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PubMedDate not supplied

The effects of atropine microinjections into the motor cortex of rats on the development of a motor habit.

Acetylcholine modulates the responses of motor cortex neurons during learning. Studies were carried out on the effects of atropine microinjections into the motor cortex on the development of a habit consisting of procuring food with the forelimbs in freely mobile rats. Animals received unilateral intracortical injections of atropine (5 and 15 micrograms in 0.6 microliter over 40 sec) in the forelimb representation area of the motor cortex. Rats were trained to procure food from a horizontal tube, using the forelimb contralateral to the injection site. Data were obtained which suggested that atropine has a dose-dependent effect on the development of this movement habit. The general effect of atropine doses consisted of suppressing the inhibition of concurrent movements during learning. The higher atropine concentration had a depressive effect on the initiation of the learned movement.

Animals↗

PubMed1987

Role of secretin and CCK in the stimulation of pancreatic secretion in conscious dogs. Effects of atropine and somatostatin.

The role of gut hormones, such as secretin and CCK, in the stimulation of pancreatic secretion by duodenal HCl or oleate and by meat feeding has been studied in conscious dogs before and after pretreatment with atropine and somatostatin. Plasma hormones were measured by specific and sensitive radioimmunoassays. Duodenal perfusion with HCl and oleate stimulated dose-dependently pancreatic HCO3 and protein secretion and raised plasma levels of secretin and CCK, respectively. Atropine reduced significantly both HCO3 and protein secretion but did not affect plasma secretin and CCK levels in these studies. Both exocrine pancreatic secretion and plasma secretin and CCK levels were suppressed by somatostatin. Meat feeding caused a marked pancreatic HCO3 and protein secretion accompanied by a significant increase in plasma secretin and CCK which seem to play an important role in the postprandial pancreatic stimulation. Both atropine and somatostatin reduced the pancreatic secretion induced by exogenous hormones but only somatostatin, but not atropine, significantly decreased plasma secretin and CCK responses to intestinal stimulants. We conclude that both atropine and somatostatin reduce the pancreatic responses to duodenal HCl or oleate or to meat feeding but only somatostatin is capable of suppressing the release of secretin and CCK.

Animals↗

PubMedDate not supplied

The comparison of therapeutic effects of atropine and pralidoxime on cardiac signs in rats with experimental organophosphate poisoning.

Organophosphate poisoning causes disturbances in cardiac conduction and potentially fatal severe cardiac rhythm abnormalities. This study investigated the cardiac effects of atropine and pralidoxime in the treatment of organophosphate poisoning in rats. Three groups of 10 adult male Wistar rats were anesthetized with an intraperitoneal injection of ketamine 100 mg/kg and xylazine 10 mg/kg and connected to a computerized electrocardiographic monitor. Each rat was then injected intraperitoneally with the pesticide dichlorvos 70 mg/kg. Sixty seconds after the injection, 10 rats were injected with saline, 10 with pralidoxime mesylate 20 mg/kg, and 10 with atropine 10 mg/kg. During the computerized electrocardiographic monitoring, each rat's heart rate and QT(c) intervals were recorded and analyzed as the injections were administered. The heart rates in all 3 groups did not differ before the dichlorvos was administered, nor at 60 seconds afterward, but in the atropine group, the time elapsed before the first decline in heart rate was significantly longer than that in the control group (P<.05). In addition, the interval before death was significantly longer in the atropine group than in either the control group or the pralidoxime group (P<.05 for both). The QT(c) was almost identical in each of the groups. Atropine has beneficial effects on the heart rate, prolongs the time before the heart rate declines, and delays death but has no effect on the QT(c) interval. Further research about the toxic effects of organophosphate compounds on myocardial cells is warranted.

Animals↗

PubMed1990

Atropine-induced heart rate changes: a comparison between midazolam-fentanyl-propofol-N2O and midazolam-fentanyl-thiopentone-enflurane-N2O anaesthesia.

