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PubMedDate not supplied

Effects of atropine on refractive development, dopamine release, and slow retinal potentials in the chick.

Atropine has previously been found to suppress visually induced myopia both in animals and humans. The mechanism of its action is unclear. We have studied its retinal effects in an in vitro preparation, using the retina-pigment epithelium-choroid complex of the chick eye. In vivo, deprivation myopia was induced by translucent goggles. Atropine solution was injected into the vitreous at two-day intervals. Dopamine release from the retina following atropine injection in vivo and from the in vitro retina preparation was quantified by HPLC-EC. In vitro preparations of the isolated chick retina-pigment epithelium-choroid were superfused with atropine. Light-induced potentials (local ERG), slow standing potentials from the retinal pigment epithelium/neural retina, and extracellular potassium concentrations were recorded. In line with previous findings, intravitreal injections of atropine (25 microg, 250 microg) reduced deprivation myopia in a dose-dependent manner. Atropine increased the release of the neurotransmitter dopamine into the superfusate in vitro at 100-500 microM and into the vitreous in vivo at 250 microg. Before an increase was measured in the vitreous, the retinal dopamine content was elevated. In concentrations equivalent to the intravitreal concentration to suppress myopia in vivo (200-800 microM), atropine induced spreading depression (SD) in the in vitro preparation. In contrast, muscarinic agonists, acetylcholine and pilocarpine, did not induce SD. Atropine reduced the ERG b- and d-wave, led to damped oscillations of RPE potentials, and reversed the ERG c-wave. Atropine suppressed myopia only at doses at which severe nonspecific side effects were observed in the retina. Atropine seems to intrude massively into the vital functions of the retina as indicated by the occurrence of SD. We conclude that atropine, by inducing SD, boosts neurotransmitter release from cellular stores, which may cancel out a presumed retinal signal that controls eye growth and through this, myopia.

Acetylcholine↗
PubMed2000

Safety and prognostic value of early dobutamine-atropine stress echocardiography in patients with spontaneous chest pain and a non-diagnostic electrocardiogram.

AIMS: To risk stratify and shorten hospital stay in patients with spontaneous (resting) chest pain and a non-diagnostic electrocardiogram (ECG). METHODS AND RESULTS: The study comprised 102 patients (mean age 58+/-12 years, 67 men) with spontaneous chest pain and a non-diagnostic ECG. Forty-three patients had suspected coronary artery disease and 59 had known (but of unknown actual significance) coronary artery disease. All patients underwent serial creatine kinase enzyme measurements, continuous ECG monitoring for at least 12 h and early dobutamine-atropine stress echocardiography in patients with negative creatine kinase enzymes and normal findings at ECG monitoring. Dobutamine-atropine stress echocardiography was considered positive in patients with new or worsening wall thickening abnormalities. Patients with negative dobutamine-atropine stress echocardiography were discharged after the test. In-hospital and 6 month follow-up events noted were cardiac death, non-fatal myocardial infarction, unstable angina, and coronary artery bypass surgery or angioplasty. Thirteen patients had evidence of evolving myocardial infarction by elevated creatine kinase enzymes, or unstable angina by ECG monitoring. In the remaining 89 patients, dobutamine-atropine stress echocardiography was performed after a median observation period of 31 h (range 12-68 h). During dobutamine-atropine stress echocardiography no serious complications (death, non-fatal myocardial infarction, sustained ventricular tachycardia or ventricular fibrillation) occurred. Dobutamine-atropine stress echocardiography results were of poor quality in three, non-diagnostic in six, negative in 44 and positive in 36 patients. In the 80 patients with diagnostic dobutamine-atropine stress echocardiography, variables associated with in-hospital events (n=7) were history of exertional angina (P<0. 005), chest pain score (P<0.005), stress-induced angina (P<0.001) and positive dobutamine-atropine stress echocardiography (P<0.005). Variables associated with follow-up events (n=11) were history of exertional angina (P<0.05), chest pain score (P<0.001), stress-induced angina (P<0.01) and positive dobutamine-atropine stress echocardiography (P<0.01). At multivariate analysis the only significant predictor of events was positive dobutamine-atropine stress echocardiography (P<0.01). CONCLUSION: Early dobutamine-atropine stress echocardiography may safely distinguish between low- and high-risk subsets for subsequent cardiac events in patients with spontaneous chest pain and a non-diagnostic ECG.

