Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ATROPINE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources
PubMed1989

Atropine and/or diazepam therapy protects against soman-induced neural and cardiac pathology.

Toxic doses of the organophosphonate anticholinesterase agent soman can produce neural and cardiac lesions in animals that survive the acute poisoning. The ability of two standard antidote drugs, atropine and diazepam, along with the oxime pralidoxime (2-PAM) Cl, were evaluated for their ability to block these pathological effects. Rats were challenged with a fixed dose (85 micrograms/kg, sc) of soman and treated im 5 min later with 25 mg/kg 2-PAM Cl and one of the following combinations of atropine (0.0, 1.0, 3.2, 10.0, or 32.0 mg/kg) and diazepam (0.0, 0.1, 0.32, 1.0, or 3.2 mg/kg) in a balanced design. The severity of acute anticholinesterase intoxication signs was rated 1 hr after exposure; Body weights and behavioral reactivity ratings were obtained daily for 16 days after exposure; brains and hearts of all surviving subjects were then evaluated for pathological changes. Soman challenge resulted in 33% lethality in animals that received only 2-PAM therapy; both atropine and diazepam reduced lethality in a dose-dependent fashion. Across all treatment conditions greater than 50% of the deaths occurred later than 24 hr after intoxication and treatment. Acute intoxication signs were differentially moderated by the two drugs: atropine reduced all six signs in a dose-dependent fashion; diazepam had no effect on lacrimation and eye bulb protrusion, antagonized signs of salivation and motor abnormalities in a dose-dependent manner, and antagonized the effects of soman on signs of physical activity and coordination only at low doses. All doses of diazepam and the highest dose of atropine moderated body weight loss and a syndrome of behavioral hyperreactivity observed after exposure. Brain pathology was significantly reduced by all doses of diazepam and/or the highest dose of atropine, but no single drug or drug combination was effective in protecting all animals in a group from some brain pathology. Both drugs blocked the development of cardiac lesions in a dose-dependent fashion. The results demonstrate that diazepam or high doses of atropine can antagonize the development of brain lesions that result from soman exposure. Pharmacological management of epileptiform motor abnormalities during the acute intoxication is critical for this effect. In contrast, soman-induced cardiac pathology may occur secondarily as a consequence of the severe brain lesions or develop independently of brain lesion formation due possibly to sympathetic overstimulation.

Animals↗
PubMed1995

Effect of atropine and bispyridinium oximes on respiratory and circulatory function in guinea-pigs poisoned by sarin.

During the past decade the oxime HI 6(1-[[[4-(aminocarbonyl)pyridinio]methoxy]methyl]-2- [(hydroxyimino)methyl] pyridinium dichloride) was shown to improve survival in nerve agent poisoning (in combination with atropine). Recent studies indicate, that HLö 7 (1-[[[4-(aminocarbonyl)pyridinio]methoxy]methyl]-2,4-bis [(hydroxyimino)methyl] pyridinium diiodide or dimethanesulfonate) is also an effective antidote in nerve agent poisoning but, with both oximes, data on restoration of respiration and circulation are scarce. The ability of HLö 7 or HI 6 with atropine to improve the respiratory and circulatory function in sarin-poisoned guinea-pigs was therefore investigated. Female Dunkin-Hartley guinea-pigs were anaesthetised with urethane (1.8 g/kg) and the arteria carotis, vena jugularis and trachea were cannulated. After baseline measurements the animals received 100 or 200 micrograms/kg sarin, and 2 min later the antidotes (all i.v.): 10 mg/kg atropine sulfate or a combination of atropine and HLö 7 or HI 6 (30 mumol/kg, each). Respiratory and circulatory parameters were recorded for the whole experimental period of 60 min or until the death of the animal. Brain and diaphragm acetylcholinesterase (AChE) activity was determined in each animal after the experiment. Poisoning by sarin resulted in a rapid respiratory arrest within 5 min. Atropine treatment was only partially effective in improving respiration after 100 micrograms/kg sarin but was ineffective after 200 micrograms/kg sarin. Therapy of sarin-poisoned animals with atropine plus oxime further improved respiration to various extents, restored circulation and increased survival time, HLö 7 being more effective than HI 6. Diaphragm and brain AChE were reactivated by HLö 7 and, to a minor extent, by HI 6. The results of this investigation suggest, that at equimolar doses (30 mumol/kg) the new bispyridinium dioxime HLö 7 has a higher therapeutic efficacy in sarin-poisoned guinea-pigs when compared to HI 6 (both in combination with atropine).

