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PubMed1985

Effect of atropine on plasma gastrin and somatostatin concentrations during sham feeding in man.

The purpose of these studies was to measure circulating gastrin and somatostatin concentrations during sham feeding in humans and to evaluate the effect of two doses of intravenous atropine on circulating concentrations of these peptides. Gastric acid and bicarbonate secretion and pulse rate were also measured. Sham feeding increased plasma gastrin concentrations by approximately 15 pg/ml but had no effect on plasma somatostatin-like immunoreactivity (SLI). A small dose of atropine (5 micrograms/kg) augmented plasma gastrin concentrations during sham feeding significantly (P less than 0.01), but did not affect plasma SLI. Atropine also significantly inhibited gastric acid secretion and gastric bicarbonate secretion (by 62% and 52%, respectively), but pulse rate was not affected. A larger dose of atropine (15 micrograms/kg intravenously) suppressed plasma gastrin concentrations significantly compared to the smaller 5 micrograms/kg atropine dose (P less than 0.02), so that plasma gastrin concentrations when 15 micrograms/kg atropine was given were not significantly different from those during the control study. 15 micrograms/kg atropine reduced gastric acid and bicarbonate secretion by 81% and 66%, respectively, and also increased pulse rate by 15 min-1. These studies indicate that small doses of atropine enhance vagally mediated gastrin release in humans, probably by blocking a cholinergic inhibitory pathway for gastrin release. Although the nature of this cholinergic inhibitory mechanism is unclear, we found no evidence to incriminate somatostatin. Our finding that the larger dose of atropine reduced serum gastrin concentrations compared with the smaller dose suggests that certain vagal-cholinergic pathways may facilitate gastrin release.

Adult↗
PubMed1992

Atropine administration in experimental electromechanical dissociation.

Atropine can have a place during cardiopulmonary resuscitation (CPR) in the management of asystole, where parasympathetic influence might be excessive. However, the beneficial effects of atropine in electromechanical dissociation (EMD) have not been clearly demonstrated. The authors studied the effects of atropine in combination with epinephrine on an experimental model of EMD in the closed-chested dog. In 15 pentobarbital-anesthetized, mechanically ventilated dogs (mean weight 20 kg), EMD was induced by ventricular fibrillation followed by an external countershock, and was observed for 2 minutes before CPR was started. After 5 minutes of chest compression using a CPR thumper, either atropine 0.5 mg or D5W was administered, and the same injection was repeated every 5 minutes until recovery. Epinephrine 1 mg was administered in alternans. Each dog was submitted to two successive episodes of CPR, using either atropine or D5W, in a randomized order. Of a total of 28 CPRs, five were successful with chest compression alone. In the treatment groups, 10 of 11 were successful with atropine, but only eight of 12 with D5W (P < .01). The duration of CPR was also significantly shorter when atropine was used (9 minutes 56 seconds +/- 14 seconds versus 12 minutes 08 seconds +/- 43 seconds, P < .001). During the recovery period, atropine-treated animals had higher arterial pressure, heart rate, cardiac output and stroke volume. On this experimental model, the administration of high doses of atropine together with epinephrine enhances the recovery from EMD and results in a better cardiac function during recovery.

Animals↗
PubMed2005

Carotid angioplasty and stent-induced bradycardia and hypotension: Impact of prophylactic atropine administration and prior carotid endarterectomy.