Atropine-induced heart rate (HR) changes were studied in 19 patients (ASA physical status I) during anaesthesia-maintained predominantly with propofol-N2O or thiopentone-enflurane-N2O. Ten patients (Group A) received midazolam (0.07 mg.kg-1), fentanyl (1 microgram.kg-1), propofol (2 mg.kg-1) and succinylcholine (1 mg.kg-1). Following tracheal intubation, anaesthesia was maintained with propofol (6 mg.kg-1.hr-1), N2O (67 per cent) and O2 (33 per cent). In nine patients (Group B) thiopentone (4 mg.kg-1) was substituted for propofol and anaesthesia maintained with N2O (67 per cent) O2 (33 per cent), and enflurane (0.5 per cent inspired concentration). The study was non-randomised because Group B patients were only included if HR before administration of atropine less than 90 beats.min-1. IPPV was performed in all patients using a Manley ventilator (minute vol. 85 ml.kg-1; tidal vol. 7 ml.kg-1). Ten minutes after tracheal intubation, incremental doses of atropine (equivalent cumulative doses: 1.8, 3.6, 7.2, 14.4, 28.8 micrograms.kg-1) were administered at two-minute intervals and HR responses calculated during the last 45 sec of each intervening period. No differences were observed between the groups following 1.8 and 3.6 micrograms.kg-1 atropine, but propofol-N2O anaesthesia was associated with reduced responses (P less than 0.01) following 7.2, 14.4 and 28.8 micrograms.kg-1 atropine. These results suggest that there is a predominance of parasympathetic influences during propofol-N2O anaesthesia compared with thiopentone-enflurane-N2O anaesthesia.

Adult↗

PubMed1981

Anatomical dead space and airway resistance after glycopyrrolate or atropine premedication.

The effects of atropine and glycopyrrolate on anatomical dead space, one and three second forced expiratory volume, maximal expiratory flow rate, and total forced expiratory volume were determined in ten healthy volunteers. Using Fowler's single breath nitrogen analyzing technique, atropine was found to increase dead space by 19.2 per cent at one hour, declining to 11.02 per cent at four hours. Glycopyrrolate increased dead space by 21.57 per cent at one hour, 29.28 per cent at two hours, and 26.65 per cent at four hours. When compared to the effects of saline control injection, the dead space increases are significant. The difference between glycopyrrolate and atropine is significant only at four hours. Increases in maximal expiratory flow rate induced by atropine and glycopyrrolate were significant at one-half hour, while atropine alone induced a significant increase in one second forced expiratory volume. Three second forced expiratory volume and total forced expiratory volume were not significantly altered.

Adult↗

PubMed1989

Haemodynamic effects of atropine during halothane or isoflurane anaesthesia in infants and small children.

In this study, two-dimensional and pulsed Doppler echocardiography were used to measure cardiovascular changes before and after IV atropine in 31 infants and small children during halothane (n = 15) or isoflurane (n = 16) anaesthesia. Prior to induction of anaesthesia heart rate (HR), mean blood pressure (MBP), and two-dimensional echocardiographic dimensions of the left ventricle and pulmonary artery blood flow velocity were measured by pulsed Doppler echocardiography. Cardiovascular measurements were repeated while anaesthesia was maintained at 1.5 MAC halothane (n = 15) or isoflurane (n = 16). Atropine 0.02 mg.kg-1 IV was then administered and two minutes later, a third set of cardiovascular data was obtained. Heart rate decreased during halothane anaesthesia but did not change significantly during isoflurane anaesthesia. Mean blood pressure, cardiac output (CO) and stroke volume (SV) decreased similarly during 1.5 MAC halothane or isoflurane anaesthesia. Ejection fraction (EF) decreased and left ventricular end-diastolic volume (LVEDV) increased significantly in both groups, but decreases in EF (32 +/- 5 per cent vs 18 +/- 5 per cent) and increases in LVEDV (18 +/- 7 per cent vs 7 +/- 5 per cent) were significantly greater during halothane than during isoflurane anaesthesia. Following atropine, HR increased more in the patients maintained with halothane (31 +/- 6 per cent), than during isoflurane anaesthesia (18 +/- 5 per cent). Atropine increased CO in both groups of patients, but SV and EF remained unchanged. When compared with awake values, HR increased similarly and significantly (18 +/- 4 per cent) following atropine in both groups, and CO returned to control levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗

PubMed1988

Heart rate response to atropine in humans anaesthetized with five different techniques.