Acetylcholinesterase↗
PubMed1990

Evidence for a central site of action to explain the negative chronotropic effect of atropine: studies on the human transplanted heart.

The chronotropic response to atropine is biphasic; low doses cause slowing of the sinus rate and high doses cause acceleration. Although it is accepted that atropine functions as a competitive antagonist at high doses, the mechanism of the negative chronotropic response at low doses is controversial. Specifically, it is unclear whether the effect is mediated centrally or peripherally. Since at the time of cardiac replacement all central nervous system connections to the heart are severed, the transplanted heart is a unique model for separating these effects. Graded doses of atropine sulfate (0.5, 1.0, 2.0, 4.0, 8.0 and 40.0 micrograms/kg body weight) were administered to 12 human heart transplant recipients to test the hypothesis that the bradycardiac effect of low dose atropine is centrally mediated. The baseline sinus cycle lengths of the decentralized donor and innervated native sinus nodes were 694 +/- 20 and 733 +/- 27 ms, respectively. At the 0.5 and 1.0 microgram/kg doses, the cycle lengths of the native sinus node increased by 29.1 +/- 13.5 and 23.1 +/- 14.2 ms, respectively. At the 2.0 micrograms/kg dose the sinus cycle length again shortened to control. At the maximal dose of atropine the sinus cycle length shortened by 138.3 +/- 29.7 ms compared with control. In contrast, the decentralized donor sinus node exhibited a flat dose response to atropine. High dose atropine (40 micrograms/kg) caused no change in the donor heart's atrial effective refractory period, corrected sinus node recovery time, or sinoatrial conduction time measured by either the Strauss or the Narula method.(ABSTRACT TRUNCATED AT 250 WORDS)

Atropine↗
PubMed1976

Coronary occlusion site as a determinant of the cardiac rhythm effects of atropine and vagotomy.

We have previously demonstrated that atropine pretreatment increases the incidence of fatal ventricular arrhythmias induced by left anterior descending coronary artery (LAD) occlusion. The purpose of the present study was to determine whether the deleterious effect of atropine also applies to arrhythmias induced by right coronary artery (RCA) occlsusion. Occlusion of the RCA resulted in ventricular arrhythmias in all 20 animals studied, followed by ventricular fibrillation in three animals (15 per cent). Right coronary occlusion also resulted in bradycardia (-30.3 +/- 5.1 beats per minute) and hypotension (-23.1 +/- 4.9 mm. Hg). Pretreatment of 15 animals with atropine caused no significant increase in the incidence of ventricular fibrillation (i.e., 20 per cent). In addition, atropine pretreatment had no effect on the fall in heart rate and hypotension associated with RCA ligation. Sectioning the vagus nerves produced results similar to atropine pretreatment with the exception that a significant portion of the bradycardia was prevented. These results indicate that the increase in deaths after atropine observed in animals undergoing experimental LAD occlusion in not demonstrated with RCA occlusion. The results also indicate that the potential for deleterious effects of atropine in acute infarction might depend on the anatomic location of the involved myocardium.

Animals↗
PubMed1982

Atropine resistance of transmurally stimulated isolated human bladder muscle.

Human detrusor strips were obtained from patients undergoing reimplantation of ureters because of reflux, transvesical prostatectomy, or cysto-urethrectomy en bloc because of bladder malignancy. The strips were electrically stimulated. A frequency-dependent contractant response was obtained that was potentiated by physostigmine and abolished by tetrodotoxin. The maximum response approximately equaled that of acetylcholine in a maximum concentration. In most bladder preparations from patients without known functional bladder disturbances, atropine (0.01 to 0.1 microM) had a marked inhibitory effect, and at concentrations exceeding 1 microM the blockade was complete. In strips obtained from patients undergoing transvesical prostatectomy, and who also had a cystometrically verified unstable bladder, there was a varying degree of atropine resistance, with some preparations showing a 50 per cent resistance to atropine. Prazosin, phentolamine, yohimbine, guanethidine, clonidine, and noradrenaline had no consistent effects on the electrically induced bladder contraction. Nifedipine and nimodipine caused a maximum of 65 per cent inhibition of the response. Addition of nimodipine to atropine-resistant strips when maximum atropine inhibition had been reached abolished the contractions. Omitting calcium from the bath solution rapidly abolished the electrically induced contraction. It is suggested that in the normal human bladder the contraction induced by electrical stimulation is mainly atropine sensitive. However, in the functionally disturbed bladder, part of the bladder contraction is atropine resistant, a finding that may have clinical implications.