OBJECTIVE: We compared the physiologic effect of selective atropine administration for bradycardia with routine prophylactic administration, before balloon inflation, during carotid angioplasty and stenting (CAS). We also compared the incidence of procedural bradycardia and hypotension for CAS in patients with primary stenosis vs those with prior ipsilateral carotid endarterectomy (CEA). METHODS: A total of 86 patients were treated with CAS at 3 institutions. Complete periprocedural information was available for 75 of these patients. The median degree of stenosis was 90% (range, 60%-99%). Indications for CAS were severe comorbidities (n = 49), prior CEA (n = 21), and prior neck radiation (n = 5). Twenty patients with primary lesions were treated selectively with atropine only if symptomatic bradycardia occurred (nonprophylactic group). Thirty-four patients with primary lesions received routine prophylactic atropine administration before balloon inflation or stent deployment (prophylactic group). The 21 patients with prior CEA received selective atropine treatment only if symptomatic bradycardia occurred (prior CEA group) and were analyzed separately. Mean age and cardiac comorbidities did not vary significantly either between the prophylactic and nonprophylactic atropine groups or between the primary and prior CEA patient groups. Outcome measures included bradycardia (decrease in heart rate >50% or absolute heart rate <40 bpm), hypotension (systolic blood pressure <90 mm Hg or mean blood pressure <50 mm Hg), requirement for vasopressors, and cardiac morbidity (myocardial infarction or congestive heart failure). RESULTS: The overall incidence of hypotension and bradycardia in patients treated with CAS was 25 (33%) of 75. A decreased incidence of intraoperative bradycardia (9% vs 50%; P < .001) and perioperative cardiac morbidity (0% vs 15%; P < .05) was observed in patients with primary stenosis who received prophylactic atropine as compared with patients who did not receive prophylactic atropine. CAS after prior CEA was associated with a significantly lower incidence of perioperative bradycardia (10% vs 33%; P < .05), hypotension (5% vs 32%; P < .05), and vasopressor requirement (5% vs 30%; P < .05), with a trend toward a lower incidence of cardiac morbidity (0% vs 6%; not significant) as compared with patients treated with CAS for primary carotid lesions. There were no significant predictive demographic factors for bradycardia and hypotension after CAS. CONCLUSIONS: The administration of prophylactic atropine before balloon inflation during CAS decreases the incidence of intraoperative bradycardia and cardiac morbidity in primary CAS patients. Periprocedural bradycardia, hypotension, and the need for vasopressors occur more frequently with primary CAS than with redo CAS procedures. On the basis of our data, we recommend that prophylactic atropine administration be considered in patients with primary carotid lesions undergoing CAS.

Aged↗
PubMed1999

Atropine pharmacokinetics and pharmacodynamics following endotracheal versus endobronchial administration in dogs.

Emergency endotracheal and endobronchial drug administration provide an effective alternative for intravenous drug delivery during cardiopulmonary resuscitation. The purpose of the present study was to determine the immediate pharmacokinetic and pharmacodynamic properties of atropine following administration by either of these routes. Atropine (0.02 mg/kg) was given to seven anaesthetized mongrel dogs. Each dog was studied twice: once when atropine was injected into the endotracheal tube, and on another day when atropine was given via a flexible catheter wedged into a peripheral bronchus. Plasma atropine concentrations and blood gases were measured during 60 min following drug administration. Both routes of atropine administration differed significantly in three measures: the maximal atropine concentration (Cmax) was significantly higher with the endobronchial administration 40.0 +/- 7.8 ng/ml compared to 23.9 +/- 5 ng/ml endotracheally (P = 0.008); atropine's elimination (t1/2beta) half-life was significantly longer with the endobronchial route (39.3 +/- 5.2 min vs. 28.0 +/- 7.9 min; P = 0.05); Endobronchial administration resulted in an increase of 16% in heart rate, beginning immediately after drug delivery and peaking after 5 min. Other pharmacokinetic parameters were not significantly different. We conclude that endobronchial administration of atropine has a clear advantage over the endotracheal route.

Animals↗
PubMed1999

The efficacy of atropine in the treatment of hemodynamically unstable bradycardia and atrioventricular block: prehospital and emergency department considerations.

