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PubMed1979

Effect of physostigmine and atropine on acetylcholine turnover in mouse brain.

The effect of physostigmine salicylate (0.5 mg/kg, i.p.) alone and in combination with atropine sulfate (25 mg/kg, i.p.) on levels of acetylcholine (ACh) and choline (Ch) and turnover of ACh has been studied in whole brain and striatum of mice. The animals were killed by focussed microwave irradiation and the turnover of ACh was studied after i.v. injection of deuterium labelled Ch by employing mass fragmentography. Physostigmine increased the levels of ACh in whole brain from 24.5--28.0 nmol/g(P less than 0.001) whereas there was no significant increase in striatum. The levels of Ch were also increased. The turnover rate of ACh was decreased in whole brain from 15.4 to 8.4 and in striatum from 52.9 to 24.4 nmol/g . min. Physostigmine given before or after atropine did not completely block the ACh lowering effect of atropine. When atropine was given before physostigmine the turnover rate of ACh in whole brain was increased to 24.2 nmoles/g . min. The results seem to indicate that there is no clear cut relation between the turnover rate and level of ACh in vivo. The increase of the turnover rate induced by atropine is masked unless a cholinesterase inhibitor is given to protect the newly synthesized labelled ACh released by atropine.

Acetylcholine↗
PubMed1984

Comparison of radioreceptor assay and radioimmunoassay for atropine: pharmacokinetic application.

A membrane suspension prepared from rat brain was able to bind the potent muscarinic antagonist quinuclidinyl benzilate (QNB). The KD for binding was 0.48 nM and Bmax was 1.42 pmol/mg protein. Atropine competitively inhibited the binding of tritiated QNB to muscarinic receptors. This new radioreceptor assay (RRA) for atropine has been compared with a radioimmunoassay (RIA) for atropine. The RRA measures only the active component of atropine, 1-hyoscyamine and in this respect it differs from the RIA. As little atropine as 1.25 ng/ml (4.33 nmol/l) in a 25 microliters serum sample could be reliably assayed by the RRA. Using both assay techniques the pharmacokinetics of atropine was studied after a single 0.02 mg/kg i.v. dose given to 8 anaesthetized patients. The half-life calculated by the RRA was 3.7 +/- 2.3 h (m +/- SD) and by the RIA 4.3 +/- 1.7 h. Both the volume of distribution and the total clearance were higher according to the RRA than the RIA: 3.9 +/- 1.5 vs 1.7 +/- 0.71/kg and 15.4 +/- 10.3 vs 5.9 +/- 3.6 ml/min/kg, respectively. The AUC measured by the RRA and RIA was 29.8 +/- 18.9 and 103.9 +/- 110.7 micrograms X h/l, respectively. The differences in the pharmacokinetics according to the 2 methods are presumably due to preferential tissue uptake of the l-form.

Adult↗
PubMed1979

Placental transfer of atropine at the end of pregnancy.

In a first study, 28 pregnant women received a fast intravenous injection of atropine sulphate 12.5 microgram/kg, as in a classical atropine test. Fetal tachycardia resulted. The maternal venous blood concentration of atropine, determined by bioassay on guinea pig ileum, decreased rapidly in the first 3--5 min and very slowly therafter. In a second study, 45 women in labour received the same dose i.v., and at birth atropine was measured both in maternal and cord blood. Placental transfer of atropine had occurred in every case and was highly variable, depending on the maternal blood concentration of the drug. This suggests that the atropine test is not mainly dependent on placental function.

Adult↗
PubMed1987

Cutaneous blood flow and local sweating after systemic atropine administration.

Localized cutaneous vasodilation (flush) is seen following systemic atropine administration. To verify calculated enhanced dry heat loss with actual changes in cutaneous blood flow, four men were studied in both control and atropine (0.025 mg.kg-1; im) experiments (Ta = 30 degrees C, Tdp = 7 degrees C) during moderate exercise (55% VO2 peak). Esophageal temperature (Tes) and arm sweating (ms) by local dewpoint were measured continously. Skin (forearm) blood flow (FBF) was measured twice each minute by venous occlusion plethysmography. Injection of atropine (2 mg) caused an increased sensitivity (+85%, p less than 0.01) in FBF to Tes with no change in the vasodilator threshold. An elevated Tes onset (0.3 degrees C, p less than 0.05) for sweating occurred with no change in the sensitivity of ms to Tes (-27%, p less than 0.20). No elevation in either forearm or Tsk occurred before the onset of vasodilation, however, both mean skin (Tsk) and local arm temperatures were higher in the atropine experiments after 15 min of exercise. Systemic atropine resulted in higher cutaneous vasodilation at the same core temperature with the local skin temperature following passively. The effect of systemic atropine in stimulation of increased cutaneous vasodilation is suggested to result by a combination of central and local responses which may be mediated through the release of vasoactive sustances.

