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PubMed1984

Morphine sulfate inhibits bronchoconstriction in subjects with mild asthma whose responses are inhibited by atropine.

To determine whether morphine sulfate alters the bronchoconstrictive response to inhalation of distilled water, we gave 13 subjects with mild asthma 0.15 mg/kg morphine sulfate or normal saline intravenously, after which they inhaled increasing volumes of nebulized distilled water from an ultrasonic nebulizer. We constructed stimulus-response curves, and by interpolation determined the provocative output of the nebulizer that resulted in a 50% increase in SRaw from baseline (PO50). On a separate day the subjects inhaled 2.0 mg of atropine sulfate 30 min before they inhaled distilled water. We compared the bronchoconstrictive response after morphine and after atropine with the bronchoconstrictive response after saline by determining the ratio of the PO50 values. Atropine was considered effective in inhibiting bronchoconstriction in 7 of the 13 subjects in whom the ratio of PO50 after atropine to the PO50 after saline was greater than 2.0. By similar criteria, morphine was also considered effective in 5 of these 7 subjects. Neither atropine nor morphine was effective in the remaining 6 subjects. By chi-square analysis, we found a positive correlation between the inhibitory effects of morphine and those of atropine (p less than 0.05). In the 5 subjects in whom morphine was effective, naloxone reversed the inhibitory effect of morphine. Atropine caused significant baseline bronchodilation when compared with placebo (normal saline), whereas morphine did not. We conclude that opiate receptor stimulation by morphine causes inhibition of the vagally mediated component of water-induced bronchoconstriction.

Adult↗
PubMed1986

Comparative absorption of inhaled and intramuscularly administered atropine.

The inhalation of atropine sulfate was investigated in a randomized, 4-period, rising-dose study. Atropine sulfate 2, 4, and 6 mg by inhalation, and atropine free base 1.67 mg (equivalent to 2.0 mg atropine sulfate) by intramuscular (IM) injection were given to 8 healthy, nonsmoking subjects. Serum atropine sulfate concentrations were monitored during an 8-h period by radioimmunoassay. Mean serum concentrations and area under the serum concentration-versus-time curves (AUC) increased as the inhaled dose increased. Peak concentrations (mean +/- SD) were 11.5 +/- 3.4, 16.4 +/- 6.2, and 18.0 +/- 3.1 ng/ml for the 2, 4, and 6 mg doses, and 11.7 +/- 2.5 ng/ml for the IM dose. The time to peak concentration for each dose was similar (mean, 0.8 to 1.9 h). The AUC ratio of the 2-mg inhaled and IM doses was 1.11 +/- 0.41. The observed bronchodilating, anticholinergic, and other pharmacologic effects were seen after all dose concentrations and were typical of atropine. This study showed that inhalation is an efficient way to administer atropine sulfate for systemic use.

Absorption↗
PubMed1985

Effects of atropine and gastric inhibitory polypeptide on hepatic glucose uptake and insulin extraction in conscious dogs.

