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 451 records · Page 25Linked to original sources
PubMed2002

Influence of atropine on fractal and complexity measures of heart rate variability.

BACKGROUND: Measurement of short-term fractal-like correlation properties of heart rate dynamics has been shown to be a useful prognostic indicator of adverse events in cardiac patients. Complexity measurements of heart rate variability (HRV) have already provided important information in many cardiac conditions. However, data on the physiological background of these newer nonlinear measures of HRV are limited. METHODS: Nine healthy subjects (aged from 22 to 35 years, 6 males, 3 females) had an electrocardiographic (ECG) recording during controlled breathing in supine position. HRV was analyzed for 5 min periods before and after intravenous injection of 0.6 mg of atropine using conventional HRV measures and newer nonlinear HRV measures including the short-term scaling exponent (alpha(1)) and approximate entropy (ApEn). RESULTS: The short-term scaling exponent alpha(1) increased significantly after atropine injection (1.01 +/- 0.23 vs 1.43 +/- 0.19, P = 0.001). There was no significant difference between ApEn values before and after atropine injection (0.87 +/- 0.17 vs 0.70 +/- 0.31, respectively, P = 0.27). At baseline before atropine administration, alpha(1) had a significant negative correlation with SDNN, RMSSD, and HF (r = -0.70, -0.76, -0.67, respectively, P < 0.05 for all), and a significant positive correlation with heart rate (r = 0.76, P < 0.05). After atropine injection, alpha(1) did not have significant correlation with any of the HRV parameters or heart rate. There were no significant correlations between ApEn and any of the HRV measures or heart rate either before or after atropine administration. CONCLUSIONS: Vagal tone has an important influence on the values of the short-term scaling exponent alpha(1). However, vagal modulation is not a major determinant of the values of ApEn.

Adult↗
PubMed1993

Atropine and oxime treatment in lethal soman poisoning of anaesthetized guinea-pigs: HLö 7 dimethanesulfonate versus HI 6 dichloride.

The oxime HI 6 is considered to be effective in soman poisoning and less effective in tabun poisoning. Recently, HLö 7 was shown to reactivate acetylcholinesterase (AChE) inhibited by soman and tabun. Therefore, the efficacy of HLö 7 and HI 6 was compared in soman poisoned guinea-pigs. Female Pirbright-white guinea-pigs were anaesthetized with urethane (1.8 g/kg) and the a. carotis, v. jugularis and trachea were cannulated. After base line measurements soman 0.08 mg/kg (= 5 x LD50) or 0.16 mg/kg (= 10 x LD50) was injected intravenously, 2 min. later the antidotes were applied intravenously: HLö 7 0.03 or 0.1 mmol/kg, HI 6 0.03 or 0.1 mmol/kg, atropine 10 mg/kg, or a combination of atropine and an oxime. Respiratory and circulatory parameters were recorded for 60 min. or until the death of the animal. The injection of 5 x LD50 soman resulted in a rapid respiratory arrest followed by circulatory failure in the soman and soman plus oxime groups (survival time about 7 min). Atropine restored the circulatory parameters to base line but was unable to provide a sufficient respiratory function (survival time 26 min.). The combination therapy with atropine plus HLö 7 or HI 6 improved the respiration sufficiently, restored the circulation completely, and prolonged the survival time to about 50 min. Atropine treatment was insufficient in animals poisoned with 10 x LD50 soman. The combination of atropine and HLö 7 or HI 6 improved respiration, circulation, and survival time to various extent. Despite of the striking therapeutic effect no reactivation of erythrocyte AChE by the antidotes was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholinesterase↗
PubMed1990

Atropine treatment induced cholinergic supersensitivity at receptor and second messenger levels in the rat salivary gland.