OBJECTIVE: To determine the efficacy of atropine therapy in patients with hemodynamically compromising bradycardia or atrioventricular block (AVB) in the prehospital and emergency department settings. METHODS DESIGN: Retrospective review of prehospital, emergency department, and hospital records. PARTICIPANTS: Prehospital patients with hemodynamically compromising bradycardia or AVB with evidence of spontaneous circulation who received atropine as delivered by emergency medical services personnel (advanced life support level). SETTING: Urban/suburban fire department-based emergency medical service system with on-line medical control serving a population of approximately 1.6 million persons. DEFINITIONS: Hemodynamic instability was defined as the presence of any of the following: ischemic chest pain, dyspnea, syncope, altered mental status, and systolic blood pressure less than 90 mmHg. Bradycardia was defined as sinus bradycardia, junctional bradycardia, or idioventricular bradycardia (grouped as bradycardia) while AVB included first-, second- (types I and II), or third-degree (grouped as AVB). The response that occurred within one minute following each dose of atropine was defined as none, partial, complete, or adverse. MAIN RESULTS: Of 172 patients meeting entry criterion complete data was available for 131 (76.1%) and constitutes the study population. The mean age was 71 years. Fifty-one percent were female. Forty-five patients had AVB and 86 bradycardia. Patients with AVB were more likely to have a presenting systolic blood pressure less than 90 mmHg than those with bradycardia. In the 131 patients, responses to atropine were as follows: 26 (19.8%) = partial, 36 (27.5%) = complete, 65 (49.6%) = none, and 4 (2.3%) = adverse. Patients presenting with bradycardia (compared to AVB) more commonly: (1) received a single dose of atropine; (2) a lower total dose of atropine in the prehospital interval; (3) were more likely to arrive in the ED with a normal sinus rhythm; and (4) were less likely to receive additional atropine or isoproterenol in the ED. Those patients who achieved normal sinus rhythm over the total course of care were likely to have achieved that rhythm during the prehospital interval. There was no difference between groups in the likelihood of leaving the ED with a normal sinus rhythm achieved during the ED interval. Acute myocardial infarction was more common in patients presenting with AVB (55.5%) than with bradycardia (23.2%, P = 0.001). CONCLUSIONS: Approximately one-half of patients who received atropine in the prehospital setting for compromising rhythms had either a partial or complete response to therapy. Adverse responses were uncommon. Those patients who presented with hemodynamically unstable bradycardia to EMS personnel responded more commonly to a single dose and a lower total dose of atropine compared to similar patients with AVB. Those patients who achieve normal sinus rhythm by ED discharge were likely to have achieved it during the prehospital interval.

Aged↗
PubMed2001

Comparison of myocardial blood flow during dobutamine-atropine infusion with that after dipyridamole administration in normal men.

OBJECTIVES: The present study was designed to compare the absolute myocardial blood flow (MBF) after intravenous dipyridamole infusion with that during dobutamine-atropine administration in normal healthy male volunteers. BACKGROUND: Both safety and usefulness of dobutamine-atropine stress in myocardial perfusion imaging have been reported. However, no information exists on whether the magnitude ofhyperemia achieved with dipyridamole and dobutamine-atropine is comparable. METHODS: Myocardial blood flow was measured with positron emission tomography and 15O-labeled water in 20 healthy young men (23 +/- 3 years) 1) at baseline, 2) after dipyridamole infusion (0.56 mg/kg over 4 min), and 3) during dobutamine (40 microg/kg/min) and atropine (0.25 to 1.0 mg) infusion. RESULTS: The MBF was significantly increased during dipyridamole infusion and during dobutamine-atropine stress compared with at rest (4.33 +/- 1.23 and 5.89 +/- 1.58 vs. 0.67 +/- 0.16 ml/min/g, respectively, p < 0.0001). Moreover, dobutamine-atropine infusion produced greater MBF compared with dipyridamole (p = 0.0011), while coronary vascular resistance did not differ significantly after dipyridamole administration and during dobutamine-atropine infusion (17.6 +/- 7.9 vs. 18.6 +/- 5.6 mm Hg/[ml/min/g], respectively). CONCLUSIONS: Near maximal coronary vasodilatation caused by dipyridamole is attainable using dobutamine and atropine in young healthy volunteers. Dobutamine in conjunction with atropine is no less effective than dipyridamole in producing myocardial hyperemia.

Adult↗
PubMed1999

Difference between the effect of acute and chronic surgical vagotomy on the cytoprotective action of atropine against indomethacin-induced mucosal lesions on the gastrointestinal tract in rats.