Previous studies comparing the effects of oral, intraportal, and peripheral venous administration of glucose in conscious dogs demonstrated a significant increase in hepatic extraction of insulin only after oral glucose, but similar hepatic uptake of glucose after oral and intraportal glucose, which was greater than that after peripheral intravenous glucose infusion. This study evaluated the effect of atropine blockade of the parasympathetic nervous system on the increased fractional hepatic extraction of insulin and the role of gastric inhibitory polypeptide (GIP) on augmented hepatic uptake of oral glucose in conscious dogs with chronically implanted Doppler flow probes on the portal vein and hepatic artery, and catheters in the portal and hepatic veins and carotid artery. Since atropine infusion decreased absorption of glucose, and in order to achieve comparable portal vein levels of glucose and insulin, the dogs receiving atropine were given 1.9 +/- 0.1 g/kg glucose, compared with the control dogs who received 1.1 +/- 0.1 g/kg. The percentage of the glucose load that was absorbed was greater in the dogs not given atropine (80 +/- 4 vs. 44 +/- 7%), but because of the different loads, the absolute amount of glucose absorbed was similar in both groups (20.2 +/- 1.6 vs. 21.7 +/- 4.1 g). Although delayed by atropine, the peak portal vein glucose and insulin concentrations and the amounts presented to the liver were similar in both groups. However, the increased portal vein plasma flow and fractional hepatic extraction of insulin observed after oral glucose was not observed in the dogs infused with atropine. The net hepatic glucose uptake after oral glucose was significantly less at 10, 20, and 45 min in the atropine-treated dogs, and the area under the curve over the 180-min period was 44% less. However, the latter was not statistically significant. Infusion of GIP with peripheral intravenous glucose did not increase hepatic uptake of glucose or the fractional hepatic extraction of insulin compared with peripheral intravenous glucose alone. These results indicate an important role for parasympathetic innervation in the augmented fractional hepatic extraction of insulin, and increased portal vein plasma flow after oral glucose. Although a relationship between the augmented fractional extraction of insulin and the net hepatic glucose uptake may exist, it does not necessarily indicate that the former is required for the latter. Such parasympathetic innervation may be involved in the greater removal of glucose by the liver after oral compared with peripheral glucose administration. The augmented hepatic uptake of glucose and fractional hepatic extraction of insulin after oral glucose doesn not appear to be mediated by gastric inhibitory polypeptide.

Administration, Oral↗
PubMed1978

Effect of atropine on meal-stimulated gastrin and gastric inhibitory polypeptide (GIP) release.

The effect of atropine on meal-stimulated gastric inhibitory polypeptide (GIP) and gastrin release was studied in 5 purebred foxhounds and compared with control studies done in the same animals given a meal without atropine, peak incremental serum gastrin occurred between 5 and 15 min after the meal whereas the greatest increment in serum GIP occurred 60 min postcibal. Atropine had no effect on basal concentrations of gastrin or GIP. However, when atropine was given before feeding serum gastrin concentrations from 75 to 120 min postcibal were significantly higher (P less than 0.04) than after the meal alone. The normal meal-stimulated rise in serum GIP was almost completely inhibited by atropine. We conclude that: 1) the rise in serum gastrin adter a meal preceeds the rise in serum GIP; 2) atropine potentiates the late gastrin response while suppressing the increase in serum GIP after a meal; and 3) the mechanism by which atropine potentiates gastrin release may be related to its suppressive effects on intestinal inhibitors of gastrin secretion, such as GIP.

Animals↗
PubMed2000

Low-dose atropine attenuates muscle sympathetic nerve activity in healthy humans.

Central muscarinic receptors play an important role in the regulation of cardiac vagal nerve activity. We studied the inhibition of central muscarinic receptors and sympathetic nerve function in humans, since very little information is currently available on this subject. We examined the effects of graded doses of atropine (five doses, range 0.001 to 0.016 mg/kg) on heart rate, arterial pressure, heart rate variability, and muscle sympathetic nerve activity in 13 healthy young volunteers. Atropine caused biphasic effects on heart rate and the high-frequency (HF) power of R-R interval variability. At lower doses (< or =0.002 mg/kg for heart rate, 0.001 mg/kg for HF power), atropine decreased heart rate and increased HF power. In contrast, at higher doses, atropine increased heart rate and decreased HF power. Low-dose atropine significantly attenuated muscle sympathetic nerve activity, burst rate (bursts/min) by -30.5 +/- 6.0% and burst incidence (bursts/100 heart beats) by -23.8 +/- 6.9% at 0.002 mg/kg. Systolic and diastolic arterial pressure did not change with atropine infusion. Low-dose atropine (< or =0.002 mg/kg) did not significantly affect either low frequency (LF) power or LF/HF. These results suggest that central muscarinic receptors may modulate not only cardiac vagal nerve activity but also sympathetic nerve activity in the skeletal muscle vasculature.