Adult↗
PubMed1997

A re-appraisal of the nature of the atropine-resistant contraction to electrical field stimulation in the human isolated detrusor muscle.

We investigated whether in human isolated detrusor strips the atropine-resistant contractile response to electrical field stimulation was mediated by ATP (or a related purine), as previously shown in the urinary bladder of other mammalian species. Electrical stimulation (1-50 Hz for 5 s at 1 min intervals, 0.1 ms pulse width, 60 V) elicited reproducible, frequency-dependent twitch contractions, which were markedly reduced by atropine (10 microM). Tetrodotoxin (TTX: 1 microM) inhibited contractile responses to a similar degree. When applied together, atropine and TTX caused an inhibition which was superimposable to that caused by either drug alone. The TTX-resistant contractions were totally unaffected by omega-conotoxin GVIA (omega-CTX: 0.1 microM). The atropine-resistant contractions were unaffected by the P2-purinoceptor antagonists suramin (300 microM) and PPADS (30 microM), at concentrations which virtually suppressed the contractile response induced by applied ATP (10 microM(-1) mM). As previously described, antagonism of the ATP-induced contractions by suramin (30, 100, 300 microM) and PPADS (3, 10, 30 microM) was insurmountable, with apparent 'pA2' values (calculated at the lowest antagonist concentrations) of 4.9 and 5.2, respectively. It is concluded that, under our experimental conditions, the non-cholinergic (atropine-resistant) component of the excitatory transmission in the human detrusor is not mediated by neural release of ATP, in spite of the presence of excitatory P2-purinoceptors on the effector cells. The TTX- and omega-CTX-resistant, non-cholinergic component might be related to the release of unknown transmitter(s) through a mechanism independent of both Na+- and N-type Ca2+-channels. More likely, the atropine-resistant component may reflect direct smooth muscle excitation since the human detrusor has a very short chronaxie (Sibley 1984).

Adenosine Triphosphate↗
PubMed2000

Atropine test and circulatory arrest in the fossa posterior assessed by transcranial Doppler.

OBJECTIVE: To evaluate whether a negative atropine test (i.e., increase in heart rate of less than 3% after intravenous administration of 3 mg atropine) correctly predicts circulatory arrest in the fossa posterior during craniocaudal herniation in patients with primary supratentorial lesions. MATERIAL AND METHODS: Prospective, observational clinical study. SETTING: Two surgical intensive care units in a university hospital. PATIENTS: In 45 consecutive patients with suspected brain death, an atropine test (AT) and a transcranial Doppler sonography were performed simultaneously and, if necessary, repeatedly. MEASUREMENTS AND RESULTS: Forty-four patients fulfilled the typical criteria of a supratentorial and infratentorial circulatory arrest as the atropine test became negative. In one patient, who had undergone a decompressive craniectomy for uncontrollable intracranial pressure 4 h prior to the AT testing, we found a negative AT in the presence of an antegrade supratentorial and infratentorial flow. CONCLUSION: A negative atropine test indicates a circulatory arrest in the fossa posterior in patients with primary supratentorial lesions and craniocaudal herniation. In patients with brain-stem lesions, however, a negative atropine test does not unequivocally indicate a circulatory arrest.

Adolescent↗
PubMed1995

Cardiorespiratory function in nerve agent poisoned and oxime + atropine treated guinea-pigs: effect of pyridostigmine pretreatment.