The cytoprotective effect of a small dose of atropine was proved against the indomethacin (IND)-caused gastrointestinal (GI) mucosal damage. This protective effect of atropine disappeared in the acute phase of surgical vagotomy (ASV) on the vagally-innervated parts of GI tract. The aims of our observations were: 1) to examine the effect of chronic surgical vagotomy (CSV) on the cytoprotective action of atropine in the GI tract; and 2) to compare the effects of ASV and CSV on the GI cytoprotection caused by atropine against IND-induced mucosal damage and vascular permeability in rats. The IND was given s.c. 24 h prior to the killing of the animals in a dose of 20 mg x kg(-1). Bilateral surgical vagotomy or sham operation were carried out 24 h (ASV) or 14 d (CSV) before IND-application. Atropine was given i.p. every 5 h after IND-treatment in a dose of 0.1 mg x kg(-1). The number of macroscopical mucosal ulcerations was noted and its severity was calculated by semiquantitative scale in the stomach, small intestine and three equal parts of colon. Vascular permeability was measured by Evans-blue leakage into the mucosal tissue. It has been found that: 1) Tte small dose of atropine significantly decreased the IND-induced mucosal damage and vascular permeability on the stomach, small intestine and the vascular permeability on the proximal colon; 2) the small dose of atropine did not cause any changes in the appearance of IND-induced mucosal lesions and in Evans blue concentration in the mucosa after ASV, but it significantly decreased the IND-caused mucosal damage and Evans blue concentration in the mucosa of stomach, small intestine and proximal colon after CSV; 3) the IND-induced mucosal damage and vascular permeability treated with atropine (given in cytoprotective dose) were significantly smaller after CSV than that after ASV on the stomach, small intestine and proximal colon. It has been concluded that the intact vagal nerve has an essential role in the appearance of cytoprotective mechanisms of atropine in GI tract.

Animals↗
PubMed1998

The role of tachykinin NK1 and NK2 receptors in atropine-resistant colonic propulsion in anaesthetized guinea-pigs.