Adult↗
PubMed1977

Comparative bronchodilator responses to atropine and terbutaline in asthma and chronic bronchitis.

We have compared bronchodilator responses to atropine and terbutaline in 39 chronic bronchitics and 16 stable asthmatics. Fasting subjects were given either 1.05 mg atropine of 5.0 mg terbutaline orally. Pulmonary function was assessed using the peak responses, namely: three 60-minute intervals for terbutaline and three 30-minute intervals for atropine. A subgroup of five reactive bronchitis patients was given a placebo with no response. Areas under the percent response-time interval curve were compared. Both patient groups responded to the same degree to atropine and terbutaline with respect to reduction of airway resistance. However, the FEV1 and V50 responses to terbutaline were markedly enhanced compared to atropine in the asthmatics while equal to the atropine response in the bronchitis patients. Thus, atropine appears to exert its effect upon both large and small airways in bronchitis, but predominantly on large airways in asthma. The results are consistent with a state of enhanced vagal tone in small airways in bronchitis compared to asthma, but other explanations are conceivable.

Airway Resistance↗
PubMed1980

The effect of atropine inhalation in "irreversible" chronic bronchitis.

Fifteen patients with chronic bronchitis and airflow obstruction which was not improved by inhalation of isoproterenol (increase in forced expiratory volume in one second [FEV1] less than 15 percent) received an aerosol of atropine sulfate (0.05 mg/kg of body weight), in order to determine their response to an anticholinergic bronchodilator drug. The improvement over initial values for FEV1 at 15 minutes following inhalation of isoproterenol and at 90 minutres following inhalation of atropine averaged 5.9 percent and 19.2 percent, respectively (P less than 0.01). Eleven of 15 patients demonstrated a 15 percent or greater increase in FEV1 following inhalation of atropine, and six subjects demonstrated more than 25 percent improvement. The maximum effect of atropine was observed at or later than 90 minutes following inhalation in nine of 11 patients who were responsive to atropine. Minimal systemic toxic effects resulted from inhalation of atropine, although dryness of the mouth was frequent. In patients with chronic bronchitis, airflow obstruction resistant to isoproterenol may respond to inhalation of an aerosol of atropine sulfate.

Aged↗
PubMed1981

The response to atropine sulfate given by aerosol and intramuscular routes to patients undergoing fiberoptic bronchoscopy.

Two groups of 11 patients each were studied in their responses to intramuscular (IM) or aerosolized atropine sulfate, given in preparation for fiberoptic bronchoscopy. The patients in group 1 received 1.0 mg of atropine IM, and those in group 2 were given a prepared solution of atropine in saline (5 mg/ml) at a dosage of 0.1 mg/kg by nebulization (IPPB). Statistical analysis of the FVC, FEV1, FEF25-75%, and FEFmax showed excellent protective bronchodilatory effects of both IM and aerosolized atropine. In fact, the beneficial result was more prolonged when the drug was administered by inhalation. One possible factor to consider, however, is that atropine given by the aerosol route did not inhibit the vasovagal response in three of the 11 patients. Another factor to take into account is that atropine by IM injection is quicker to administer, more convenient, and requires less instrumentation than atropine given by aerosol.

Adult↗
PubMed1992

A comparative analysis of the neuroendocrine mechanisms regulating ovulation, affected by a unilateral implant of atropine in the preoptic-anterior hypothalamic area, in intact and hemiovariectomized adult rats.