Adolescent↗
PubMed1993

Atropine for the treatment of biliary tract pain: a double-blind, placebo-controlled trial.

STUDY OBJECTIVE: To compare the efficacy of IM atropine with placebo for the treatment of pain caused by biliary tract disease. DESIGN: Prospective randomized, double-blind, crossover study. SETTING: Emergency departments of a university medical center and affiliated county hospital. PARTICIPANTS: Fifty-five adults with biliary tract disease. INTERVENTIONS: Subjects were randomized to receive either 0.6 mg (0.5 mL) IM atropine or normal saline placebo in a double-blinded manner. If pain relief with the initial injection was inadequate, patients received the alternate injection. Pain was assessed by visual analog scale (0 to 100 mm) before the initial injection and 30 to 40 minutes after each subsequent injection. MEASUREMENTS AND MAIN RESULTS: Relief of pain was complete after the initial injection in four of 28 (14%) who received atropine and four of 27 (15%) who received normal saline (P = .956). For subjects who received both injections, atropine and placebo resulted in similar pain relief (-12.0 mm versus -16.0 mm; P = .316). There also was no difference in pain relief between atropine and placebo for the subset of patients with biliary colic receiving both injections (-15.2 mm versus -17.0 mm; P = .658). This study had more than 80% power to detect a 7.5-mm difference in pain relief between atropine and placebo in all patients with biliary tract disease and a 12.5-mm difference in those with biliary colic. CONCLUSION: Atropine is no better than placebo in the treatment of biliary tract pain.

Adult↗
PubMed1987

Canine cardiovascular responses to endotracheally and intravenously administered atropine, isoproterenol, and propranolol.

This study compared canine cardiovascular responses observed after endotracheally administered atropine, isoproterenol, and propranolol to those observed following IV administration. Acetylcholine and isoproterenol dose response curves for arterial pressures and heart rate were established following IV boluses of each drug. Once the dose response curves were established, atropine and propranolol were administered endotracheally and intravenously in different groups to alter the established dose response curves. The time required for endotracheally and intravenously administered atropine and propranolol to inhibit 50% of the mean arterial pressure response following an IV infusion of acetylcholine and isoproterenol, respectively, was determined. Atropine and propranolol administered by either route significantly altered the arterial pressure response to acetylcholine and isoproterenol (P less than .05), respectively. Atropine altered the heart rate response to acetylcholine when administered by either route (P less than .05). IV-administered propranolol altered the heart rate response to isoproterenol (P less than .05); endotracheally administered propranolol did not. Atropine administered IV inhibited 50% of the mean arterial pressure response during an acetylcholine infusion within 21 seconds, and within 48 seconds following endotracheal administration. Propranolol administered intravenously inhibited 50% of the mean arterial pressure response during an isoproterenol infusion within 23 seconds, and within 49 seconds following endotracheal administration. The arterial pressure and heart rate responses immediately following endotracheally and intravenously administered isoproterenol also were measured and compared. The arterial pressure and heart rate responses after endotracheally administered isoproterenol were much less than those following IV administration (P less than .005). In dogs the pharmacological effects following endotracheally and intravenously administered atropine and propranolol are similar, while the effects of endotracheally and intravenously administered isoproterenol differ greatly.

Animals↗
PubMedDate not supplied

Atropine-induced gastrointestinal cytoprotection dependences to the intact of vagal nerve against indomethacin-induced gastrointestinal mucosal and microvascular damage in rats.