1. The role of endogenous tachykinins on guinea-pig colonic propulsion was investigated by using potent and selective tachykinin NK1 and NK2 receptor antagonists. Colonic propulsion and contractions were determined by means of a balloon-catheter device, inserted into the rectum of guanethidine (68 micromol kg(-1), s.c., 18 and 2 h before)-pretreated, urethane-anaesthetized guinea-pigs. Propulsion of the device (dynamic model) was determined by measuring the length of the catheter expelled during 60 min filling of the balloon (flow rate 5 microl min(-1)). 2. In control conditions the tachykinin NK1 receptor antagonist SR 140333 (1 micromol kg(-1), i.v.) did not affect either colonic propulsion or the amplitude of contractions. The tachykinin NK2 receptor antagonists MEN 10627 and MEN 11420 (1 micromol kg(-1), i.v.) increased colonic propulsion at 10 min (+120% and 150%, respectively) but at 60 min the effect was significant only for MEN 10627 (+84%). SR 48968 (1 micromol kg(-1), i.v.) did not significantly enhance the colonic propulsion. None of these tachykinin NK2 receptor antagonists modified the amplitude of colonic contractions. In contrast, both atropine (6 micromol kg(-1), i.v., plus infusion of 1.8 micromol h(-1)) and hexamethonium (55 micromol kg(-1), i.v., plus infusion of 17 micromol h(-1)) abolished propulsion (81% and 87% inhibition, respectively) and decreased the amplitude of contractions (68% inhibition for either treatment). 3. In atropine-treated animals (6 micromol kg(-1), i.v., plus infusion of 1.8 micromol h(-1)), apamin (30 nmol kg(-1), i.v.) restored colonic propulsion (+416%) and increased the amplitude of contractions (+367% as compared to atropine alone). Hexamethonium (55 micromol kg(-1), i.v., plus infusion of 17 micromol h(-1)) abolished the apamin-induced, atropine-resistant colonic propulsion (97% inhibition) and reduced the amplitude of the atropine-resistant contractions (52% inhibition). 4. The apamin-induced, atropine-resistant colonic propulsion was inhibited by SR 140333 (-69% at 1 micromol kg(-1)), SR 48968 (-78% at 1 micromol kg(-1)), MEN 11420 (-59% at 1 micromol kg(-1)) and MEN 10627 (-50% at 1 micromol kg(-1)), although the latter effect was not statistically significant. The combined administration of SR 140,333 and MEN 10,627 (1 micromol kg(-1) for each antagonist) almost completely abolished colonic propulsion (90% inhibition). The amplitude of colonic contractions was also reduced by SR 140333 (-42%), SR 48968 (-29%), MEN 11420 (-45%) but not by MEN 10627 (-16%). The combined administration of SR 140333 and MEN 10,627 reduced the amplitude of contractions by 47%. SR 140603 (1 micromol kg(-1), i.v.), the less potent enantiomer of SR 140333, was inactive. 5. In control animals, apamin (30 nmol kg(-1), i.v.) enhanced colonic propulsion (+84%) and increased the amplitude of contractions (+68%), as compared to the vehicle. Hexamethonium (55 micromol kg(-1), i.v. plus infusion of 17 micromol h(-1)) inhibited propulsion (86% inhibition) and decreased the amplitude of contractions (49% inhibition). SR 140333, SR 48968, MEN 11420, MEN 10627, or the coadministration of SR 140333 and MEN 10627 had no effect. 6. In a separate series of experiments, the mean amplitude of colonic contractions was also recorded under isovolumetric conditions through the balloon-catheter device kept in place at 75 mm from the anal sphincter (static model). In control conditions, neither SR 140333 nor MEN 11420 modified the amplitude of contractions. In atropine-pretreated guinea-pigs, SR 140333 and MEN 11420 (0.1-1 micromol kg(-1)) dose-dependently decreased the amplitude of contractions. In apamin- and atropine-pretreated animals, only the highest (1 micromol kg(-1)) dose of SR 140333 or MEN 11420 significantly decreased the amplitude of contractions. The inhibitory potency of atropine (0.3-1 micromol kg(-1)) was similar in apamin-pretreated animals and in controls. 7. It was concluded that, in anaesthetized guinea-pigs, endogenous tachykinins, acting through both NK(1) and NK(2) receptors, act as non-cholinergic excitatory neurotransmitters in promoting an apamin-evoked reflex propulsive activity of the distal colon.

Anesthesia↗
PubMed1994

[Cardiac effects of atropine in patients treated with antidepressive medication].

UNLABELLED: It is often suggested that atropine should be avoided in patients on treatment with tricyclic or tetracyclic antidepressants. It is feared that the strong anticholinergic side effects of these drugs could exaggerate the effects of atropine on the heart. METHODS: In a controlled prospective study, 31 patients on treatment with tri- or tetracyclic antidepressants were given atropine in incremental doses. ECG-changes and changes in heart rate were recorded and compared to a control group. Atropine 2 micrograms/kg was administered in 60 sec. intervals up to a total dose of 10 micrograms/kg. RESULTS: The patients on antidepressant treatment had a higher incidence of common anticholinergic side effects (dryness of mouth, accommodation disorders, constipation) due to the anticholinergic properties of the antidepressants. In addition, the basal heart rate of these patients was significantly higher compared to the control group (81/min vs. 73/min). After administration of 2 and 4 micrograms/kg of atropine the patients of the control group showed a 5% resp. 4% decrease in heart rate. 26% of these patients developed conduction disturbvances. These changes could be explained by the parasympathetic effect of low doses of atropine. They were less pronounced in the patients on treatment with antidepressants. Here, only the administration of 2 micrograms/kg of atropine led to a 2% decrease in heart rate. Only 6% of these patients developed conduction disturbances. Both groups showed an increase in heart rate when higher doses of atropine were administered (8 and 10 micrograms/kg). However, the increase in heart rate after administration of 10 micrograms/kg was significantly less in the patients on antidepressant treatment compared to the control group (11.4% vs. 16.2%). There were no changes of blood pressure during these investigations. CONCLUSION: The results of this study suggest that the anticholinergic properties of tri- and tetracyclic antidepressants include an increase in basal heart rate, but do not render the heart more susceptible to the cardiac effects of atropine.