Atropine, 0.01 mg.kg-1, was given intravenously before the start of surgery to 169 patients who were anaesthetized with one of five different techniques; halothane, enflurane, cervical epidural, lumbar epidural or narcotic anaesthesia in addition to nitrous oxide and oxygen. Atropine produced a significant increase in heart rate (HR) within 1 min in all patients studied; the HR increases in patients anaesthetized with halothane (37 +/- 11 beats.min-1, n = 37) or narcotic (34 +/- 12 beats.min-1, n = 30) were significantly greater than in those anaesthetized with enflurane (25 +/- 10 beats.min-1, n = 35; P less than 0.01) or epidural anaesthesia. Because of the presence of an acute cardiac sympathectomy, the patients who received cervical epidural anaesthesia were expected to have different responses to the atropine. However, there was no significant difference in the HR increases between the patient groups with cervical (19 +/- 12 beats.min-1, n = 32) and lumbar (22 +/- 8 beats.min-1, n = 35) epidural anaesthesia. Atropine also produced a small but significant increase in arterial pressure in all five groups of patients. These results suggest that the cardiac responses to atropine may differ depending on the individual anaesthetic agent used, and are likely dependent upon the agent's effect on autonomic nervous system activity.

Adolescent↗

PubMed2006

Conservative treatment of infantile hypertrophic pyloric stenosis with intravenous atropine sulfate does not replace pyloromyotomy.

Pyloromyotomy as described by Weber and Ramstedt has been the standard therapy for infantile hypertrophic pyloric stenosis since the 1960's and conservative therapy has been abandoned. The objective of this study was to test the effectiveness of systemic atropine applied intravenously for 7 days as a conservative therapeutic strategy and as an alternative to primary operation. Forty-two consecutive term infants with infantile hypertrophic pyloric stenosis were enrolled in the study over a period of 5 years. After confirmation of the diagnosis they all received intravenous atropine at a dose of 0.04 mg/(kg day) and increased by 0.01 mg/(kg day) up to 0.12 mg/(kg day), given as 6-8 single doses per/day. Nine pairs of parents requested that their child should be operated before completing the 7 days of medical therapy. Surgery was necessary in 8 of the remaining 33 infants (24,.2%) who did not improve after 7 days of conservative treatment. Successful treatment with i.v. atropine sulfate was achieved only in 25/33 term infants at an average maximal dose of 0.11 mg/(kg day), without any major side effects. Intravenous atropine sulfate has been considered as a potential alternative therapeutic strategy in the treatment of infantile hypertrophic pyloric stenosis. Clinical improvement however was often not seen before the 6th or 7th day of intravenous treatment. A success rate for the conservative approach of only 75% at day 7 in our study does not favour atropine therapy, in view of success rates above 95% with surgical repair.

Atropine↗

PubMed1992

Enhanced sensitivity for detection of coronary artery disease by addition of atropine to dobutamine stress echocardiography.

Patients undergoing dobutamine stress echocardiography often take beta antagonists which limit heart rate response and sensitivity in the test for detection of coronary artery disease. The aim of this study was to assess the effect of the addition of atropine to dobutamine stress echocardiography on clinical, electrocardiographic and echocardiographic outcomes. Dobutamine stress echocardiography was performed starting at and increasing every 3 minutes with 10 micrograms/kg/min to a maximum of 40 micrograms/kg/min (stage 4), which was continued for 6 minutes. In patients not achieving 85% predicted maximal exercise heart rate and in whom the test was not judged positive on echocardiographic or electrocardiographic criteria, atropine (0.25 mg intravenously, repeated up to a maximum of 1 mg if necessary) was added and dobutamine continued for up to a further 5 minutes, or until an adequate heart rate was achieved or the test was stopped because of chest pain or electrocardiographic changes. Of 80 consecutive patients undergoing dobutamine stress echocardiography within 2 weeks of coronary angiography, 49 required atropine (group A) and 31 required only dobutamine (group B). After dobutamine alone, heart rate (mean +/- SD) was higher in group B than in group A: 129 +/- 20 vs 90 +/- 18 beats/min, p less than 0.0001; but after the addition of atropine, heart rate in group A increased to 120 +/- 20 beats/min. Overall sensitivity for the detection of coronary disease was 70%, 95% confidence interval (CI) 55 to 83%; after the addition of atropine, sensitivity for group A was 65%, 95% CI 45 to 81%; in group B, sensitivity was 81%, 95% CI 54 to 96%.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1986