The effects were analysed of a unilateral implant of atropine on ovulation in intact and hemiovariectomized adult rats, together with the response of the atropine-implanted rats to hormone replacement. An outer cannula directed to the left or right preoptic (POA)-anterior-hypothalamic area (AHA) was implanted into cyclic adult rats. A group of animals in oestrus was hemiovariectomized and some were also implanted with a cannula. After two consecutive 4-day cycles, the hemiovariectomized animals were implanted with atropine (23 +/- 4 micrograms) or cholesterol (25 +/- 2 micrograms) on the day of oestrus. Atropine implanted into the left side of the POA-AHA blocked ovulation and compensatory ovarian hypertrophy, whilst implants in the right side had no effects. Administration of gonadotrophin-releasing hormone (GnRH; 3.7 micrograms/kg) at 13.00 h on the expected day of pro-oestrus induced ovulation in six out of seven treated animals. Of 19 rats with an implant of atropine in the left side of the POA-AHA, one ovulated after treatment with pregnant mare serum gonadotrophin (PMSG) on oestrus, or oestradiol benzoate or human chorionic gonadotrophin (hCG) on day 2 of dioestrus. The effects on ovulation of a unilateral implant of atropine into the POA-AHA of cyclic adult rats and the responses of such rats to GnRH, PMSG, hCG and oestradiol benzoate replacement were also studied. Ovulation was induced in rats with a unilateral implant of atropine and which had been treated with GnRH or hCG at 13.00 h on the expected day of pro-oestrus after the implant.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Effects of atropine sulfate on rat harderian glands: correlation between morphological changes and porphyrin levels.

We examined the correlation between histopathological changes and porphyrin levels in the Harderian glands of male rats after treatment with atropine sulfate. After a single administration of atropine sulfate (250 mg/kg/day), the porphyrin levels in the Harderian glands gradually increased, beginning from 2 hr after administration, and at 36 hr reached a maximum level, which was about 7 times higher than that of the control animals. Histopathologically, the Harderian glands showed marked luminal dilatation and a brownish pigment accumulation in the lumina 6 hr after a single dose. Under daily repeated administrations of atropine sulfate (250 mg/kg/day), the highest porphyrin levels in the Harderian glands were observed 24 hr after the third dose, and were about 9 times higher than those of the control animals. However, beginning from one week after the initial dose, much lower peak porphyrin levels were observed 6 hr after each dose. The maximum porphyrin levels were only twice as high as those of the control animals, and they returned to the control levels 24 hr after each atropine dose. Histological examinations of the Harderian glands revealed that repeated administrations of atropine sulfate induced the same histopathological changes observed after a single atropine administration, and that no aggravated dilation of the lumina or pigmentation in the lumina appeared after such repeated administrations. The degree and incidence of the histopathological changes observed correlated well with the porphyrin levels. Some animals showed a degeneration of the glandular epithelium after 4 weeks of treatment, and the frequency increased slightly after 13 weeks of treatment. The present study suggests that atropine suppresses the expulsion of secretory materials, including porphyrin, from the glandular lumen of the Harderian glands, and thereafter an excessive accumulation of porphyrin induces luminal dilatation. These changes were gradually reduced by repeated administrations. The degeneration of the glandular epithelium after repeated administration might be a consequence of retention of an excessive accumulation of porphyrin.

Animals↗
PubMed2005

Atropine-induced inhibition of sperm and semen transport impairs fertility in male rats.

Previous studies revealed that atropine reduced male fertility in rats without any effects on mating performance, sperm production and motility, and testicular morphology. The present study was conducted to investigate whether the impairment of male fertility induced by atropine was related to the inhibition of sperm and semen transports from the vas deferens and seminal vesicle to the urethra during the process of emission. Male rats were treated with atropine at 125 mg/kg/day for 10-17 days prior to mating with untreated females. After confirmation of mating, male rats were euthanized and sperm number in the vas deferens and weights of the seminal vesicle and copulatory plug were determined as indicators of inhibition of sperm and semen transports, respectively. Reproductive status of mated females was determined on gestation days 15-17. A low pregnancy rate associated with a decreased number of implants was observed in females that mated with the atropine-treated males. The average number of sperm in the vas deferens was increased in the atropine-treated males. The average seminal vesicle weight in the atropine-treated males was greater than that of controls. The copulatory plug weights were decreased in the atropine-treated males. These results suggest that inhibitions of sperm and semen transports from the vas deferens and seminal vesicle to the urethra during the process of emission result in reduced male fertility in rats.