Adult↗
PubMed2002

Heart rate response to intravenous atropine during propofol anesthesia.

UNLABELLED: We studied the dose-response relationships for atropine-induced heart rate (HR) changes in 61 patients during propofol anesthesia. The control group (n = 15) received no propofol. Group P-5 (n = 22) received IV propofol 1.25 mg/kg over 1 min followed by propofol at 5 mg. kg(-1). h(-1). After tracheal intubation, anesthesia was maintained with propofol 5 mg. kg(-1). h(-1) and 67% nitrous oxide in oxygen. Group P-10 (n = 24) received IV propofol 2.5 mg/kg over 1 min followed by propofol at 10 mg. kg(-1). h(-1). The P-10 protocol was otherwise identical. All patients received incremental doses of IV atropine 5 microg/kg over 5 s at 2-min intervals until HR increased >20 bpm from baseline values. Heart rate response to atropine 10 microg/kg was attenuated in Groups P-5 (12 +/- 7 bpm) and P-10 (9 +/- 6 bpm) compared with the control group (28 +/- 13 bpm, P<0.05). When atropine 20 microg/kg was administered, HR increased >20 bpm in all patients of the control group, but in only 43% and 13% of patients in Groups P-5 and P-10, respectively (P<0.05). These results indicate the decreased HR responsiveness to IV atropine in patients receiving propofol, which cannot be effectively overcome by a large dose of atropine, is possibly attributable to propofol-induced suppression of the sympathetic nervous system. IMPLICATIONS: Heart rate response to IV atropine is attenuated during propofol anesthesia, and the decreased responsiveness to atropine cannot be effectively overcome by a large dose of atropine.

Adjuvants, Anesthesia↗
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↗
PubMed2004

Preparing for chemical terrorism: stability of injectable atropine sulfate.

OBJECTIVE: A massive nerve agent attack may rapidly deplete in-date supplies of atropine. The authors considered using atropine beyond its labeled shelf life. The objective was to determine the stability of premixed injectable atropine sulfate samples with different expiration dates. METHODS: This was an in-vitro study using gas chromatography and mass spectrometry (GC/MS). Four atropine solutions (labeled concentration of 400 microg/mL) ranging from in date to 12 years beyond expiration (exp) and an additional sample of atropine sulfate (labeled concentration of 2,000 microg/mL) obtained from a World War II era autoinjector were assayed for atropine stability. Standards of atropine sulfate and tropine were prepared and quantified by GC/MS. Study samples were prepared by adding a buffer solution to free the base, extracting with an isopropanol/methylene chloride mixture and followed by evaporating the organic layer to dryness. Pentafluoropropionic anhydride and pentafluoropropanol were then added as derivatization reagents. Study samples were heated, the derivitization reagents were evaporated, and the remaining compound was reconstituted in ethyl acetate for injection into the GC/MS. RESULTS: All solutions were clear and colorless. Atropine concentrations were as follows: in date, 252 microg/mL; 2001 exp, 290 microg/mL; 1999 exp, 314 microg/mL; 1990 exp, 398 microg/mL; and WW II specimen, 1,475 microg/mL. Tropine was found in concentrations of <10 microg/mL in all study samples. CONCLUSIONS: Significant amounts of atropine were found in all study samples. All samples remained clear and colorless, and no substantial amount of tropine was found in any study sample. Further testing is needed to determine clinical effect.

Antidotes↗
PubMedDate not supplied

Hemodynamic effects of atropine, dobutamine, nitroprusside, phenylephrine, and propranolol in conscious horses.