Physiological, biochemical and morphological correlates of chronic treatment of rats with the classical muscarinic antagonist atropine for 14 days (20 mg kg-1 day-1 s.c.) were studied in submandibular salivary glands. The amount of saliva collected from submandibular glands following a single injection of isoproterenol (30 mg kg-1 i.p.) was significantly larger and had higher protein concentration in rats treated with atropine than in saline-treated animals. In the glands of atropine-treated rats a conspicuous increase in the amount of rough endoplasmic reticulum (RER) along with a decrease in the mucous volume was observed in the acinus when examined by light microscopy. Several biochemical changes were observed in an enriched plasma membrane fraction from the submandibular gland of the atropine-treated rats: (1) an increase in the number of muscarinic antagonist binding sites (31 + 3.4%), (2) a decrease in the specific activity of basal adenylate cyclase, (3) a significantly lower Vmax of the adenylate cyclase in the presence of GTP (10 microM) and varying concentrations of Mg2+ (0-22.5 mM) with no apparent change in affinity of the enzyme for Mg2+ but (4) higher magnitude of stimulation in the presence of GTP (100 microM), vasoactive intestinal polypeptide (5 microM), isoproterenol (100 microM), NaF (10 microM) and forskolin (10 microM). There was however no change in the density of beta-adrenergic receptors upon atropine treatment. In tissue slices from the submandibular glands of atropine-treated rats we found lower basal cAMP levels (decrease 29 +/- 6.9%) and no significant change in the phosphatidylinositol breakdown stimulated by carbachol (10(-6) to 10(-4) M). It appears that chronic blockade of an inhibitory muscarinic input to the adenylate cyclase system is compensated by lowered adenylate cyclase activity. Phosphoinositide metabolism is not subject to the same adaptation, suggesting that cAMP may be the pivotal second messenger in the supersensitive salivary response.

Adenylyl Cyclases↗
PubMed2001

Preanaesthetic use of atropine in small animals.

Although it is unwise to recommend any preanaesthetic drug or regimen to be used routinely without consideration for the individual patient, the procedure being undertaken or the other drugs that will be used during the anaesthetic, of all anaesthetic-related drugs that might be under review, atropine is probably one of the least 'toxic' and least likely to cause life-threatening complications when used correctly. In most small veterinary practices there isn't the luxury of a dedicated anaesthetist available to monitor and manage each anaesthetised patient and the best form of cardiac monitor available may be an audible rate monitor. In this situation the advantages combined with the usual indications probably far outweigh the disadvantages of using atropine prophylactically. If a choice must be made, a sinus tachycardia under anaesthesia is probably preferable to a profound bradyarrhythmia. Absolute contraindications for using atropine are rare; the drug, when used alone, has low incidence of toxicity at clinically recommended doses in dogs and cats. Further, the new inhalation agents available to veterinarians (enflurane and isoflurane) do not sensitise the heart to the effect of catecholamines, so that the predominance of sympathetic tone produced when atropine is used is unlikely to precipitate dysarrthythmias during gaseous anaesthesia. Rhythm disturbances that occur under halothane anaesthesia when atropine is used, suggest there is some other cause, or agent, that is arrhythmogenic, such as an alpha 2 agonist, excessively deep level of anaesthesia, hypercapnia or hypoxaemia. Notwithstanding the above arguments, my preference, as a specialist anaesthetist, is that a drug is given only as required (not before) and that when, for example, any unusual heart rhythm occurs, all possible reasons for the occurrence (such as excessively deep anaesthesia or hypoventilation) are eliminated before other drugs like atropine or antiarrhythmics are administered.

Adjuvants, Anesthesia↗
PubMed2001

Reactions to tick antitoxin serum and the role of atropine in treatment of dogs and cats with tick paralysis caused by Ixodes holocyclus: a pilot survey.

OBJECTIVE: To determine the incidence and nature of adverse reactions of dogs and cats to tick antitoxin serum and to re-evaluate the role of atropine in the treatment of tick paralysis. DESIGN: A retrospective questionnaire of veterinarians. PROCEDURE: Questionnaires were posted to 320 veterinarians in tick-endemic regions of Australia. Questions referred to dogs and cats treated for tick paralysis over a period of three years: the number treated, treatment protocols and adverse systemic reactions to tick antitoxin serum. Ninety completed questionnaires were returned and responses analysed. RESULTS: Veterinarians reported that approximately 3% of dogs exhibited adverse reactions immediately following treatment with tick antitoxin serum. Eighteen percent of these reactions were described as anaphylaxis, with the remaining 82% attributed to the Bezold-Jarisch reflex. Six percent of cats treated with tick antitoxin serum reacted adversely and the majority of reactions (63%) were ascribed to the Bezold-Jarisch reflex. Atropine was used routinely by 10% of responding veterinarians in the treatment of dogs and cats with tick paralysis. A similar number of veterinarians used atropine only in selected cases. Most veterinarians (76%) reported that they never used atropine in the treatment of tick paralysis in either dogs or cats. Within the survey population, premedication with atropine reduced the number of Bezold-Jarisch reactions following tick antitoxin administration approximately five-fold in dogs and four-fold in cats. CONCLUSIONS: Data from this pilot survey indicate that more cats than dogs have adverse systemic reactions to tick antitoxin serum and that the majority of these reactions in both dogs and cats could be related to the Bezold-Jarisch reflex. The number of reactions to tick antitoxin serum in dogs and cats could be significantly reduced by the routine use of atropine prior to administration of tick antitoxin serum.