The effect of pyridostigmine pretreatment on the efficacy of oxime + atropine treatment in sarin and VX poisoning was investigated in a guinea-pig model with on-line monitoring of respiratory and circulatory parameters. The carotid artery, jugular vein and trachea were cannulated in female urethane-anesthetized Pirbright-white guinea-pigs. After baseline measurements the animals received pyridostigmine (PYR, 0.05 mumol/kg, i.v.), 30 min later sarin (100 or 200 micrograms/kg = 5 or 10 x LD50, i.v.) or VX (45 or 90 micrograms/kg = 10 or 20 x LD50, i.v.), followed 2 min later by atropine (10 mg/kg, i.v.) plus HI 6 or HLö 7 (30 mumol/kg each, i.v.). Sixty-minute survival time and rate and respiratory and circulatory parameters were recorded. Diaphragm acetylcholinesterase (AChE) activity was determined spectrophotometrically. Identical groups without PYR were included for comparison. With regard to survival time and rate, PYR pretreatment slightly improved the efficacy of HI 6 plus atropine in sarin 5 x LD50 poisoned animals, reduced the efficacy of oxime + atropine treatment in the other sarin groups and had no effect in VX poisoning. Compared to non-pretreated oxime + atropine groups, PYR slightly improved respiratory function in sarin and in VX poisoning (only HI 6). PYR did not affect circulatory function in VX poisoning but reduced circulatory parameters in sarin poisoning to varying extent's. The oxime efficacy in reactivating diaphragm AChE decreased in the order sarin > VX without significant differences between pretreated and non-pretreated groups. The data suggest that pyridostigmine pretreatment does not enhance the efficacy of oxime + atropine in sarin or VX poisoning.

Animals↗
PubMed2003

Inhibitory effects of atropine and hexamethonium on the angiotensin II-induced contractions of rat anococcygeus smooth muscles.

We have evaluated the interaction between angiotensin II (Ang II) and the cholinergic transmission in anococcygeus smooth muscles isolated from rats treated (sympathectomised group) or not (vehicle group) with reserpine and alpha-methyl-p-tyrosine. For this, we contracted the tissues with Ang II in the presence and absence of atropine and hexamethonium. Ang II induced concentration-dependent contractions, which did not undergo temporal changes in tissues isolated from both groups of rats. In the vehicle group, Ang II induced more potent contractions than in the sympathectomised group. In the sympathectomised rat group, atropine inhibited the contractions induced by Ang II in a concentration-dependent fashion with no decrease in E(max). Additionally, hexamethonium inhibited the contraction induced by Ang II in a concentration-dependent fashion with a decrease in E(max). Association of atropine and hexamethonium produced Ang II-induced curves with rightward shifts from the control curve with a decrease in E(max). Incubation with N(G)-nitro-L-arginine methyl ester (L-NAME) reversed the effects of atropine and hexamethonium association. Conversely, in the vehicle group of rats, atropine and hexamethonium did not produce any significant effect. However, in the presence of yohimbine, atropine shifted the Ang II-induced curves to the right of the control curve with no E(max) decrease. Results suggest that there is a positive interaction between Ang II and cholinergic transmission in the rat anococcygeus smooth muscle mediated by angiotensin receptors located on pre-ganglionic cells.

Angiotensin II↗
PubMed2005

Cholinergic effects on fear conditioning II: nicotinic and muscarinic modulations of atropine-induced disruption of the degraded contingency effect.

RATIONALE: In a companion study (Carnicella et al., 2005), we showed that the muscarinic antagonist atropine, when administered after extensive training during both conditioning and testing, affected neither cued nor contextual fear memories when both of them did not compete for the control of the overt behaviour. In contrast, atropine altered the degraded contingency effect (DCE), that is, the processes by which contextual fear memory competes with the cued one for the control of the conditioned response. Atropine-induced disruption of the DCE was fully reversed by the administration of the anticholinesterase inhibitor physostigmine, which suggests a direct cholinergic implication. OBJECTIVE: The present series of experiments was conducted in order to define more precisely the involvement of the cholinergic system in such an effect. METHODS: Oxotremorine (0.0, 0.0075, 0.015, or 0.03 mg/kg), pilocarpine (0.0, 0.3, 1, or 3 mg/kg), xanomeline (0.0, 2.5, 5.0, 10.0 or 20.0 mg/kg) and nicotine (0.0, 0.1, 0.2, or 0.4 mg/kg) were tested for reversal of the atropine-induced alteration of the DCE. RESULTS: Oxotremorine and pilocarpine did not reverse the atropine-induced alteration of the DCE. In contrast, xanomeline and nicotine reversed the effect of atropine on the DCE. CONCLUSION: The present series of experiments reveals complex pharmacological interactions within the cholinergic system when cued and contextual fear memories interact. Results are discussed in this connection and with regard to the relation between the properties of cholinergic agonists and their therapeutic values.