Administration, Oral↗
PubMed2001

Effects of preemptive atropine administration on incidence of medetomidine-induced bradycardia in dogs.

OBJECTIVE: To determine the cardiorespiratory effects of preemptive atropine administration in dogs sedated with medetomidine. DESIGN: Randomized crossover trial. ANIMALS: 12 healthy adult dogs. PROCEDURES: Dogs underwent 6 treatments. Each treatment consisted of administration of atropine (0.04 mg/kg [0.018 mg/lb] of body weight, IM) or saline solution (0.9% NaCl, 1 ml, IM) and administration of medetomidine (10, 20, or 40 microg/kg [4.5, 9.1, or 18.2 microg/lb], IM) 10 minutes later. Treatments were administered in random order, with a minimum of 1 week between treatments. Cardiorespiratory effects before and after atropine and medetomidine administration were assessed. Duration of lateral recumbency and quality of sedation and recovery were assessed. RESULTS: Bradycardia (heart rate < 60 beats/min) was seen in all dogs when saline solution was administered followed by medetomidine, and the dose of medetomidine was not associated with severity or frequency of bradycardia or second-degree heart block. However, a medetomidine dose-dependent increase in mean and diastolic blood pressures was observed, regardless of whether dogs received saline solution or atropine. Preemptive atropine administration effectively prevented bradycardia and second-degree heart block but induced pulsus alternans and hypertension. The protective effects of atropine against bradycardia lasted 50 minutes. Blood gas values were within reference limits during all treatments and were not significantly different from baseline values. Higher doses of medetomidine resulted in a longer duration of lateral recumbency. CONCLUSIONS AND CLINICAL RELEVANCE: Preemptive administration of atropine in dogs sedated with medetomidine effectively prevents bradycardia for 50 minutes but induces hypertension and pulsus alternans.

Adrenergic alpha-Agonists↗
PubMed1990

Comparison of loxiglumide, a cholecystokinin receptor antagonist, and atropine on hormonal and meal-stimulated pancreatic secretion in man.

The effects of loxiglumide, a potent cholecystokinin (CCK)-receptor antagonist, and atropine, a muscarinic receptor blocker, on exocrine pancreatic secretion stimulated by hormones (secretin plus CCK) and a Lundh test meal were studied in healthy young volunteers. Loxiglumide infused intravenously in gradually increasing doses (2-16 mumol/kg-h) caused a dose-dependent inhibition of pancreatic enzyme secretion induced by intravenous infusion of a constant dose of secretin (82 pmol/kg-h) plus CCK-8 (85 pmol/kg-h) but had relatively smaller influence on duodenal volume flow and bicarbonate output. Atropine (20 nmol/kg) also caused a significant reduction in pancreatic enzyme secretion but failed to affect the volume flow or bicarbonate secretion induced by secretin plus CCK, possibly owing to the high doses of secretin and CCK used in these tests. Both loxiglumide and atropine inhibited the pancreatic enzyme response to a Lundh meal, but atropine was more effective in the early phase and loxiglumide in the late phase of the postprandial secretion. Neither loxiglumide nor atropine affected the plasma gastrin and CCK levels, but both antagonists reduced plasma pancreatic polypeptide responses to the Lundh meal. We conclude that 1) loxiglumide results in a relatively stronger suppression of the pancreatic enzyme than aqueous-alkaline secretion induced by secretin plus CCK, whereas atropine inhibits only enzyme secretion; and 2) both loxiglumide and atropine suppress the pancreatic enzyme responses to the meal stimulation without affecting the postprandial plasma gastrin and CCK responses.

Adult↗
PubMedDate not supplied

Topological distribution of atropine in dipalmitoylphosphatidylcholine liposomes.