UNLABELLED: The non-steroidal antiinflammatory drugs, such as an indomethacin (IND), cause mucosal ulceration and increase the mucosal vascular permeability in the gastrointestinal (GI) tract. Some exogenous agents, e.g. the atropine, can protect the GI mucosa against these ulcerogenic effects. The gastrointestinal functions and mucosal protection, however, are regulated by the vagal nerve. The aims of this study was to examine the dependence of atropine-induced GI cytoprotection to the vagal innervation against the development of IND-caused ulcers and microvascular damage in the mucosa of stomach and small intestine in rats. METHODS: the observations were carried out on CFY-strain rats. The mucosal damage was produced by subcutaneous administration of IND in a 20 mg/kg dose 24 h prior to the killing of animals at the same time as the start of atropine-application, which was given in a small dose (0.1 mg/kg) every 5 h. The subdiaphragmatic bilateral surgical vagotomy was done 24 h before the experiment. The vascular permeability, indicated by the microvascular endothel damage, was measured by the appearance and concentration of intravenously administered Evans blue into the GI mucosa. The number and severity of mucosal lesions and the Evans blue content of mucosa were determined in the stomach and small intestine. RESULTS: (1) The IND caused mucosal ulcers and Evans blue extravasation into the mucosa of the stomach and small intestine. (2) The IND-induced mucosal ulceration and vascular permeability significantly decreased after atropine-administration in the same parts of GI tract. (3) The extent of cytoprotective effect of atropine against the IND was decreased after bilateral surgical vagotomy. CONCLUSIONS: (1) The IND causes microvascular endothel damage in the stomach and small intestinal. (2) The atropine has a cytoprotective effect in the stomach and small intestine against the aggressive effects of IND without decrease of gastric acid secretion. (3) The intact vagal nerve is necessary to the function of cytoprotective mechanisms of atropine against the IND.

Animals↗
PubMed2001

Atropine prevents midazolam-induced core hypothermia in elderly patients.

STUDY OBJECTIVE: To test the hypothesis that core temperature is well preserved when atropine and midazolam are combined. DESIGN: Randomized, blinded study. SETTING: Department of Anesthesia, Yamanashi Medical University. PATIENTS: 40 elderly, ASA physical status I and II patients (aged more than 60 years). INTERVENTIONS: Patients were randomly assigned (n = 10 per group) to premedication with: 1) saline control; 2) midazolam 0.05 mg/kg; 3) atropine 0.01 mg/kg; and 4) midazolam 0.05 mg/kg combined with atropine 0.01 mg/kg. All premedication was given on the ward at approximately 8:30 am, approximately 30 minutes before induction of anesthesia. MEASUREMENTS AND MAIN RESULTS: Core temperatures were measured at the right tympanic membrane. Mean skin temperature was calculated as 0.3 x (T(chest) + T(arm)) + 0.2 x (T(thigh) + T(calf)). Fingertip perfusion was evaluated using forearm minus fingertip and calf minus toe, skin-surface temperature gradients. Temperatures were evaluated at the time of premedication and 30 minutes later, just before induction of anesthesia. Core temperature remained nearly constant in the control patients (0.1 +/- 0.2 degrees C; mean +/- SD), whereas it decreased significantly in the patients given midazolam alone (-0.3 +/- 0.1 degrees C). Atropine alone increased core temperature (0.3 +/- 0.2 degrees C), although the increase was not statistically significant. The combination of midazolam and atropine attenuated the hypothermia induced by midazolam alone (0.0 +/- 0.2 degrees C). Initial skin-temperature gradients exceeded 0 degrees C in all groups, indicating that the patients were vasoconstricted. The gradients were unchanged by premedication with saline or atropine. Midazolam significantly decreased the gradient (-1.8 +/- 1.1 degrees C), as did the combination of midazolam and atropine (-1.4 +/- 0.9 degrees C). CONCLUSIONS: The thermoregulatory effects of benzodiazepine receptor agonist and cholinergic inhibitors oppose each other, and the combination leaves core temperature unchanged.

Aged↗
PubMed2003

Effects of atropine on plasma amino acid profiles and on the synthesis of individual milk proteins in dairy cows fed with pasture.