Animals↗
PubMed2005

Cholinergic effects on fear conditioning I: the degraded contingency effect is disrupted by atropine but reinstated by physostigmine.

RATIONALE: The cholinergic system has been shown to modulate contextual fear conditioning. However, with the exception of trace conditioning studies, most of the available data have focussed on independent context, i.e., context that do not compete with the conditioned stimulus to control for the conditioned response (interactive context). OBJECTIVE: In the present series of experiments, the effects of the muscarinic antagonist, atropine, were assessed when contextual fear memory interacts with cued fear memory to regulate conditioned response, using a Pavlovian degraded contingency preparation in rats. This preparation not only afforded an insight into simple Pavlovian associations but also enabled us to test for the processes of competition that made use of these associations to make an appropriate response to a stimulus [degraded contingency effect (DCE)]. METHODS: In experiment 1, three doses of atropine [2.5, 5.0, and 10.0 mg/kg, intraperitoneally (i.p.)] were evaluated on male Sprague-Dawley rats. In experiment 2, physostigmine (0.037-0.3 mg/kg, i.p.) was injected after the administration of 5 mg/kg of atropine. RESULTS: Experiment 1A and its partial replication (experiment 1B) showed that at asymptotic level of training, atropine did not alter contextual and cued fear memories when the subjects were directly tested for them, whereas it suppressed the DCE for a 5 mg/kg dose. Indeed, atropine-induced suppression of the DCE was found to be an inverted U-shaped dose-response curve. Experiment 2 showed that physostigmine caused a dose-dependent reversal of the atropine-induced alleviation of the DCE, without altering the expression of simple cued and contextual fear memories. CONCLUSION: These results evidence at asymptotic level of training a cholinergic modulation of the processing of interactive context, but not of independent ones. They are discussed in the framework of the mechanisms that are involved in both types of contextual processing.

Animals↗
PubMed1983

Atropine-induced cardioacceleration in patients on chronic propranolol therapy: comparison with the positive chronotropic effect of isometric exercise.

The hemodynamic effects of intravenous atropine administration were examined in 24 patients on chronic propranolol therapy. In the first 13 patients the safety of atropine administration was tested by giving the drug in small increments to a total dose of either 1.2 mg (five patients) or 1.7 mg (eight patients). The heart rate after atropine administration in these patients varied between 57 and 82 bpm and no adverse effects were noted. The other 11 patients received 1.2 mg atropine intravenously with hemodynamic measurements obtained prior to and 3 minutes after administration of the drug. Heart rate increased from 57.5 +/- 8.7 to 72.8 +/- 13.9 bpm, mean pulmonary arterial and left ventricular end-diastolic pressure declined, and cardiac index increased. Total systemic resistance decreased in most of the patients. Isometric exercise performed prior to atropine administration in the same 11 patients accelerated heart rate from 57.4 +/- 8.6 to 68.4 +/- 10.8 bpm. A close correlation, r = 0.909, was demonstrated between the postatropine heart rate and the rate during isometric exercise. It is concluded that atropine in a dose of 1.2 to 1.7 mg may be administered safely in patients on chronic propranolol therapy. Isometric exercise may be useful in unmasking vagal tone in beta-blocked patients.

Adult↗
PubMed1988

Dose-dependent effects of atropine sulfate on the brainstem and cortical auditory evoked potentials in the rat.