Animals↗
PubMed1988

An evaluation of the effectiveness of intramuscular atropine or homatropine eyedrops in preventing the effects of physostigmine eyedrops on human vision.

An intramuscular injection of 2 mg atropine sulphate was given at either 8 or 120 min prior to instillation of 0.25% physostigmine sulphate eyedrops. In this way, the maximum accommodative change and the concomitant reduction in contrast sensitivity caused by physostigmine coincided with, respectively, the peak plasma atropine concentration or the fully developed mydriasis and reduction of near-point accommodation caused by atropine. Atropine at both times did not affect the miosis, the reduction in near-point, the increase in accommodation or the reduction in contrast sensitivity caused by physostigmine. Contrast sensitivity to a phase-reversed grating pattern was actually diminished by atropine, though this was not statistically significant. By contrast, 2% homatropine hydrobromide eyedrops did effectively antagonize physostigmine's actions. This indicates that the rate of delivery of atropine from the intramuscular injection was insufficient to compete against the ocular effects of physostigmine.

Accommodation, Ocular↗
PubMed1976

Effects of atropine, injected into a lateral cerebral ventricle of the rabbit, on fevers due to intravenous leucocyte pyrogen and hypothalamic and intraventricular injections of prostaglandin E1.

1. Cholinergic synapses in the hypothalamus may transmit information in those thermoregulatory pathways which function to raise body temperature. The effect of atropine, administered intracranially, on the febrile response to intravenous leucocyte pyrogen or intracranial prostaglandin E1 was therefore examined in conscious rabbits. 2. In rabbits exposed to a thermoneutral environment, micro-injections of PGE1, into the anterior hypothalamus, intraventricular injections of PGE1, and intravenous injection so leucocyte pyrogen all caused fever accompanied by vasoconstriction in the ears and reduced respiratory rate. Intraventricular injection of 200 mug atropine during such fevers attenuated their development. This was due to the activation of heat loss mechanisms through vasodilatation in the ears and an increase in the frequency of respiration. This suggests a similarity in the pattern of neuronal activity evoked by PGE1 and leucocyte pyrogen, at least at the site(s) where atropine directly or indirectly exerted its effect and in the efferent pathways from this site. 3. In rabbits exposed to a cold environment, intraventricular injection of PGE1 caused fever through the activation of shivering accompanied by increased O2 consumption. Intraventricular injection of atropine during the development of fever caused an inhibition of shivering accompanied by increased O2 consumption. Intraventricular injection of atropine during the development of fever caused an inhibition of shievering and a decrease in O2 consumption so that temperature ceased to rise and returned to normal. 4. During fever, reversal by atropine of the increased heat conservation of rabbits in a neutral environment, and of their increased heat production in a cold environment adds further support to the concept that cholinergic synapses provide an important link in central temperature-rasising pathways.

Animals↗
PubMed1977

The effect of anaesthesia on the inhibition of pentagastrin-evoked gastric acid secretion induced by atropine in the rat.

1. In the anaesthetized, vagally intact rat, with a perfused gastric lumen, atropine produced a maximum inhibition of 60% of maximal pentagastrin-evoked gastric acid secretion. Sub-maximal pentagastrin-stimulated secretion was also inhibited by atropine.2. In the anaesthetized, vagotomized rat, with a perfused gastric lumen, atropine had no inhibitory effect on maximal pentagastrin-evoked gastric acid secretion.3. In the conscious fistula rat, atropine totally abolished both the basal gastric acid secretion and the maximal gastric acid secretion evoked by pentagastrin. In the anaesthetized chronic fistula rat, doses of atropine up to 1.6 mg.kg(-1) administered subcutaneously produced a maximum inhibition of 70% of maximal pentagastrin-evoked gastric acid secretion. Vagotomy did not affect the response to atropine.4. In the conscious Heidenhain pouch rat, doses of atropine up to 1.6 mg.kg(-1) administered subcutaneously produced a maximum inhibition of 70.9% of maximal pentagastrin-evoked gastric acid secretion. Both anaesthesia and vagotomy, alone or in combination, did not affect the response to atropine.