Atropine↗
PubMed1997

Effects of antianginal therapy with a calcium antagonist and nitrates on dobutamine-atropine stress echocardiography. Comparison with exercise electrocardiography.

BACKGROUND: Anti-ischaemic therapy with nitrates and/or calcium channel blockers profoundly affects the results of pharmacological stress echocardiography with coronary vasodilators but the influence on catecholamine stress testing remains unsettled. AIMS: The present study aimed to assess the effects of non-beta-blocker antianginal therapy on dobutamine (up to 40 micrograms.kg-1.min-1)-atropine (up to 1 mg) stress. echo-cardiography and to evaluate whether drug-induced changes in the dobutamine atropine stress echocardiography response may predict variations in exercise tolerance. METHODS: Twenty six patients with angiographically assessed coronary artery disease (seven patients with single-, 10 with double-, and nine with triple-vessel disease) performed a dobutamine atropine stress echocardiography and an exercise electrocardiography test in random order both off and on antianginal drugs (nitrates and calcium antagonists). In doubtamine-atropine stress echocardiography, we evaluated: dobutamine time (i.e. the time from initiation of the dobutamine infusion to obvious dyssynergy), wall motion score index (in a 16-segment model of the left ventricle, each segment ranging from 1 = normal, to 4 = dyskinetic), and rate-pressure product at peak stress. RESULTS: Dobutamine-atropine stress echocardiography positivity occurred in 26 out of 26 patients off and in 23 patients on therapy (100 vs 88%, P = ns). Atropine coadministration was needed to evoke echo positivity in no patient off and in five out of 26 on therapy (0 vs 19% P < 0.01). The achieved rate pressure product during dobutamine-atropine stress echocardiography was comparable on and off therapy (17 +/- 4 vs 19 +/- 5 x 10(3) mmHg x heart rate. min-1, P = ns). Therapy induced an increase in dobutamine time (on = 16 +/- 3 vs of = 13 +/- 3 min, P < 0.01) and a decrease in peak wall motion score index (on = 1.3 +/- 0.2 vs off = 1.5 +/- 0.3, P < 0.01). The therapy induced changes in exercise time during the exercise electrocardiography test were not significantly correlated to dobutamine-atropine stress echocardiography variations in either dobutamine time (r = 0.07, P = ns), or peak rate pressure product (r = 0.24, P = ns), or peak wall motion score index (r = 0.02, P = ns). CONCLUSIONS: (1) non-beta-blocker antianginal therapy only modestly reduces dobutamine-atropine stress echocardiography sensitivity, although atropine coadministration is more often required to reach stress echo positivity under therapy; (2) therapy reduces the severity of dobutamine atropine stress echocardiography ischaemia stratified in the time and space domain, but these changes are only poorly correlated to variations in exercise tolerance.

Atropine↗
PubMed1991

Dose-response for atropine and heart rate in infants and children anesthetized with halothane and nitrous oxide.

The dose recommendations for atropine in anesthetized children vary, and the dose-response for heart rate has not been defined. We determined the dose-response for atropine and heart rate in 181 healthy children anesthetized with halothane and nitrous oxide. After induction of anesthesia, atropine in a dose of 5, 10, 20, 30, or 40 micrograms.kg-1 was administered by rapid intravenous infusion of each subject. The effects of atropine on heart rate, heart rhythm, and systolic blood pressure were compared among dosage groups, and a dose-response curve for peak heart rate was constructed. The effects of atropine were compared also between younger and older subjects. For the group of all 181 subjects, atropine increased heart rate in a dose-related manner up to 30 micrograms.kg-1. Fifty percent maximal response corresponded to 9 micrograms.kg-1, and 90% maximal response corresponded to 26 micrograms.kg-1. Some subjects had nonsinus supraventricular rhythms before atropine, but none had nonsinus rhythm after atropine except after the smallest dose, 5 micrograms.kg-1. Systolic blood pressure increased significantly after all doses of atropine except 5 mu.kg-1. Subjects less than 6 months old had higher control and peak heart rates than did subjects greater than or equal to 2 yr old, but the older subjects had greater change in heart rate after atropine. For subjects greater than or equal to 2 yr old, all doses of atropine produced a significant increase in heart rate. The same was true for younger subjects, less than 6 months old, except that 5 micrograms.kg-1 did not increase heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1996