Because brainstem auditory evoked potentials (BAEPs) are frequently recorded in anesthetized animals and humans, it is important to become familiar with the effects on the BAEP of drugs used during anesthesia, including pre-anesthetics. The dose-dependent and stimulus intensity-dependent effects on the BAEP of a pre-anesthetic, atropine sulfate, were studied in the unanesthetized rat. The animal subjects were 11 adult female Long-Evans rats. BAEPs in response to 0.1 ms clicks (12.5/s) were recorded from skull screw electrodes during a baseline period, as well as after saline and atropine treatments. Atropine sulfate was given i.p. in doses ranging from 0.250 to 40 mg/kg. Contrary to a prior report, doses in the standard pre-anesthetic range (i.e. 0.250-1.000 mg/kg) did not convincingly influence the BAEP. Only the highest dose (40 mg/kg) produced a significant and noteworthy change in the BAEP. This effect was characterized by significant amplitude increases in the P1, P2 and P3 components, but not in the P4, P5 and P6 components. This selective effect occurred at the highest stimulus intensity of 110 dB peak equivalent sound pressure level, but not at lower intensities. There were no convincing atropine-induced changes in BAEP latencies. Atropine-induced changes in the cortical auditory evoked potential (CAEP) were characterized by amplitude decrements. Thus, atropine seemed to have an excitatory effect on the BAEP and an inhibitory or depressive effect on the CAEP.

Animals↗
PubMed1990

Inhibition of nicotinic acetylcholine response by atropine in frog isolated sympathetic neurons.

The effect of atropine on nicotinic acetylcholine (ACh) response was studied in frog isolated sympathetic ganglion cells using a 'concentration clamp' technique which combines intra-cellular perfusion with a rapid external solution change within 3 ms. When atropine (more than 6 x 10(-7) M) was simultaneously applied to neurons with ACh (6 x 10(-6) M), the current amplitude was instantaneously reduced in a dose-dependent fashion. Further decreases in the current amplitude were observed in a time-dependent manner during about 20 min after the start of drug-application. Thereafter the current amplitude gradually restored toward the control level in the following 90-120 min in spite of the continuous presence of atropine. However, because d-tubocurarine greatly inhibited the 'restored' current, the last-mentioned is suggested to be also mediated by nicotinic ACh receptor-ionophore complex. Therefore, the inhibitory action of atropine on the peak amplitude of ACh response was examined at 15-20 min after adding the agent. It was dose-dependent but not voltage-dependent. Respective concentrations of atropine and d-tubocurarine causing half the maximum inhibition (IC50) of the peak current evoked by ACh (6 x 10(-6) M) were 1.8 x 10(-5) M and 1.8 x 10(-6) M. Thus, the inhibitory potency was 10 times less than that of d-tubocurarine, an antagonist of nicotinic ACh receptors. The blockade of ACh response by d-tubocurarine was competitive while that by atropine was non-competitive. The current elicited by ACh consisted of two (fast and slow) exponential components plus a steady-state one in the control period.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMedDate not supplied

The effect of atropine on the turnover of acetylcholine in the mouse brain.

The effect of atropine on the acetylcholine (ACh) turnover in the mouse brain has been studied and related to the central effect (motor activity) of the drug. At the threshold dose for maximal increase in motor activity, atropine had no measurable effect in the brain on the initial rate of formation of labelled ACh from labelled choline (Ch) i.v. injected. However, if atropine was injected 3 min after the injection of labelled Ch, when the labelled ACh had reached its peak value in the brain, there was a more rapid exponential decline of labelled ACh. This was assumed to be an indication that atropine increases the turnover of ACh in the brain. The specific radioactivity of ACh was not changed 2-17 min after the atropine injection, which indicates that atropine does not preferentially increase the release of newly synthetized ACh.

Acetylcholine↗
PubMed1984

Comparison of the gastric cytoprotective properties of atropine, ranitidine and PGE2 in rats.

In view of the controversy as to whether antisecretory agents such as H2 antagonists and antimuscarinics might be cytoprotective like the PGs, the oral activity of atropine, ranitidine and PGE2 against absolute ethanol-induced lesions was evaluated in rats. The results showed that atropine and PGE2, but not ranitidine, were effective in preventing absolute ethanol-induced gastric damage. The effects were related to the doses of the ulcerogenic agent and of the cytoprotective compound. The anti-ulcer activity of atropine is considered to be an expression of cytoprotection, since the pathogenesis of ethanol-induced gastric damage was independent of gastric pH and atropine, like PGE2, does not affect basal acid secretion at a fully cytoprotective dose. Some studies were undertaken to elucidate the mechanism of gastric cytoprotection by atropine. The possibility that the anti-muscarinic agent might work as a mild irritant was ruled out since, like PGE2, the agent was still effective in PG-deficient rats. The evidence that neostigmine markedly aggravated gastric damage caused by low doses of absolute ethanol and that atropine completely prevented this damage postulates mechanisms involving specific muscarinic receptor interactions.