Difference in effects of pirenzepine and atropine on carbachol-induced pepsinogen secretion from isolated gastric glands.

The effect of pirenzepine on carbamylcholine (carbachol)-stimulated pepsinogen secretion was compared with that of atropine in the isolated guinea pig gastric glands. Pirenzepine and atropine caused a dose dependent inhibition of carbachol-stimulated pepsinogen secretion. Moreover, pirenzepine as well as atropine produced a rightward shift in the dose response curve of carbachol-stimulated pepsinogen secretion but did not alter the maximum increase in pepsinogen secretion. Results therefore demonstrate that pirenzepine acts as a specific receptor antagonist in the interaction of carbachol with its receptor on gastric chief cells. However, pirenzepine was 50 times less potent than atropine in inhibiting pepsinogen secretion. Half maximal inhibitory concentration of pirenzepine was 2 X 10(-5) M when a maximally effective concentration of carbachol was used, while that of atropine was 4 X 10(-7) M. Results, therefore, suggest that muscarinic receptor on gastric chief cells to which pirenzepine binds may be an intermediate affinity type.

Animals↗

PubMed1980

Behavior-dependent evoked potentials in the hippocampal CA1 region of the rat. II. Effect of eserine, atropine, ether and pentobarbital.

The correlations of the rat's behaviors and the hippocampal EEG with the averaged evoked potentials (AEPs) evoked by the Schaffer collaterals in the hippocampal CA1 region of the rat were studied after intraperitoneal injections of several drugs known to affect hippocampal EEG. Ether and eserine induced continuous train of rhythmical slow activity (RSA) of 5-6/sec in the hippocampal EEG, during which the AEPs showed waveforms intermediate between those elicited during large irregular activity (LIA) in the awake, immobile control and those elicited during walking in the control. Low dose nembutal and atropine induced high amplitude LIA during immobility, resembling EEG during slow-wave sleep (SWS). The AEPs during these LIA states, and that during LIA of wake-immobility were of similar waveforms. The AEP waveforms are proposed to form a continuum which corresponds to the continuum of EEG from high amplitude LIA to RSA of increasing frequency. AEP waveforms do not depend only on walking or similar movements which correlate with high frequency RSA. Atropine sulfate (25-50 mg/kg i.p.) severely dampened the oscillations in the AEPs of rats during walking or similar movements, even though the high frequency RSA was essentially unaffected. The difference between AEPs during immobility and those during walking was markedly reduced after atropine, even though the EEG-behavior relationship persisted. The effect of atropine on AEPs may be interpreted as a direct effect on the hippocampus which is apparently inconsistent with present knowledge. If the effect was on inputs from the brain stem or the septum to the hippocampus, the hypothesis that there are two pharmacological types of RSA (atropine-sensitive and -resistant) requires re-definition and re-examination.

Animals↗

PubMed1978

Quinidine-like activity of atropine in rabbit atria.