Effects of atropine on blood plasma amino acid profile and on the yields and concentration of milk components were investigated in 12 Friesian cows in early lactation. Cows were housed indoors and fed with cut pasture ad libitum. Each cow received four treatments over 12 d during a replicated 4 x 4 Latin square experiment. Treatments were: control (saline); low dose (L; 30 microg atropine/kg body weight (BW)); medium dose (M; 40 microg atropine/kg BW); and 2 x L dose, 2 h apart (2 x L). On each of four treatment days, cows were milked at about 7.00, after which treatments were administered by subcutaneous injection. Cows were milked again at 2 h, 6 h and 10 h after injection. Milk samples were collected at each milking. Immediately after the 2 h milking, blood samples were drawn from each cow and the second injection was given for the 2 x L treatment. Atropine reduced hourly milk yield, and concentrations and hourly yields of total protein, casein, whey protein, alpha-casein, beta-casein, kappa-casein, beta-lactoglobulin and alpha-lactalbumin, but by differing amounts. Milk concentrations of bovine serum albumin and immunoglobulin G were increased by atropine, and overall yields of these proteins were mostly unchanged. Atropine lowered concentrations of most, but not all, amino acids in blood plasma, with essential amino acids reduced more than non-essential amino acids. Concentrations of alpha-amino N in whole blood, and glucose and insulin in blood plasma, fell after atropine injection. There was no difference between the L and M doses of atropine, but the 2 x L dose had greater effects on milk composition than the single doses. For yields of milk and milk components, the effect of the 2 x L dose was also more persistent. The results highlight the differential synthesis of individual milk proteins, and suggest that atropine might be useful for evaluating the mechanisms regulating milk protein composition.

Amino Acids↗
PubMed2001

Differential effects of atropine and isoproterenol on inducibility of atrioventricular nodal reentrant tachycardia.

BACKGROUND: Radiofrequency ablation of the "slow pathway" in atrioventricular nodal reentrant tachycardia (AVNRT) relies on tachycardia non-inducibility after ablation as success criterion. However, AVNRT is frequently non-inducible at baseline. Thus, autonomic enhancement using either atropine or isoproterenol is frequently used for arrhythmia induction before ablation. METHODS: 80 patients (57 women, 23 men, age 50+/-14 years) undergoing slow pathway ablation for recurrent AVNRT were randomized to receive either 0.01 mg/kg atropine or 0.5-1.0 microg/kg/min isoproterenol before ablation after baseline assessment of AV conduction. The effects of either drug on ante- and retrograde conduction was assessed by measuring sinus cycle length, PR and AH interval, antegrade and retrograde Wenckebach cycle length (WBCL), antegrade effective refractory period (ERP) of slow and fast pathway and maximal stimulus-to-H interval during slow and fast pathway conduction. RESULTS: Inducibility of AVNRT at baseline was not different between patients randomized to atropine (73%) and isoproterenol (58%) but was reduced after atropine (45%) compared to isoproterenol (93%, P<0.001). Of the 28 patients non-inducible at baseline isoproterenol rendered AVNRT inducible in 21, atropine in 4 patients. Dual AV nodal pathway physiology was present in 88% before and 50% after atropine compared to 83% before and 73% after isoproterenol. Whereas both drugs exerted similar effects on ante- and retrograde fast pathway conduction maximal SH interval during slow pathway conduction was significantly shorter after isoproterenol (300+/-48 ms vs. 374+/-113 ms, P=0.012). CONCLUSION: Isoproterenol yields higher AVNRT inducibility than atropine in patients non-inducible at baseline. This may be caused by a more pronounced effect on antegrade slow pathway conduction.

Adult↗
PubMed1985

Previous experience disrupts atropine-induced stereotyped "trapping" in rats.

Three experiments were conducted to investigate the phenomenon of atropine-induced stereotypic trapping in rats reported by Schallert, De Ryck, and Teitelbaum (1980). The first two showed that such trapping was disrupted by previous experience with the specific trapping task or the test context alone. The third showed that, in response to the test context, specific behaviors were altered in rats experienced with the context. Inexperienced atropine-treated animals moved slowly and showed a strong thigmotaxis to surfaces with the body and particularly the snout. The hindquarters did not cooperate well with the movements of the forequarters. In contrast, atropine-treated animals familiar with the context moved with medium-speed, coordinated movements, were independent of surface contact with body and snout, and the hindquarters cooperated fully with forequarter movements. These reactions of drugged animals were exaggerated forms of those of undrugged animals to the unfamiliar and familiar context, respectively. Thus, atropine enhances the reactions of the rat to both a novel and a familiar environment. The enhanced reactions to a novel environment appear as stereotyped behaviors that trap the animal in particular configurations of surfaces. The enhanced reactions to a familiar environment abolish the stereotypic trapping normally produced by atropine. This pattern of results indicates that it is not atropine per se that leads to trapping. Rather, stereotypic trapping develops as a consequence of an interaction between the adaptive responses of the rat to a novel environment and atropine.

