kg hr. Pepsin secretion was much more strongly inhibited than acid secretion by atropine with Ki 0.27 mug/kg hr and the inhibition was uncompetitive. Calculated maximal inhibition of H+ secretion by atropine was 89% and of pepsin 95%. Furthermore the shape of the response to pentagastrin was altered by atropine so that the peak response was delayed to the third and fourth hour of pentagastrin infusion.

Animals↗
PubMed1976

Halothane anaesthesia and suxamethonium I: the significance of preoperative atropine administration. A double-blind study.

Preoperative administration of atropine was evaluated during induction of halothane anaesthesia with two administrations of suxamethonium 1 mg/kg body weight, 5 min apart. Sixty-eight healthy, adult patients were studied. They were divided into five groups according to dose and route of administration of atropine. ECG was continuously monitored. Serum potassium, pH, PaCO2, PaO2 and standard bicarbonate were measured at appropriate intervals. It was found that neither atropine 0.01 mg/kg body weight given intramuscularly 1 h beofre the anaesthesia nor atropine 0.01 mg/kg body weight given intravenously 5 min prior to induction protected against serious bradycardias (defined as heart rate below 20 beats per minute) following the second dose of suxamethonium. No serious brady-arrhythmias were seen in patients given either a combination of intramuscular and intravenous atropine in the above-mentioned doses or in patients given atropine 0.015 mg/kg body weight intravenously 5 minutes prior to induction. However, a decrease in heart rate to around 40-50 beats per minute occurred in some of these patients. Furthermore, these large doses of atropine caused an increase in heart rate during induction to more than 120 beats per minute in about 50% of the patients and to more than 140 beats per minute in about 25% of the patients. Our results suggest that preoperative administration of atropine does not protect against serious brady-arrhythmias following a second dose of suxamethonium, unless doses of atropine are used which cause tachycarida of considerable degree.

Adolescent↗
PubMed1979

Effects of atropine on induction and maintenance of atrioventricular nodal reentrant tachycardia.

The electrophysiologic effects of atropine were studied in 14 patients with dual atrioventricular (AV) nodal pathways and recurrent paroxysmal supraventricular tachycardia (PSVT). During PSVT, all patients used a slow pathway (SP) for antegrade and fast pathway (FP) for retrograde conduction. Atropine enhanced both SP antegrade and FP retrograde conduction, shown by a decrease in paced cycle lengths (atrial and ventricular) producing AV and ventriculoatrial block. Five patients had induction of sustained PSVT before and after atropine. Seven patients failed to induce or sustain PSVT before atropine, because of retrograde FP refractoriness. All seven had induction of sustained PSVT after atropine due to facilitation of FP retrograde conduction. Two patients had only single atrial echoes before atropine, reflecting SP antegrade refractoriness. After atropine, sustained PSVT was inducible in one, and nonsustained in the other, PSVT cycle length could be compared in seven patients before and after atropine and decreased from 383 +/- 25 to 336 +/- 17 (p less than 0.05). Thus, in patients with dual AV nodal pathways, atropine facilitated SP antegrade and FP retrograde conduction, shortened cycle length of PSVT and potentiated ability to sustain PSVT.

Adult↗
PubMed1979

The effect of large doses of atropine sulfate on heart rate and blood pressure in rats.

Atropine sulfate causes bradycardia in doses which are greater than the usual anticholinergic doses producing tachycardia (Shucard and Andrew, 1977, Res. Comm. Chem. Path. Pharmacol. 16, 401-410). The present study was designed to evaluate the effects of large doses of atropine sulfate on heart rate and systemic blood pressure in rats. Six groups of urethane anesthetized, male, Sprague Dawley rats (200-450 g) were injected with varying doses of atropine via the jugular vein. Groups I through IV received 5 mg/kg, 20 mg/kg, 40mg/kg and 80 mg/kg, respectively. Group V was bilaterally vagotomized before the injection of 80 mg/kg of atropine. Animals in Group VI were bilaterally vagotomized and pretreated with propranolol-HCl before injection of 40 mg/kg of atropine. Atropine caused a significant (p less than 0.005) dose-dependent reduction in both heart rate and blood pressure. The negative chronotropic property of atropine shown in these experiments is in agreement with recent in vitro and in vitro studies. The cause of bradycardia in these doses appears to be an intrinsic property of atropine rather than being centrally mediated. Possible direct action by atropine on peripheral vascular resistance is discussed.

Animals↗
PubMed1976

Electrophysiologic effects of atropine on sinus node and atrium in patients with sinus nodal dysfunction.