Anesthesia, General↗
PubMed2006

Anticonvulsants for nerve agent-induced seizures: The influence of the therapeutic dose of atropine.

Two guinea pig models were used to study the anticonvulsant potency of diazepam, midazolam, and scopolamine against seizures induced by the nerve agents tabun, sarin, soman, cyclosarin, O-ethyl S-(2-(diisopropylamino)ethyl)methylphosphonothioate (VX), and O-isobutyl S-(2-diethylamino)ethyl)-methyl phosphonothioate (VR). Animals instrumented for electroencephalogram recording were pretreated with pyridostigmine bromide (0.026 mg/kg i.m.) 30 min before challenge with 2 x LD50 (s.c.) of a nerve agent. In model A, atropine sulfate (2.0 mg/kg i.m.) and pyridine-2-aldoxime methylchloride (2-PAM; 25.0 mg/kg i.m.) were given 1 min after nerve agent challenge, and the tested anticonvulsant was given (i.m.) 5 min after seizure onset. In model B, a lower dose of atropine sulfate (0.1 mg/kg i.m.) was given along with 2-PAM 1 min after nerve agent challenge, and the anticonvulsant was given at seizure onset. With the lower dose of atropine, seizure occurrence increased to virtually 100% for all agents; the time to seizure onset decreased for sarin, cyclosarin, and VX; the signs of nerve agent intoxication were more severe; and coma resulted frequently with cyclosarin. The anticonvulsant ED50 doses for scopolamine or diazepam were, in general, not different between the two models, whereas the anticonvulsant ED50 values of midazolam increased 3- to 17-fold with the lower atropine dose. Seizure termination times were not systematically effected by the different doses of atropine. The order of anticonvulsant effectiveness within each model was scopolamine > or = midazolam > diazepam. The findings indicate that the dose of atropine given as antidotal therapy can significantly influence measures of nerve agent toxicity and responsiveness to anticonvulsant therapy.

Animals↗
PubMed2002

Intravenous atropine treatment in infantile hypertrophic pyloric stenosis.

AIMS: To assess the efficacy of a new regimen of intravenous atropine treatment for infantile hypertrophic pyloric stenosis (IHPS) with special reference to regression of pyloric hypertrophy. METHODS: Atropine was given intravenously at a dose of 0.01 mg/kg six times a day before feeding in 19 patients with IHPS diagnosed from radiographic and ultrasonographic findings. When vomiting ceased and the infants were able to ingest 150 ml/kg/day formula after stepwise increases in feeding volume, they were given 0.02 mg/kg atropine six times a day orally and the dose was decreased stepwise. RESULTS: Of the 19 infants, 17 (89%) ceased projectile vomiting after treatment with intravenous (median seven days) and subsequent oral (median 44 days) atropine administration. The remaining two infants required surgery. No significant complications were encountered. Ultrasonography showed a significant (p < 0.05) decrease in pyloric muscle thickness, but no significant shortening of the pyloric canal after completion of the atropine treatment. The patients exhibited failure to thrive at presentation, but were thriving at 6 months of age (p < 0.01). CONCLUSIONS: This atropine therapy resulted in satisfactory clinical recovery. Pyloric muscle thickness was significantly reduced.

Atropine↗
PubMed1998

Effect of atropine on gastro-oesophageal reflux and transient lower oesophageal sphincter relaxations in patients with gastro-oesophageal reflux disease.

BACKGROUND: Atropine reduces the rate of reflux episodes in normal subjects by inhibition of transient lower oesophageal sphincter (LOS) relaxations. The aim of this study was to investigate the effect of atropine on the rate and mechanisms of reflux in patients with reflux disease. METHODS: Oesophageal motility and pH were recorded for one hour after a meal in 15 patients with reflux disease. On separate days, atropine (15 micrograms/kg bolus intravenously, 4 micrograms/kg/h infusion) or saline were given and maintained for the recording period. RESULTS: Atropine significantly reduced basal LOS pressure from 7.1 (2.2) to 2.9 (1.3) mm Hg (mean (SEM)). Atropine also reduced the rate of reflux episodes from 5.0 (2.0-8.75) to 1.0 (0-6.25) per hour (median (interquartile range)) largely because of a decrease in the rate of transient LOS relaxations from 2.0 (0-4.75) to 0 (0-0) per hour and abolition of reflux during swallow induced LOS relaxation. There was no change in the rate of reflux episodes because of absent basal LOS pressure. CONCLUSIONS: Atropine inhibits reflux in patients with reflux disease largely by inhibition of transient LOS relaxations and swallow induced LOS relaxation. These findings suggest that pharmacological control of reflux through control of transient LOS relaxations is possible in patients with reflux disease.