Animals↗
PubMed1988

Systemic absorption of topically applied ocular atropine.

We quantitated atropine plasma levels and monitored blood pressure, heart rate, and salivary secretion after ocular application. Eight patients received 40 microliters 1% atropine in the lower cul-de-sac of one eye in connection with ocular surgery. Atropine plasma levels were determined for 90 minutes by radioreceptor assay. The peak plasma atropine concentration of 860 +/- 402 pg/ml was reached within 8 minutes in all patients. The ocular absorption of atropine was at least as rapid as that reported for intramuscular administration. Ocular atropine did not affect patients' blood pressure or heart rate when compared with those of the placebo group. Thirty minutes after administration of atropine eyedrops, the salivary secretion in the experimental group was reduced, but was statistically insignificant from the placebo group.

Adult↗
PubMed2003

Interactions of atropine with heterologously expressed and native alpha 3 subunit-containing nicotinic acetylcholine receptors.

(1) Atropine, a classical muscarinic antagonist, has been reported previously to inhibit neuronal nicotinic acetylcholine receptors (nAChRs). In the present study, the action of atropine has been examined on alpha3beta4 receptors expressed heterologously in Xenopus oocytes and native nAChRs in medial habenula neurons. (2) At concentrations of atropine often used to inhibit muscarinic receptors (1 micro M), responses induced by near-maximal nicotine concentrations (100 micro M) at negative holding potentials (-65 mV) are inhibited (14-30%) in a reversible manner in both alpha4 and alpha3 subunit-containing heteromeric nAChRs. Half-maximal effective concentrations (IC(50) values) for atropine inhibition are similar for the four classes of heteromeric receptors studied (4-13 micro M). (3) For alpha3beta4 nAChRs in oocytes, inhibition by atropine (10 micro M) is not overcome at higher concentrations of agonist, and is increased with membrane hyperpolarization. These results are consistent with non-competitive antagonism--possibly ion channel block. (4) At low concentrations of both nicotine (10 micro M) and atropine (<10 micro M), potentiation ( approximately 25%) of alpha3beta4 nAChR responses in oocytes is observed. The relative balance between potentiation and inhibition is dependent upon membrane potential. (5) In rat medial habenula (MHb) neurons, atropine (0.3-3.0 micro M) inhibited nicotine-induced responses in both a concentration and membrane potential-dependent manner (at -40 mV, IC(50)=4 micro M), similar to the effects on alpha3beta4-nAChRs in oocytes. However, unlike heterologously expressed receptors, potentiation was barely detectable at depolarized membrane potentials using low concentrations of nicotine (3-10 micro M). Conversely, the weak agonist, choline (1-3 mM) was observed to augment responses of MHb nAChRs.

Animals↗
PubMed1998

Safety and utility of atropine addition during dobutamine stress echocardiography for the assessment of viable myocardium in patients with severe left ventricular dysfunction.

OBJECTIVE: To assess the feasibility safety and side effects of the addition of atropine to dobutamine stress echocardiography for the detection of viable myocardium in patients with left ventricular dysfunction (ejection fraction < or = 35%) prior to coronary revascularization. BACKGROUND: The assessment of viable and/or ischaemic myocardium has high prognostic value as regards improvement of function and survival after coronary revascularization. The addition of atropine to dobutamine during echocardiographic testing for the presence of viable myocardium is not common practice. Consequently, no data exist on the safety and additional diagnostic value of this practice. METHODS: Two hundred patients with left ventricular ejection fraction < or = 35% were studied. RESULTS: Test end-points were: target heart rate in 164 (82%) of the patients, severe angina in 18 (9%), maximum dobutamine-atropine dose in six (3%), severe ST segment changes in five (2%), cardiac arrhythmias in four (2%), and hypotension in three (1%). Viability could be assessed echocardiogaphically in 105/200 (53%) from a biphasic response (improvement of wall motion with low dose dobutamine and worsening with high dose), in 93 from ischaemia and in 12 from sustained or late improvements. In 36/105 (34%) patients, ischaemic myocardium could only be assessed after the addition of atropine. Cardiac arrhythmias occurred in 11/200 (6%) and hypotension (decrease of systolic blood pressure >30 mmHg) in 21/200 (11%). Neither the use of atropine nor the induction of ischaemia were associated with an increased incidence of cardiac arrhythmias or hypotension. CONCLUSIONS: In a large group of patients with severe left ventricular dysfunction, dobutamine stress echocardiography is feasible and safe in 186/200 (93%); the addition of atropine was necessary in 34% to assess myocardial viability. Hypotension and cardiac arrhythmias were the most frequent side effects, but were not related to the induction of ischaemia or addition of atropine.