Electrophysiologic studies were conducted in 21 patients with sinus nodal dysfunction before and after intravenous administration of 1 to 2 mg of atropine. The mean sinus cycle length (+/- standard error of the mean) was 1,171 +/- 35 msec before and 806 +/- 29 msec after administration of atropine (P less than 0.001). Mean sinus nodal recovery time determined at a aced rate of 130/min and maximal recovery time were, respectively, 1,426 +/- 75 and 1,690 +/- 100 msec before and 1,169 +/- 90 and 1,311 +/- 111 msec after atropine (P less than 0.001 and less than 0.001). Mean calculated sinoatrial conduction time, measured in 16 patients, was 113 +/- 8 msec before and 105 +/- 9.7 msec after atropine (difference not significant). Mean atrial effective refractory period, measured at an equivalent driven cycle length, was 262 +/- 11.1 msec before and 256 +/- 10.3 msec after atropine (not significant). Mean atrial functional refractory period was 302 +/- 12.5 msec before and 295 +/- 11.3 msec after atropine (not significant). The shortening of sinus cycle length and sinus recovery time with atropine was similar to that noted in patients without sinus nodal dysfunction. In contrast, atropine had insignificant effects on sinoatrial conduction and atrial refractoriness in this group whereas it shortens both in normal subjects. This finding may reflect altered perinodal and atrial electrophysiologic properties in patients with sinus node disease.

Adult↗
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↗
PubMed1979

[The effect of atropine on the pancreas].

The literature relating to the effect of atropine on exocrine pancreatic secretion in man and animals is critically reviewed. In most species basal secretion of volume, bicarbonate, and enzyme secretion are reduced by atropine, thus indicating some neural control of basal pancreatic secretion. The literature is replete with conflicting findings on the effect of atropine on pancreatic response to exogenous hormones. In well controlled studies atropine had no effect on the action of cholecystokinin-pancreozymin (CCK) or caerulein on the pancreas. Atropine either moderately depressed or did not alter the volume and bicarbonate response to secretin but constantly reduced enzyme secretion. With respect to pancreatic response to a meal, and to intestinal instillation of aminoacids, fat or HCL, all studies agree that pancreatic secretion is depressed by atropine. The recent finding that atropine did not alter the response of a transplanted denervated pancreas to intestinal stimulants suggests that atropine acts on the pancreas by interrupting an enteropancreatic vago-vagal reflex and not by blocking the action of hormones on the pancreas or by interfering with cholinergic facilitation of gastrointestinal hormone release.

Anesthesia↗
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↗
PubMed1978

Effect of atropine on meal-stimulated gastrin and gastric inhibitory polypeptide (GIP) release.

The effect of atropine on meal-stimulated gastric inhibitory polypeptide (GIP) and gastrin release was studied in 5 purebred foxhounds and compared with control studies done in the same animals given a meal without atropine, peak incremental serum gastrin occurred between 5 and 15 min after the meal whereas the greatest increment in serum GIP occurred 60 min postcibal. Atropine had no effect on basal concentrations of gastrin or GIP. However, when atropine was given before feeding serum gastrin concentrations from 75 to 120 min postcibal were significantly higher (P less than 0.04) than after the meal alone. The normal meal-stimulated rise in serum GIP was almost completely inhibited by atropine. We conclude that: 1) the rise in serum gastrin adter a meal preceeds the rise in serum GIP; 2) atropine potentiates the late gastrin response while suppressing the increase in serum GIP after a meal; and 3) the mechanism by which atropine potentiates gastrin release may be related to its suppressive effects on intestinal inhibitors of gastrin secretion, such as GIP.

Animals↗
PubMed1977

Comparative bronchodilator responses to atropine and terbutaline in asthma and chronic bronchitis.

We have compared bronchodilator responses to atropine and terbutaline in 39 chronic bronchitics and 16 stable asthmatics. Fasting subjects were given either 1.05 mg atropine of 5.0 mg terbutaline orally. Pulmonary function was assessed using the peak responses, namely: three 60-minute intervals for terbutaline and three 30-minute intervals for atropine. A subgroup of five reactive bronchitis patients was given a placebo with no response. Areas under the percent response-time interval curve were compared. Both patient groups responded to the same degree to atropine and terbutaline with respect to reduction of airway resistance. However, the FEV1 and V50 responses to terbutaline were markedly enhanced compared to atropine in the asthmatics while equal to the atropine response in the bronchitis patients. Thus, atropine appears to exert its effect upon both large and small airways in bronchitis, but predominantly on large airways in asthma. The results are consistent with a state of enhanced vagal tone in small airways in bronchitis compared to asthma, but other explanations are conceivable.

Airway Resistance↗