Direct effects of atropine and quinidine on contractile force, overdrive suppression, and effective refractory period was studied in rabbit atria. Left atrial contractile force at normal CaCl2 concentration (2.2 mM) and the contractile force response to elevated CaCl2 (5 mM) were unchanged over 30 min. Atropine exposure (1.7 X 10(-5) M) for 30 min significantly reduced contractile force at both normal and elevated CaCl2 levels. Quinidine exposure (6.2 X 10(-6) M) for 30 min produced similar but statistically insignificant changes. At 4 h, control contractile force at 2.2 mM CaCl2 decreased to the post-atropine level, but the response to 5 mM CaCl2 was unchanged. The asystolic interval of right atria following overdrive (for 2 min at 3 rates) was increased after 30 min by 4% for controls, 14% after atropine (1.7 X 10(-5) M) and 45% after quinidine. The effective refractory period of left atria (evaluated by paired pulse stimulation) was unchanged after 30 min for controls, but increased by 20% after atropine and 45% after quinidine.

Animals↗

PubMed1986

Differences in cardiac but not in neuroendocrine responses in healthy volunteers after administration of two antimuscarinic agents, atropine and pirenzepine.

Neuroendocrine and cardiac responses were studied in healthy volunteers with the classical muscarinic antagonist, atropine and the new antimuscarinic agent, pirenzepine. The secretion of prolactin (PRL) and growth hormone (GH) was increased after metoclopramide. Typically, an antidopaminergic drug such as metoclopramide decreases rather than increases GH concentrations in serum. Pretreatment with both atropine and pirenzepine abolished the increase of GH secretion, which suggests an important role of cholinergic mechanisms in the regulation of GH secretion. The increase of PRL secretion was not inhibited by the two muscarinic antagonists. With the doses used, antimuscarinic activities in serum were comparable after atropine and pirenzepine treatments for the most part of the study. Heart rate was, however, significantly increased during atropine and higher than during saline or pirenzepine treatments throughout the study period. When compared to placebo, pirenzepine lowered heart rate slightly but significantly. The exact mechanism of this effect is unclear. We conclude that in contrast to the identical neuroendocrine effects, the cardiac responses clearly differ during atropine and pirenzepine treatments which confirms the ability of pirenzepine to distinguish muscarinic receptor sites in the central nervous system from those of the heart.

Adult↗

PubMed1992

Effects of atropine on operant test battery performance in rhesus monkeys.

The acute behavioral effects of atropine sulfate were assessed using a battery of complex food-reinforced operant tasks that included: temporal response differentiation (TRD, n = 7); delayed matching-to-sample (DMTS, n = 6), progressive ratio (PR, n = 8), incremental repeated acquisition (IRA, n = 8), and conditioned position responding (CPR, n = 8). Performance in these tasks is thought to depend primarily upon specific brain functions such as time perception, short-term memory and attention, motivation, learning, and color and position discrimination, respectively. Atropine sulfate (0.01-0.56 mg/kg iv), given 15-min pretesting, produced significant dose-dependent decreases in the number of reinforcers obtained in all tasks. Response rates decreased significantly at greater than or equal to 0.03 mg/kg for the learning and discrimination tasks, at greater than or equal to 0.10 mg/kg for the motivation and short-term memory and attention tasks, and at greater than or equal to 0.30 mg/kg for the time perception task. Response accuracies were significantly decreased at doses greater than or equal to 0.10 mg/kg for the learning, discrimination, and short-term memory and attention tasks, and at greater than or equal to 0.30 mg/kg for the time perception task. Thus, the order of task sensitivity to any disruption by atropine is learning = color and position discrimination greater than time perception = short-term memory and attention = motivation (IRA = CPR greater than TRD = DMTS = PR). Thus in monkeys, the rates of responding in operant tasks designed to model learning and color and position discrimination were the most sensitive measures to atropine's behavioral effects. Accuracy in these same task was also disrupted but at higher doses. These data support the hypothesis that cholinergic systems play a greater role in the speed (but not accuracy) of performance of our learning and discrimination tasks compared to all other tasks. Accuracy of responding in these and the short-term memory task, all of which involve the use of lights as visual stimuli, was more sensitive to disruption by atropine than those tasks which did not utilize such strong visual stimuli.

Animals↗

PubMed1978

Effects of atropine on conditioned taste aversion.