Adult↗
PubMed1992

Effects of atropine on autonomic indices based on electrocardiographic R-R intervals in healthy volunteers.

The dose dependent responses to atropine of 11 indices of autonomic function were investigated in 10 healthy volunteers. Five subjects were given cumulative doses of atropine (0.1-2.0 mg/70 g, intravenously). The other five received equivalent volumes of water for injection. The ratio of the longest to the shortest R-R intervals in the electrocardiogram during forced expirations and deep inspirations (respiratory ratio), deviations in the periods of consecutive cardiac cycles, the ratio of the longest to the shortest R-R intervals during a Valsalva manoeuvre (Valsalva ratio), the ratio of the 30th to the 15th R-R intervals after standing up from a low sitting position (30:15 ratio), and the means of R-R intervals recorded in standing or lying positions were calculated with different computer algorithms. Sympathetic orthostatic effects on the above indices were measured by comparing values in supine and standing positions after atropinization. The recumbent respiratory ratio was the most sensitive test to atropinization. Its maximum response was a 97% decrease, indicating specificity for the vagal tone. The decrease in other indices in response to atropine ranged from 34% to 94%. The average orthostatic effect on the indices after atropinization was a 14.6% increase. The Valsalva ratio failed to respond significantly to any degree of muscarinic antagonism. In conclusion, the Valsalva ratio is unlikely to be closely related to the parasympathetic control of the heart. However, the resting vagal tone can be selectively measured in a live and conscious person by using the respiratory ratio.

Atropine↗
PubMed1979

A comparative study of atropine methonitrate, salbutamol, and their combination in airways obstruction.

Dose-response relationships of the cholinergic antagonist, atropine methonitrate, and the beta-adrenergic agonist, salbutamol, were examined by cumulative dose techniques. A wet aerosol, 1.5 mg atropine methonitrate produced a maximum response. The response to 200 microgram of salbutamol from a pressurised aerosol was close to maximum. Secondly, the bronchodilator response of salbutamol microgram was compared with atropine methonitrate 2 mg and placebo in 18 asthmatic patients in a randomised crossover study. In 11 of them the bronchodilator response of the combination of salbutamol and atropine methonitrate was evaluated. Atropine methonitrate produced a similar peak bronchodilator effect to salbutamol, but its effect was more prolonged, the response being significantly greater at four and six hours than with salbutamol. The combination of drugs produced a significantly greater and more lasting bronchodilatation than either of the drugs alone. Despite mild side effects, atropine methonitrate, either alone or in combination with an adrenergic drug, appears to have a place in the treatment of sever reversible airway obstruction not adequately controlled by conventional treatment.

Aerosols↗
PubMed1996

Cardiopulmonary effects of combinations of medetomidine hydrochloride and atropine sulphate in dogs.

Medetomidine and xylazine are alpha 2 adrenoceptor agonists which are used as sedatives and premedicants in small animals. However, bradycardia is a side effect and the use of atropine sulphate has been recommended to counteract it. This study investigated the effects of combining medetomidine (40 micrograms/kg) and atropine (30 micrograms/kg) on the cardiopulmonary function of six dogs. Medetomidine administered alone caused severe bradycardia, but hypertension was mild and transient. Medetomidine and atropine administered together caused an initial bradycardia, but within 15 minutes there was tachycardia accompanied by a mean arterial blood pressure of 210 mm Hg. When atropine was administered 30 minutes before medetomidine, tachycardia and hypertension were observed within five minutes of the medetomidine injection. Thus, although atropine will counteract medetomidine-induced bradycardia, its use results in prolonged and severe hypertension, in association with the tachycardia. Although atropine may be life-saving when bradycardia is profound, its indiscriminate use in combination with alpha 2 adrenoceptor agonists may be disadvantageous.

Adrenergic alpha-Agonists↗
PubMed1978

Atropine blockade of cholinergic drugs on rabbit stomach muscle.