The topography of atropine entrapped in sn-3-(dipalmitoyl)phosphatidylcholine (DPPC) liposomes was determined by the electron spin resonance (ESR) technique using 5-, 7-, and 16-nitroxy-stearic acid probes. The liposome preparations, with or without entrapped atropine, were passed through a Sepharose-4B column; the entrapment efficiency and lipid recovery were determined using [3H]-atropine and [14C]-DPPC as tracers. It was found that approximately 31 per cent of the added atropine was entrapped in the liposomes. The ESR results established that the temperature range of the gel-to-liquid crystalline transition of DPPC liposomes was not altered significantly by the encapsulation of atropine. The entrapped atropine also caused no significant change in the order of hydrocarbon chains of DPPC vesicles. These results were confirmed by data obtained from differential scanning calorimetry. On the basis of these experiments, it was concluded that atropine does not interact with the hydrophobic region of the lipid bilayers but is exclusively localized within the entrapped aqueous compartment of DPPC liposomes.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1998

Effect of atropine on ciliary beat in human upper respiratory tract epithelial cells.

The mucociliary apparatus is a fundamental element among the defensive mechanisms of the airways. In man, average ciliary beat frequency (CBF) has been reported to be between 600 and 1,000 beats/min and does not vary significantly at different sites along the respiratory tract. Ciliary function is altered by numerous factors, including temperature, pH, cigarette smoke, drugs, and alcohol. The aim of the present study was to evaluate whether intravenous (i.v.) infusion of atropine alters CBF. We studied nine patients (six females and three males, mean age 42.9 years) with otosclerosis, a nonrespiratory disease. All patients were scheduled for surgical stapedectomy. In all patients, nasal brushing was performed before and 20 min following i.v. injection of 0.5 mg atropine sulphate. The cellular samples, maintained viable in tissue medium, were observed under a microscope and filmed. A quantitative evaluation of ciliary activity was obtained by playing the film back in slow motion. The mean CBF value prior to atropine infusion in the nine patients studied was 588.12 (+/- 53.29 SD) beats/min. After infusion of atropine, mean CBF was 442.33 (+/- 52.82 SD) beats/min. The mean percentage drop in CBF following atropine infusion was 24.79% (t = 5.82, p < 0.001). Our data show a drop in in vitro CBF following atropine infusion which, presumably, reflects a fall in the in vivo efficacy of mucociliary transport. Atropine treatment determined a loss in CBF that was inversely correlated with increasing age.

Adult↗
PubMed2001

The effects of atropine and methotrimeprazine on the epinephrine-induced arrhythmias in halothane-anesthetized dogs.

The effects of atropine and methotrimeprazine on epinephrine-induced ventricular arrhythmias were evaluated in halothane-anesthetized dogs. Ten mixed-breed dogs were assigned to 3 treatments (saline, atropine, and methotrimeprazine) in a randomized complete block design. Anesthesia was induced and maintained with halothane (1.5 minimum alveolar concentration) in oxygen. Controlled ventilation was used throughout to maintain eucapnia. Saline, atropine (0.05 mg/kg, i.v.) or methotrimeprazine (0.5 mg/kg, i.v.) were administered and, 5 minutes later the arrhythmogenic dose of epinephrine (ADE) was measured by i.v. infusion of progressively increasing infusion rates of epinephrine, until the ventricular arrhythmia criterion was met (at least 4 ectopic ventricular contractions (EVCs) during a 15-second period). Data were analyzed using a student's t-test for ADE values and multivariate profile analysis for heart rate (HR), arterial blood pressure (ABP), and rate pressure product (RPP). The ADE increased in atropine- and methotrimeprazine-treated groups, whereas 1 and 4 animals from these groups did not develop any ventricular arrhythmia, respectively. Epinephrine induced multiform premature ventricular contractions (PVCs) in the atropine group, whereas ventricular escape beats were observed in the control and methotrimeprazine groups. Heart rate and RPP decreased, and ABP increased at the time of ADE observation in the control group. Epinephrine infusion in the atropine group caused marked increases in HR, ABP, and RPP, which were associated with pulsus alternans in 2 animals. It was concluded that 1) the presence of cholinergic blockade influences the type of ventricular arrhythmia induced by epinephrine; 2) increased ADE values recorded following atropine administration must be cautiously interpreted, since in this situation the PVCs were associated with signs of increased myocardial work and ventricular failure; and 3) the use of a broader arrhythmia criterion (EVCs instead of PVCs) may not allow a direct comparison between ADE values, since it includes ventricular arrhythmias mediated by different mechanisms.