Management and ultrasonographic appearance of infantile hypertrophic pyloric stenosis with intravenous atropine sulfate.

Some infants with hypertrophic pyloric stenosis (HPS) have responded to oral atropine treatment. To achieve sufficient effect of atropine, it must be administered intravenously (i.v.). Therefore, with ultrasonography, we studied the changes in the pyloric muscle in HPS during and after intravenous administration of atropine. Twenty-three infants were studied. Atropine sulfate was initially administered at a dose of 0.04 mg/kg day i.v., and the dose was increased by 0.01 mg/kg/day until vomiting ceased. When vomiting ceased after administration of intravenous atropine sulfate, the infants received oral atropine sulfate at twice the effective intravenous dose; this was continued for 2 weeks. Ultrasonography was repeated until pyloric muscles normalized. Twenty-two infants were free from vomiting after 1-8 days of intravenous atropine sulfate (dosages of 0.04-0.11 mg/kg/day). In 21 infants, weight gain continued after atropine treatment even though no change in thickness of the pyloric muscles was demonstrated ultrasonographically. Only 2 infants required pyloromyotomy because of prolonged treatment or a mistake in underdosing of oral atropine. All of the 21 infants who recovered after intravenous atropine without surgery had normalization of pyloric muscle caliber, as shown by ultrasonography 4-12 months after treatment. Atropine is an effective medicine for HPS. Regression of pyloric thickening after vomiting has been controlled implies that pyloric muscle hypertrophy could be worsened by the spasm that occurs in HPS.

Administration, Oral↗
PubMed1990

Investigation into atropine-induced antinociception.

1. The effect of atropine on the nociceptive system was examined in mice and rats by use of the hot-plate, writhing and tail-flick tests. 2. Atropine dose-dependently produced analgesia, no effect and hyperalgesia. Analgesia was observed in both species with doses ranging from 1 to 100 micrograms kg-1 while hyperalgesia was obtained with 5 mg kg-1. 3. Atropine antinociception was prevented by pirenzepine (0.1 microgram per mouse, i.c.v.), dicyclomine (10 mg kg-1, i.p.), atropine-methylbromide (0.5 microgram per mouse, i.c.v.) and hemicholinium-3 (1 microgram per mouse, i.c.v.). Naloxone (1 mg kg-1, i.p.), alpha-methyl-p-tyrosine (100 mg kg-1, s.c.) and reserpine (2 mg kg-1, i.p.) were ineffective. 4. The site of atropine analgesia is in the CNS since it exerts its antinociceptive effect also when injected i.c.v. (1-10 ng per mouse). Moreover drugs which do not cross the blood-brain barrier, such as hemicholinium-3, pirenzepine and atropine methylbromide, were unable to antagonize atropine analgesia if administered i.p. 5. Atropine also in vitro, showed a biphasic action on electrically-evoked guinea-pig ileum contractions. Concentrations between 10(-14) and 10(-12) M increased electrically and nicotine-evoked contractions but did not affect acetylcholine- and oxotremorine-evoked contractions. Concentrations above 10(-9) M inhibited both electrically- and drug (acetylcholine, nicotine and oxotremorine)-evoked contractions while they were ineffective on unstimulated ileum. 6. On the basis of the above findings, amplification of cholinergic transmission by very low doses of atropine is postulated, through a selective blockade of presynaptic muscarinic autoreceptors, as the likely mechanism of action. 7. Atropine antinociception, unlike oxotremorine antinociception, was obtained without any impairment of mouse rota-rod performance. 8. The antagonism by pirenzepine and dicyclomine of oxotremorine and atropine antinociception suggests that M1 muscarinic receptor subtypes are responsible for cholinergic analgesia.