The competition between atropine and a full agonist, carbachol, was tested on dibenamine-pretreated smooth muscle of rabbit stomach. Even after extensive irreversible blockade by dibenamine, atropine blockade of the response to carbachol was still competitive and the atropine affinity constant was unchanged. This differed from the noncompetitive action of atropine in blocking the contractile effects of partial agonists such as pilocarpine or heptyl trimethylammonium. The results thus indicate that it is not possible to convert a full agonist into a partial agonist merely by reducing the number of available cholinergic receptors. The present study compares the competitive effect of atropine on the actions of the full agonist carbachol, under conditions of irreversible blockade, with the competitive effect of atropine on partial agonists such as pilocarpine or heptyl trimethylammonium.

Animals↗
PubMed2005

Atropine-induced HRV alteration is not amended by electroacupuncture on Zusanli.

Acupuncture is known to influence autonomic nervous activity. Acupuncture on Zusanli points has been shown to enhance the regularity of gastric myoelectrical activity and accelerate gastric emptying, partly through the vagal pathway, in dogs. The aim of this study was to evaluate whether atropine-induced autonomic nervous alteration, measured by heart rate variability (HRV), could be amended by electroacupuncture on Zusanli points. HRV measurements were recorded in 15 healthy volunteers before, during and after electroacupuncture. Each subject was studied for three sessions in a randomized sequence, which included electroacupuncture on the Zusanli (St 36) points with or without premedication of atropine and placebo stimulation on a non-acupoint. The analysis of low frequency (LF), high frequency (HF) and LF/HF ratios were compared between different sessions. Serum levels of gastrin, motilin and pancreatic polypeptide (PP) levels were also measured. There was an increase in the LF/HF ratio (indicating increased sympathetic activity) during the post-acupuncture period with 2 Hz of electrical stimulation on the Zusanli acupoints. When IV atropine was used immediately before the electroacupuncture, there was a decrease in the LF power and HF power during the acupuncture and post-acupuncture periods. In addition, there was a significant increase in the LF/HF ratio during the acupuncture and post-acupuncture periods. There was a significant decrease in serum PP in the post-acupuncture period after premedication with IV atropine. In conclusion, atropine-induced HRV change might be mediated via the vagal pathway. However, atropine-induced HRV alteration is not amended by electroacupuncture on Zusanli points.

Adult↗
PubMed1979

Effect of atropine and vagotomy on response of transplanted pancreas.

It is well established that atropine and vagotomy inhibit pancreatic enzyme secretion in response to intestinal stimulants such as fat or amino acids. These effects are usually attributed to interference with hypothetical vagal cholinergic mechanisms that facilitate release of cholecystokinin. To determine whether atropine or vagotomy interferes with release of humoral stimulants of pancreatic enzyme secretion, we studied their effect on protein secretion from an autotransplanted portion of pancreas in response to intestinal stimulants in dogs. The transplanted pancreas was as sensitive as the intact pancreas to stimulation by exogenous caerulein, a cholecystokinin-like peptide, and this response was not altered by atropine or vagotomy. Therefore, if vagotomy or atropine interferes with release of humoral pancreatic stimulants, they would be expected to reduce the response of the transplanted pancreas just as they do of the intact pancreas. Truncal vagotomy caused no significant change in protein secretion from the transplant in response to intestinal perfusion with sodium oleate or tryptophan. Atropine was tested only against sodium oleate and caused no change in response. We conclude that release of humoral pancreatic excitants of protein secretion in response to intestinal stimulants is not significantly changed by atropine or vagotomy.

Animals↗
PubMed1981

Effect of atropine on pancreatic response to HCl and secretin.

In dogs with gastric and pancreatic fistulas, we studied the effect of atropine on the pancreatic secretory response to secretin and intestinal HCl. Atropine sulfate (20 micrograms.kg-1.h-1 iv) significantly depressed basal bicarbonate and protein output. Atropine depressed bicarbonate responses to low doses (62.5, 125, 250, and 500 ng.kg-1.h-1) of secretin but had no significant effect on responses to high doses (1,000 and 2,000 ng.kg-1.h-1). Secretin, with or without atropine, did not stimulate pancreatic protein output above basal. Atropine depressed bicarbonate responses to low loads (3, 6, and 12 mmol.h-1) of HCl but had no significant effect on responses to high loads (12, 24, and 48 mmol.h-1). Intraduodenal HCl produced a dose-dependent increase in protein output. Atropine abolished protein responses to low loads (3 and 6 mmol.h-1) but did not affect responses to high loads (24 and 48 mmol.h-1) of HCl. These findings are compatible with the hypotheses that a) endogenous cholinergic activity augments the pancreatic bicarbonate response to secretin, and b) the pancreatic protein response to intraduodenal HCl is, at least in part, mediated cholinergically.

Animals↗