Analgesics, Non-Narcotic↗
PubMed2001

Successful management of infantile hypertrophic pyloric stenosis with atropine sulfate.

OBJECTIVE: To evaluate the effectiveness of atropine sulfate in management of infantile hypertrophic pyloric stenosis (IHPS). DESIGN: Prospective observational. SUBJECT: Patients attending the hospital with complaints of persistent vomiting and later clinically and sonographically diagnosed as cases of IHPS were selected for the trial. METHODS: Atropine was initially administered intravenously in a dose of 0.06 mg/kg/day in eight divided doses, increased by 0.15 mg/kg/day till vomiting ceased and remained so for a period of 24 hours at a stretch and ultrasonography showed a transit time (of gastric contents through pyloric canal) of less than 1 minute. Intravenous atropine was then substituted by oral atropine at double the effective IV dose for 3 weeks. Ultrasonographic evaluation of pyloric muscle thickness and length was done at the commencement of IV treatment, after completion of oral treatment and at 3,6,9,12 and 15 months follows up. Transit time of gastric contents was measured at the commencement of intravenous treatment and then daily after the vomiting stopped for more than 24 h at a stretch. RESULTS: Medical treatment of IHPS with atropine was successful in 50/52 (96.2%) cases. Vomiting ceased in 1-3 days in all patients with mild hypertrophy and in 4-7 days in all the cases with moderate hypertrophy. In all except 2 patients with severe hypertrophy, vomiting ceased in 8-12 days. These two cases continued to vomit at least once daily even after 2 weeks of IV treatment and ultimately opted out for pyloromyotomy. All the 50 medically treated children made uneventful recovery during oral therapy except 3 cases (6%) in whom vomiting recurred during the follow-up. These 3 children later responded by increasing the dose of oral atropine. All of them began to gain weight by the time oral therapy was commenced and ultrasonographic evidence of normalization of pylorus was observed in all these children 3-15 months after completion of oral therapy. CONCLUSION: Atropine sulfate proved to be an effective and safe treatment option for IHPS.

Atropine↗
PubMed2002

Adverse reaction to atropine and the treatment of organophosphate intoxication.

Atropine is the drug of choice for treatment of organophosphate nerve agent and insecticide intoxication and has been used for this indication for several decades. Adverse reactions to atropine may occur, and are of two types: toxic and allergic. Toxic reaction, the most common form, results from the anti-muscarinic effects of the drug. Since it is most probably related to interpersonal variation in sensitivity to atropine, toxic effects may appear at the usual therapeutic doses. The second type, allergic reaction, includes local manifestations, usually after the administration of eyedrops, and systemic reaction in the form of anaphylaxis. Since most patients manifest only a mild reaction, allergy testing is not performed and the prevalence of allergy to atropine is therefore not known. Severe allergic reaction to atropine is rare, as evidenced by the small number of case reports in the literature despite the drug's extensive use. Alternative anti-muscarinic drugs recommended for OP poisoning include glycopyrrolate and scopolamine. Glycopyrrolate is a peripheral anti-muscarinic drug that has been studied in comparison to atropine for many clinical indications, while scopolamine is an anti-muscarinic drug with both peripheral and central effects. An acceptable alternative regimen for patients with proven allergy to atropine is a combination of glycopyrrolate with centrally active drugs such as benzodiazepines or scopolamine.

Atropine↗