Analgesics↗
PubMed1983

Kinetic analysis of atropine-induced alterations in bullfrog ganglionic fast synaptic currents.

The concentration- and voltage-dependent effects of atropine on the fast excitatory post-synaptic current (e.p.s.c.) of bullfrog sympathetic ganglion cells have been analysed and fitted to a kinetic scheme of open-channel blockade. Atropine (1-75 microM) reduced the peak e.p.s.c. amplitude without altering the quantal content or the reversal potential. The e.p.s.c. decay was complex in the presence of atropine, being well fitted by two exponential components. With increasing concentrations of atropine the time constant of the fast component, tau 2, decreased and the time constant of the slow component, tau 1, increased. Over the voltage range -30 to -100 mV tau 2 exhibited little or no voltage dependence and tau 1 increased with hyperpolarization. The amount of charge moved during the e.p.s.c. was reduced as a function of atropine concentration. Driving functions, which represented the rate of channel opening, were derived from e.p.s.c.s both from control and atropine-treated cells. The characteristics of the driving functions did not vary with membrane voltage, but the driving functions were shorter in duration from atropine-treated than control cells. The area under the driving function decreased as a function of atropine concentration. The decay time constants and the amplitude ratio of the exponential components were used to calculate the closing, blocking, and unblocking rate constants, alpha, G, and F. alpha and F remained constant with increasing atropine concentration, but G declined significantly. The voltage dependence of the equilibrium constant, G/F, implied that the transient blocking site for atropine is halfway through the ionic channel. The sequential model does not predict the concentration-dependent decrease in the blocking rate, G, or in the charge moved during an e.p.s.c. We conclude that atropine has an action more complex than simple channel blockade in sympathetic ganglion cells.

Animals↗
PubMed2007

Atropine pretreatment enhances airway hyperreactivity in antigen-challenged guinea pigs through an eosinophil-dependent mechanism.

Airway hyperreactivity in antigen-challenged animals is mediated by eosinophil major basic protein (MBP) that blocks inhibitory M(2) muscarinic receptors on parasympathetic nerves, increasing acetylcholine release onto M(3) muscarinic receptors on airway smooth muscle. Acutely, anticholinergics block hyperreactivity in antigen-challenged animals and reverse asthma exacerbations in the human, but are less effective in chronic asthma. We tested whether atropine, given before antigen challenge, affected hyperreactivity, M(2) receptor function, eosinophil accumulation, and activation. Sensitized guinea pigs received atropine (1 mg/kg ip) 1 h before challenge and 6 h later. Twenty-four hours after challenge, animals were anesthetized, vagotomized, paralyzed, and ventilated. Airway reactivity to electrical stimulation of the vagi and to intravenous acetylcholine was not altered by atropine pretreatment in nonsensitized animals, indicating that atropine was no longer blocking postjunctional muscarinic receptors. Antigen challenge induced airway hyperreactivity to vagal stimulation that was significantly potentiated by atropine pretreatment. Bronchoconstriction induced by acetylcholine was not changed by antigen challenge or by atropine pretreatment. M(2) receptor function was lost in challenged animals but protected by atropine pretreatment. Eosinophils in bronchoalveolar lavage and within airway tissues were significantly increased by challenge but significantly reduced by atropine pretreatment. However, extracellular MBP in challenged airways was significantly increased by atropine pretreatment, which may account for reduced eosinophils. Depleting eosinophils with antibody to IL-5 before challenge prevented hyperreactivity and significantly reduced MBP in airways of atropine-pretreated animals. Thus atropine pretreatment potentiated airway hyperreactivity by increasing eosinophil activation and degranulation. These data suggest that anticholinergics enhance eosinophil interactions with airway nerves.