Atropine sulfate, which has a deleterious effect on various learning tasks, was found to have a similar effect on the acquisition of conditioned taste aversion. Thus, intraperitoneal injection of atropine sulfate shortly before tasting was found to interfere with conditioning of the aversion, but injection of atropine after tasting did not. The interference effect was also obtained with intraventricular administration of atropine sulfate, but not with intraperitoneal injection of the peripherally-acting atropine methylnitrate. These results show that central rather than peripheral mechanisms are involved in this effect, and suggest that conditioned taste aversion, like other kinds of learning, involves cholinergic mediation.

Animals↗

PubMed1984

Effects of methamphetamine on atropine-induced conditioned gustatory avoidance.

The repeated administration of high doses of methamphetamine (MA) has been shown to cause monoaminergic damage in rhesus monkeys and rats. In view of the purported interaction between central cholinergic and monoaminergic systems, rhesus monkeys and rats previously exposed to high doses of MA were tested in conditioned gustatory avoidance studies with atropine (a muscarinic blocker) as the unconditioned stimulus. It was observed that both rhesus monkeys and rats previously exposed to high doses of MA exhibited less of an atropine-induced avoidance than control monkeys and rats. To control for the nonspecific effects of prior exposure to stimulants, an additional group of rats previously exposed to high doses of methylphenidate ( a stimulant shown to not cause catecholaminergic damage) was tested in the same paradigm. The methylphenidate treated rats showed no change in sensitivity to atropine in the conditioned gustatory avoidance paradigm as compared to control rats which indicated that prior exposure to the nonspecific effects of a stimulant without monoaminergic alterations does not alter the sensitivity of atropine's avoidance-inducing properties. The results of these experiments imply that atropine's avoidance-inducing properties may in part be mediated through the monoaminergic system.

Animals↗

PubMed1986

Change in atropine dose effect curve after subacute soman administration.

Thirty-one adult male rats were trained on a two component (FR10-extinction) operant task. After establishment of an atropine sulfate dose effect curve (vehicle, 1.0, 1.8, 3.2, 5.6 or 10.0 mg/kg), all rats were injected SC with 35.0 micrograms/kg soman three times per week for four weeks. One, twenty-eight and fifty-six days after the last soman injection, additional atropine tests were given. Atropine produced significant dose related decreases in FR10 responding at 3.2, 5.6 and 10.0 mg/kg during the initial dose effect curve with no effect on extinction responding. Although four rats died during the soman exposure period, the remaining rats exhibited neither signs of organophosphate toxicity nor significant disruptions in FR responding. However, a significant increase in extinction component responding was seen on soman injection days. The atropine dose effect curve for FR10 responding showed a significant shift to the left on the day after the last dose of soman. However, the dose effect curves at 4 and 8 weeks were the same as the initial curve. These results provide behavioral evidence that chronic soman exposure results in a supersensitivity to the antimuscarinic drug, atropine, possibly due to a down-regulation in the number of muscarinic receptors.

Animals↗

PubMed1988

Effect of eye color on heart rate response to intramuscular administration of atropine.

Melanin has been previously shown to modify the mydriatic response to atropine instillation. Skin and iris pigmentation has also been shown to modify aspects of the heart rate response to injected atropine, although these observations have been generally overlooked. In this study, 20 healthy non-smoker male subjects, ages 20-30 years, were injected by two different automatic injector devices and the mydriatic and heart rate responses in the first 90 min were reported. The group included 8 brown-eyed, 4 hazel-eyed, and 8 blue-eyed subjects. Although there were differences in the rate of atropine delivery between the two injection devices, the heart rate responses were independently modified by eye color to a magnitude of difference as great as the differences between injectors. Subjects with more pigmented irides (brown-eyed) showed a more rapid rise in heart rate compared to less pigmented irides (hazel-eyed and blue-eyed subjects). Following injection by the device with a slower atropine absorption rate, these differences were particularly enhanced and an abbreviated bradycardic phase of the heart rate response was observed for the brown-eyed subjects. This observation confirms earlier reports and suggests the possibility of an interference by melanin (in the iris or elsewhere) in atropine accessibility to selected muscarinic target sites.

Adult↗