The authors investigated the cardiovascular effects of low doses of nitroprusside, dobutamine, and phenylephrine and a beta-adrenergic blocking dose of propranolol in conscious, healthy horses with and without prior atropine administration. A parasympathetic blocking dose of atropine produced significant increases in heart rate and arterial pressures, and decreased stroke volume, ejection fraction, pulse pressure, and right-ventricular end-diastolic pressure and volume. Cardiac output was not changed by atropine administration. Nitroprusside reduced arterial pressures to a greater extent in atropinized horses but increased heart rate in both atropinized and non-atropinized horses. Dobutamine increased mean arterial pressure in both non-atropinized and atropinized horses but increased heart rate, diastolic arterial pressure, and systemic vascular resistance only in atropinized horses. Propranolol did not affect any of the hemodynamic variables that were measured. Phenylephrine, in the presence of beta-adrenergic blockade, increased mean arterial pressure and reduced cardiac output. This study showed that low doses of nitroprusside, dobutamine, and phenylephrine produce significant hemodynamic effects in conscious, healthy horses and that these effects are modified by prevailing parasympathetic tone.

Animals↗
PubMed1968

The effect of atropine on the frog sartorius neuromuscular junction.

1. The effect of atropine sulphate and of (+)-tubocurarine chloride (TC) on the amplitude and time course of end-plate potentials (e.p.p.s) and miniature end-plate potentials (m.e.p.p.s) was studied in the sartorius muscle of the frog.2. Atropine sulphate reduces the amplitude of intracellularly recorded e.p.p.s and m.e.p.p.s, in concentrations 100 times higher than TC (6 x 10(-5)M for 50% reduction of amplitude compared with 6 x 10(-7)M for TC).3. Atropine sulphate causes a marked shortening of both e.p.p.s and m.e.p.p.s: when the amplitude of e.p.p.s or m.e.p.p.s is reduced by 50%, their rise-time and half-decay time are both shortened by 40%. The corresponding shortening produced by TC is 15%.4. E.p.p.s prolonged by prostigmine 10(-6) g/ml. undergo a larger shortening (30%) in TC, while atropine-induced shortening related to the corresponding drop of amplitude is the same whether prostigmine is used or not.5. On repeated applications after recovery of amplitude and time course, TC loses its shortening effect on e.p.p.s while the atropine shortening effect remains unchanged.6. Atropine sulphate shortens the rise-time but not the falling phase of brief depolarizations produced by electrophoretic applications of acetylcholine (ACh) to the muscle fibre surface in the end-plate region. It also reduces their amplitude, in the same way that it reduces the amplitude of e.p.p.s.7. Atropine sulphate in concentrations which markedly reduce the amplitude and time course of e.p.p.s has no effect on their quantum content.8. Atropine sulphate at a concentration of 10(-4)M does not change the amplitude and time course of an electrotonic potential produced by a rectangular current pulse passed through the end-plate region of a muscle fibre.9. It is suggested that either enhanced removal of ACh or a spatial gradient of effectiveness of the blocking drugs, or both these mechanisms, participate in shortening the e.p.p. by atropine sulphate and TC.

Acetylcholine↗
PubMed2000

Effect of atropine on proximal gastric motor and sensory function in normal subjects.

BACKGROUND AND AIMS: Distension of the proximal stomach is a major stimulus for triggering transient lower oesophageal sphincter (LOS) relaxations. We have shown recently that atropine inhibits triggering of transient LOS relaxations in both normal subjects and patients with gastro-oesophageal reflux disease. Atropine could potentially act centrally by inhibiting the central integrating mechanism in the brain stem, or act peripherally by altering the response of the stomach to distension. The aim of this study was to investigate the effect of atropine on fasting gastric compliance and postprandial gastric tone using an electronic barostat. METHODS: Fasting and postprandial proximal gastric motor and sensory functions were assessed in 10 normal healthy volunteers. Oesophageal manometry and pH were simultaneously measured. On separate days, atropine (15 microg/kg bolus, 4 microg/kg/h intravenous infusion) or saline was given and maintained for the duration of the recording period. RESULTS: In the fasting period, atropine significantly reduced minimum distending pressure (5.5 (0.4) v 4.4 (0.4) mm Hg; p<0.005) and increased proximal gastric compliance (81.3 (5.3) v 102. 1 (8.7) ml/ mm Hg; p<0.05). In response to a meal, maximal gastric relaxation was similar on both study days. However, during atropine infusion, there was no recovery of proximal gastric tone in the two hour postprandial observation period. Postprandial fullness scores were higher during atropine infusion and correlated with changes in intrabag volume. Atropine significantly reduced the rate of postprandial transient LOS relaxations: first hour, 7.0 (5.3-10.0) v 3.0 (1.0-4.0) (p<0.02); second hour, 5.0 (3.3-5.8) per hour v 1.0 (0-3.0) per hour (p<0.05). CONCLUSIONS: In humans, fasting and postprandial proximal gastric motor function is under cholinergic control. Atropine induced inhibition of transient LOS relaxations is unlikely to be caused by its effect on the proximal stomach, but rather by a central action on the integrating mechanisms in the brain stem.