Animals↗
PubMed1983

Effect of route of atropine delivery on bronchospasm from cold air and methacholine.

We undertook a study to determine whether the apparent disparity between the dose of inhaled atropine required to inhibit the bronchoconstriction induced by inhaled methacholine and the dose required to inhibit the bronchoconstriction induced by eucapnic hyperpnea with cold air is a function of the route of administration of atropine. In six subjects with asthma, we constructed dose-response curves to inhaled methacholine and to eucapnic hyperpnea with cold air after treatment with inhaled atropine (0.5 mg delivered) and intravenous placebo, with inhaled placebo and intravenous atropine (0.5 mg injected), and with inhaled and intravenous placebos. Atropine by either route shifted the dose-response curves to both cold air and to methacholine to the right. In every subject, however, inhaled atropine caused a markedly greater rightward shift of the inhaled methacholine dose-response curve than did intravenous atropine, whereas inhaled and intravenous atropine had similar effects on the cold air dose-response curve. These findings suggest that the apparent disparity between the doses of atropine required to inhibit methacholine- and cold air-induced bronchoconstriction may be a function of the route of administration of atropine and thus does not imply a nonmuscarinic action of atropine. The findings support the view that cold air causes bronchoconstriction via muscarinic pathways.

Adult↗
PubMed2006

Effect of intravenous atropine on treadmill stress test results in patients with poor exercise capacity or chronotropic incompetence.

OBJECTIVE: Exercise stress test (EST) is one of the main diagnostic and prognostic tests for ischemic heart disease. However, its usefulness depends on achieving target heart rate, then chronotropic incompetence and poor exercise capacity limits its utility. We evaluated the usefulness of atropine administration during the EST to decrease the number of tests with inconclusive results in these patients. METHODS: We carried out this study in Shahid Madani Heart Center, Tabriz, Iran from September 2003 to December 2004 and comprised of 210 patients undergoing EST. In subjects experiencing fatigue when they achieved 50-75% of target heart rate (THR), or those who failed to achieve their THR, atropine was administered in doses of 0.5 mg per minute until the test conclusion (positive test results or target heart rate achieved) or until a maximum dose of 2 mg was administered. RESULTS: Forty-one (19.5%) of the 210 patients required atropine (mean dose: 1.1 mg) during the study. Among patients who received atropine, conclusive test was achieved in 38 cases (92.7%). Atropine administration resulted in a mean increase in heart rate of 38 beats/min (range 8-71 beat/min). Atropine injection resulted in a trend towards more positive results of EST in comparison to non-atropine group (31.7% versus 18.3%, p=0.053). There was no difference in response to atropine in subjects with chronotropic incompetence or poor exercise capacity (p=0.5). CONCLUSION: Use of atropine as an adjunct to standard EST can help decrease the number of inconclusive tests. Larger studies are necessary to define the role of atropine in EST and also to evaluate the accuracy of conclusive EST after atropine administration.

Atropine↗
PubMed1990

[The effects of a small dose of atropine upon sinus bradycardia during spinal anesthesia].

Positive or negative chronotropic effects of atropine and their magnitude are known to be determined by its dose given, concomitant sympathetic tone, and patient's age. Thus, the aim of the present study is to investigate the small effective dose of atropine for acceleration of heart rate in sedated bradycardic patients under spinal anesthesia, and to evaluate the relationship between the heart rate response to atropine and level of analgesia or patient's age. Significant increases in heart rate were observed in patients receiving intravenous atropine 4 micrograms.kg-1 (n = 21) or 6 micrograms.kg-1 (n = 35) except 2 micrograms.kg-1 (n = 18). However, there were wide variations in cardiac responses to atropine among patients in each group. Negative chronotropic responses to atropine were elicited in 10 (56%), 2 (9%), and 1 (3%) of the patients receiving 2 micrograms.kg-1, 4 micrograms.kg-1 and 6 micrograms.kg-1, respectively. Although there was no correlation between the heart rate response to each dose of atropine and the level of spinal anesthesia, the magnitude of positive chronotropic response to atropine of 6 micrograms.kg-1 related inversely with age. The present results suggest that atropine above 4 micrograms.kg-1 is required to accelerate the heart rate in most bradycardic patients under spinal anesthesia irrespective of the level of analgesia. However, it seems appropriate to administer atropine intravenously in a cumulative fashion, because of individual's variability including age in the chronotropic response to atropine.