Adult↗
PubMed1999

The effect of atropine in vasovagal syncope induced by head-up tilt testing.

AIMS: This single-blinded, randomized, placebo-controlled study was designed and undertaken to assess the efficacy of intravenous atropine administration on haemodynamic impairment induced by head-up tilt testing in patients with vasovagal syncope. METHODS AND RESULTS: One hundred and thirteen consecutive patients (62 male and 51 female, mean age 46.3 years) with recurrent syncope, no evidence of cardiac, neurological or metabolic disease and a positive head-up tilt test were included in the study. Within 2 weeks of the first head-up tilt test all patients underwent a second tilt test. During this second test, all patients were randomized to receive a bolus of either atropine (0.02 mg. kg(-1)) or placebo (isotonic saline solution). The administration of atropine or placebo was performed at the onset of the haemodynamic modifications (heart rate and/or blood pressure fall) in conjunction with typical vasovagal prodromal symptoms. Treatment was taken as effective when symptoms aborted and the test was completed. In 29 of 113 patients the second tilt test was negative and these patients were excluded from final data analysis. Forty-one patients received placebo, which was effective in nine cases (21.9%). Atropine was administered to 43 patients and was effective in 30 cases (69.7%, P<0.01 vs placebo). The effects of treatment were analysed further to consider the haemodynamic patterns of tilt-induced vasovagal reflex. In the cardio-inhibitory form, placebo was never effective (15 cases), while atropine was effective in 15 of 18 cases (83.3%, P<0.001 vs placebo). In the vasodepressor form, placebo was effective in nine of 26 patients (34.6%), while atropine was effective in 15 of 25 cases (60.0%, no significant difference vs placebo). CONCLUSIONS: Atropine is fully effective in the cardio-inhibitory form of tilt-induced vasovagal reflex, but is limited in the vasodepressor form.

Atropine↗
PubMed2003

Rapid atropine synthesis for the treatment of massive nerve agent exposure.

STUDY OBJECTIVE: We developed and tested a protocol for compounding a large volume of injectable atropine from powder. The resulting protocol could be used by hospitals to rapidly use large amounts of stockpiled atropine. METHODS: The protocol required 2 g of solid (powdered) atropine and 1 L of normal saline solution. The solution was filtered and mixed. One hundred syringes were filled by using a standard syringe-batching system. Modifications, including hand filling, were studied to reduce the time required to synthesize one hundred 3-mL syringes. RESULTS: A single pharmacist was able to reconstitute one hundred 6-mg atropine syringes in 29 minutes using the batching system. The quickest method for a single pharmacist filling syringes by hand was 34 minutes. The cost to the hospital for 5 g of powdered atropine was 11 dollars versus 5,000 dollars for prefilled syringes. CONCLUSION: Large quantities of atropine syringes can be compounded from a powdered form in a timely manner. Additionally, there is a significant cost advantage to using powdered atropine as a hospital stockpile.

Antidotes↗
PubMed2006

Civilian adult self injections of atropine-trimedoxime (TMB4) auto-injectors.

INTRODUCTION: The clinical effects of self injections of atropine-trimedoxime auto-injectors distributed to the civilian population as a field antidote for nerve agent attack were assessed. METHODS: Data on self injections by adults (> or = 18 years) were collected from the Israel Poison Information Center and a hospital Emergency Department's records during a 2-year period. The data included demographics, time interval from injection, type of auto-injector, clinical manifestations and atropinization score. RESULTS: Sixty-five patients, all with unintentional self injections, were reported. Systemic atropine effects were observed in 24 patients, but no severe atropinization. The atropinization score was significantly higher in the 2 mg atropine dose group than in the two lower dose groups, which were in the normal range. No specific adverse effects attributable to trimedoxime were observed. Intravenous fluids and physostigmine were not required. CONCLUSION: Only mild reactions were observed following self-injection of atropine trimedoxime auto-injectors in adults, attesting to their relative safety under these conditions.

Accidents↗