Animals↗
PubMed1995

Effect of atropine on the frequency of reflux and transient lower esophageal sphincter relaxation in normal subjects.

BACKGROUND & AIMS: Low basal lower esophageal sphincter (LES) pressure is believed to be an important mechanism of reflux. The effects of atropine on the frequency and mechanisms of gastroesophageal reflux under the experimental conditions of a low basal LES pressure in 13 normal subjects were studied. METHODS: LES pressure, esophageal pressures, esophageal pH, and crural diaphragm electromyogram were recorded simultaneously in the postprandial period for 30 minutes before and two 30-minute periods after the injection of atropine. RESULTS: Atropine reduced the basal LES pressure from 16.4 +/- 3 to 8.7 +/- 2 mm Hg. The frequencies of reflux in the control and two postatropine periods were 3.5 +/- 0.5, 0.4 +/- 0.2, and 0.8 +/- 0.3, respectively (P < 0.05). The frequencies of transient LES relaxations decreased from 3.5 +/- 0.5 in the control to 0.4 +/- 0.2 and 1.5 +/- 0.4 in the two postatropine periods (P < 0.05). Transient LES relaxation and associated inhibition of the crural diaphragm was the major mechanism of reflux under conditions of low LES pressure induced by atropine. CONCLUSIONS: Atropine-induced low LES pressure does not predispose to reflux in normal healthy subjects. Atropine reduces the frequency of reflux by its inhibitory effect on the frequency of transient LES relaxation.

Adolescent↗
PubMed1989

Dose-dependent effects of atropine on behavioral and physiologic responses in humans.

Atropine is an antimuscarinic which has been frequently studied with learning and performance tasks using both human and animal subjects. However, interpretation of data from human studies is limited by the relatively narrow range of doses used in most such studies. In the present study a wide range of atropine doses (0, 1.5, 3.0, 6.0 mg/70 kg) were given, intramuscularly, to human volunteers to assess the effects of atropine on a variety of behavioral measures, subject ratings, and physiologic function. The time course of responses was examined over 24 hours. Behavioral measures were a computerized Performance Assessment Battery (PAB) which contained measures of logical reasoning, short-term memory and rapid arithmetic, a Digit Symbol Substitution Test (DSST), and a psychomotor test of hand-eye coordination (Circular Lights). Administration of atropine produced both time- and dose-dependent effects on most measures used, although sensitivity varied across measures. At the 1.5 mg dose, no effects on performance were detected, however, after 6.0 mg reliably and 3.0 mg occasionally, impairments occurred on measures of accuracy and speed of performance. These effects generally began by 1.5 hours postdrug and returned to baseline by 7-9 hours postdrug. In contrast, certain subject ratings and physiologic variables were affected by lower doses of atropine, showing deviations from baseline at 1.5 mg and producing a time course of effects that was both earlier in onset and longer in duration than was observed with the performance measures. The present results have practical implications for the clinical utilization of atropine in situations in which optimal performance is required.

Adult↗
PubMed1985

Depletion of neuropeptides in rat parotid glands and declining atropine-resistant salivary secretion upon continuous parasympathetic nerve stimulation.

In rats the parasympathetic auriculo-temporal nerve on one side was continuously stimulated at 40 Hz for 20-80 min in the presence of adrenergic blockers (dihydroergotamine and propranolol) +/- atropine. During the first 10 min this gave rise to a flow of saliva from the parotid gland that in the atropinized rats amounted to 35% of that found in rats not treated with atropine, while the protein and amylase outputs were 75% of those in non-atropinized rats. The atropine-resistant secretion of fluid and proteins declined to 5-10% of the initial value within 40 min but did not cease completely even after 80 min. The marked reduction in secretory responses was not due to desensitization or exhaustion of the gland cells. The nerve stimulation reduced the parotid gland content of vasoactive intestinal peptide (VIP) and substance P (SP) to approximately 60 and 25% of that of contralateral glands after 20 and 60 min, respectively. The probable explanation for the decline in secretory response seems to be depletion of non-adrenergic, non-cholinergic transmitter(s). The present results suggest that neuropeptides are involved in the regulation of salivary secretion but provide no direct evidence that either VIP or SP is responsible for the atropine-resistant salivary secretion.

Amylases↗