Adult↗
PubMed1984

Varied and repeated atropine dosages and exercise-heat stress.

Comparisons of physiological responses to 0, 0.5, 1, and 2 mg atropine (IM) were made in seven males (X +/- SD: age, 24 +/- 3 years; ht, 174 +/- 12 cm; wt, 76 +/- 3 kg) while they exercised (approximately 390 W) in a hot-dry (40 degrees C, 20% rh) environment. Responses to 4 mg, as well as repeatability of responses to 2 mg, were studied in two and six of these subjects, respectively. On 8 test days an intramuscular injection of atropine or saline control was administered 20 min before subjects walked on a treadmill for two 50-min bouts. Heart rate (HR) during exercise did not change in the control trial but by min 50 increased during all atropine trials (P less than 0.01). Rectal temperature (Tre) increased (P less than 0.01) in all trials by min 50 and continued increasing (P less than 0.01) in the 2-mg trial during the second exercise bout. For the two subjects tested with all dosages (0.5 - 4 mg atropine), the change in HR and Tre between the atropine and control trials at 50 min of exercise was regressed against the various atropine dosages. The relationship (r = 0.92) for HR was curvilinear while the relationship (r = 0.99) for Tre was linear. Mean weighted skin temperature (Tsk) was relatively constant during exercise and was warmer (P less than 0.05) with increasing atropine dosage. In a repeat 2 mg trial, HR was 6 bt . min-1 lower (P less than 0.05) on the second exposure but Tre was the same (P greater than 0.05) on both days. For subjects walking in the heat, three new observations were: 1) 0.5 mg of atropine resulted in increased HR and Tsk compared to control values; 2) HR was elevated but the magnitude of change decreased with increasing dosage, while the elevation in Tre was consistent with increasing dosage; and 3) rectal temperatures (in trials with and without atropine) were unaffected by previous days of atropine administration.

Adult↗
PubMed1998

Effect of a 'vagomimetic' atropine dose on canine cardiac vagal tone and susceptibility to sudden cardiac death.

We manipulated the level of cardiac vagal tone in dogs with healed myocardial infarctions during exercise plus acute ischemia, to explore vagal involvement in the pathophysiology of sudden cardiac death. We occluded the circumflex coronary artery during the last minute of treadmill exercise in 32 dogs with healed anterior myocardial infarctions. Twenty-one dogs experienced ventricular fibrillation (susceptible) and 11 did not (resistant). On a subsequent day, we gave intravenous low-dose atropine to susceptible dogs to increase their levels of cardiac vagal tone, as estimated by moving polynomial time-series analysis of R-R interval variability (0.24-1.04 Hz). We also measured vagal responses to coronary occlusion at rest, before and after low-dose atropine. In susceptible dogs, atropine increased the average vagal tone index at rest (atropine: 7.3 +/- 0.4 versus control: 6.6 +/- 0.5 ln ms2, P < 0.01) and during maximum exercise (atropine: 2.5 +/- 0.4 versus control: 1.6 +/- 0.3 ln ms2, P < 0.01), but failed to prevent ventricular fibrillation actually decreased from 63 +/- 3 to 42 +/- 2s (P < 0.01), and R-R interval shortening elicited by coronary occlusion increased (atropine: delta -144 +/- 64 versus control: delta -55 +/- 32 ms, P < 0.01). In resting susceptible dogs, atropine significantly increased preocclusion indexes of vagal tone (atropine: 7.8 +/- 0.3 versus control: 6.9 +/- 0.4 ln ms2, P < 0.01), but did not prevent large reductions of vagal tone during ischemia (atropine: delta -4.4 +/- 0.6 versus control: delta -3.8 +/- 0.4 ln ms2, P > 0.05). We conclude that increases of resting vagal tone after low-dose atropine in dogs with healed anterior myocardial infarctions do not protect against sudden cardiac death. Quite the contrary, vagal tone is withdrawn more completely during ischemia, and the time to ventricular fibrillation during exercise plus ischemia is shortened.