Adult↗
PubMed2005

Safety and cardiac chronotropic responsiveness to the early injection of atropine during dobutamine stress echocardiography in the elderly.

OBJECTIVE: To determine the safety and cardiac chronotropic responsiveness to early atropine dobutamine stress echocardiography (DSE) in the elderly. DESIGN: Retrospective study of 258 patients >or= 70 years who underwent early atropine DSE and 290 patients >or= 70 years who underwent conventional DSE. In the early atropine protocol, atropine was started at 20 microg/kg/min of dobutamine if heart rate was < 100 beats/min, up to 2 mg. The cardiac chronotropic responsiveness in the elderly was compared with a control group of patients < 70 years matched for sex, myocardial infarction, diabetes, and treatment with beta blockers and calcium channel blockers. RESULTS: The dose of dobutamine given to elderly patients was lower during early atropine than during conventional DSE (mean (SD) 29 (7) v 38 (4) microg/kg/min, p = 0.001). Early atropine DSE resulted in diminished incidence of ventricular extrasystoles, non-sustained ventricular tachycardia, bradycardia, and hypotension compared with conventional DSE. In comparison with patients < 70 years, elderly patients required lower doses of dobutamine and atropine and achieved a higher percentage of predicted maximum heart rate (92 (9)% v 88 (10)%, p = 0.0001). Except for more common hypotension (16% v 10%, p = 0.004), no other difference in adverse effects was observed between patients >or= 70 and < 70 years. CONCLUSIONS: Early atropine DSE is a safe strategy in the elderly resulting in lower incidence of minor adverse effects than with the conventional protocol. Elderly patients presented adequate cardiac chronotropic responsiveness to early injections of atropine, requiring lower doses of drugs to reach test end points.

Aged↗
PubMed1985

Effect of atropine on digested food-induced intestinal hyperemia.

The aim of our study was to determine whether the discrepancy in the data reported on the effect of atropine on food-induced intestinal hyperemia results from a difference in experimental materials and methods. In the first two series of experiments, atropine (0.5 mg/kg iv) was given before or during intraluminal perfusion of digested food plus bile through a long jejunal loop (62% of the total small intestine) at 4 ml/min for 60 min while measuring the portion of the blood flow through the superior mesenteric artery (SMA) that perfused the loop. Atropine per se had no effect on jejunal blood flow. Before atropine food increased flow 31.5 +/- 10.1% and after atropine flow increased 54.8 +/- 11.0 and 66.0 +/- 28.0% above controls in the first and second series, respectively. Atropine also increased net fluid volume absorption. In the third series, food alone and food plus bile were placed into the lumens of the two adjacent jejunal segments. Atropine had no effect on the increases in flow and oxygen uptake produced by food alone but enhanced the hyperemia produced by food plus bile without affecting the increase in oxygen uptake. Our results suggest that the previously reported inhibition of increased SMA flow by atropine is due to the inhibitory effect of atropine on gastrointestinal motility and inhibition of pancreatic blood flow. In conclusion, food-induced jejunal hyperemia does not result from a direct vasodilator action of the cholinergic nerves.

Animals↗
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↗