Animals↗
PubMed1995

Is alpha-adrenoceptor blockade responsible for atropine flush?

Toxic amounts of atropine usually, and therapeutic doses occasionally, dilate cutaneous blood vessels, especially those in the blush area (atropine flush). However, the mechanism of this anomalous vascular response is unknown. We, therefore, investigated this action of atropine not only in functional but also in binding studies with isolated rat aorta and brain, respectively. Endothelium-denuded rat thoracic aortic rings were contracted with norepinephrine, U46619 (9,11-dideoxy-11alpha,9alpha-epoxymethanoprostaglandin F2alpha, thromboxane A2 receptor agonist) and KCl, and the relaxation in response to atropine was recorded. The norepinephrine-, but not the U46619- or KCL-mediated contraction was relaxed by atropine. Atropine caused a rightward parallel shift of the phenylephrine concentration-contraction curve with a pA2 value of 6.57 (slope 0.58), but did not affect the concentration-contraction curve for U46619. In rat cerebral cortex homogenates, atropine displaced [3H]prazosin with Ki values of 3.33 nM and 0.19 microM, respectively. These results suggest that even though atropine has low affinity for the alpha-adrenoceptor, it possesses characteristics similar to those of a competitive ligand for the alpha-adrenoceptor. Thus, atropine, especially at high concentrations, has direct alpha-adrenoceptor blocking activity, which may account, at least in part, for atropine flush.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1989

Physostigmine-insensitive behavioral excitatory effects of atropine in squirrel monkeys.

Lever press responses of squirrel monkeys were maintained under a multiple schedule in which the first response after 3 min produced either food or electric shock depending on the prevailing stimulus. Atropine sulfate (0.3-3 mg/kg, IM) given immediately before experimental sessions disrupted the temporal pattern of responding and produced dose-related decrease in rates of food- and shock-maintained responding. Increases in responding occurred when 1 mg/kg atropine was given 1 to 12 hr prior to experimental sessions. A maximal increase of 200% of control rates was seen following the 2-hr pretreatment. Qualitatively similar effects were obtained with scopolamine suggesting that the time-dependent increases may be a general consequence of muscarinic receptor blockade. Response patterning changes and response rate increases were also produced by coadministration of atropine and physostigmine both given immediately before the session. Increases in rates of responding have also been observed previously after administration of atropine with rate-decreasing doses of the direct-acting muscarinic agonist oxotremorine. Physostigmine did not reverse the rate increases or the alteration in temporal patterning produced by the 2-hr atropine pretreatment; rate decreases induced by immediate pretreatment with atropine were blocked by physostigmine. Thus, the response rate-decreasing effects of atropine were distinct from its rate-increasing effects. Whereas the rate-decreasing effects of atropine appear to involve muscarinic receptors, increases in responding may not. Such nonmuscarinic behavioral excitatory actions of atropine may be expressed when the muscarinic-related decreases are blocked by physostigmine or oxotremorine, or when the decreases are overridden by excessive nonmuscarinic stimulation, perhaps triggered by time-dependent changes in acetylcholine turnover associated with atropine.

Animals↗
PubMed2007

Intravesical atropine compared to oral oxybutynin for neurogenic detrusor overactivity: a double-blind, randomized crossover trial.

PURPOSE: We tested the efficacy and side effect profiles of intravesical atropine compared to oxybutynin immediate release when used by individuals with multiple sclerosis. MATERIALS AND METHODS: We performed a study to determine the most effective dose of atropine. Eight participants used increasing doses of intravesical atropine during a 12-day period. Bladder diary data showed that the instillation of 6 mg atropine 4 times daily was most effective for increasing bladder capacity (voided/catheter volumes). We then did a randomized, double-blind crossover trial. Participants received 14 days of treatment with oral oxybutynin or with intravesical atropine, followed by 14 days of alternative treatment. Participants recorded a bladder diary and rated side effects and quality of life. The primary outcome variable was bladder capacity. RESULTS: A total of 57 participants with multiple sclerosis completed the study. Average change in bladder capacity was higher in the atropine arm. The mean +/- SD oxybutynin change was 55.5 +/- 67.2 ml, the mean atropine change was 79.6 +/- 89.6 ml and the mean difference between arms was 24.1 ml (95% CI -0.4, 49.7; p = 0.053). Changes in incontinence events and voiding frequency were not statistically different between the arms. Changes in total side effect and dry mouth scores were significantly better in the atropine treatment arm. CONCLUSIONS: Intravesical atropine was as effective as oxybutynin immediate release for increasing bladder capacity and it was probably better with less antimuscarinic side effects. We recommend that intravesical atropine should be made available to patients with neurogenic detrusor overactivity and voiding problems requiring intermittent catheterization as an alternative to oral therapy, which often has troublesome side effects.

Administration, Intravesical↗
PubMed2003

Use of atropine in patients with chronotropic incompetence and poor exercise capacity during treadmill stress testing.

BACKGROUND: Treadmill stress testing (TMST) is a valuable diagnostic test for ischemic heart disease. However, the inability to achieve the target heart rate because of either chronotropic incompetence or poor exercise capacity is a major limitation to its utility. We evaluated the usefulness of atropine in decreasing the number of tests with inconclusive results in patients with a poor chronotropic response or exercise capacity during TMST. METHODS: The study comprised 126 patients undergoing TMST. In subjects experiencing fatigue at submaximal exercise, atropine was administered in doses of 0.5 mg per minute until the test conclusion (positive test results or target heart rate achieved) or until a maximum dose of 2 mg was administered. RESULTS: Thirty-three of the 126 patients (26%) required atropine (mean dose, 1 mg) during the study; 23 of the 33 patients (70%) proceeded to achieve their target heart rate (n = 17) or positive test results (n = 6). The mean increase in heart rate after atropine administration was 25 beats/min (range 3-53 beats/min). Atropine was required in 39% of patients receiving beta-blockers, versus 21% of patients not receiving beta-blockers (P =.02). Among patients receiving atropine, a conclusive test was achieved significantly more often in patients not receiving beta-blockers (94% vs 46%, P =.01). No adverse events were associated with the use of atropine. Atropine administration resulted in conclusive tests more often in subjects with poor chronotropic response than in subjects with poor exercise capacity (78% vs33%, P = <.001). CONCLUSION: The use of atropine as an adjunct to standard TMST can help decrease the number of inconclusive tests, even in patients taking beta-blockers. Larger studies are warranted to further define the role of atropine in diagnostic TMST.

Adrenergic beta-Antagonists↗
PubMed1998

Reduced test time by early identification of patients requiring atropine during dobutamine stress echocardiography.

In a randomized, controlled clinical trial, we evaluated the ability of an algorithm to identify, before peak stress, patients who will ultimately require atropine during dobutamine stress echocardiography. The effects of early atropine administration on test duration, atropine dose, dobutamine dose, and heart rate response also were studied. Compared with conventional atropine administration at peak dobutamine infusion, early atropine administration reduced test duration 8% (1.1 minutes, p = 0.02) and total dobutamine use 11% (0.41 mg/kg, p = 0.02) but required 90% more atropine (0.36 mg, p < 0.001). Conventional atropine administration resulted in a late, rapid rise in both heart rate and rate-pressure product. However, the heart rate and rate-pressure product curves for patients receiving early atropine paralleled those seen in patients not requiring atropine during dobutamine stress echocardiography. In conclusion, early atropine administration provides a more balanced stress and reduces test duration, thus decreasing total exposure to dobutamine and potentially increasing test efficiency.

Algorithms↗