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 253 records · Page 14Linked to original sources
PubMed1975

[Effects of physostigmine and duvadilan on an atropine-resistant contraction of dog's stomach (author's transl)].

Effects of atropine, physostigmine, duvadilan and tetrodotoxin on the mechanical activity of the longitudinal muscle preparation of dog's stomach in vitro experiments and on the motility of stomach in the same animal in vivo experiments were investigated. 1. The latency of an atropine-resistant contraction which was produced by stimulation of vagus nerve was increased in period in accordance with the augmentation of concentration of atropine in vitro experiments. 2. Physostigmine reconstructed the atropine-resistant contraction which was abolished by duvadilan as well as the cholinergic contraction which was abolished by atropine in vivo experiments. 3. Duvadilan abolished the cholinergic and atropine-resistant contractions in vitro, but in vivo experiments duvadilan abolished only the atropine-resistant contraction. 4. An atropine-resistant contraction was completely abolished by administration of tetrodotoxin. But the direct electrical stimulation of the muscle caused the contraction of it which was blocked by tetrodotoxin.

Animals↗
PubMed2006

Influence of atropine on the dose requirements of propofol in humans.

OBJECTIVE: The purpose of this study was to evaluate the effect of atropine on the dose requirement of propofol for induction of anesthesia and propofol concentrations during continuous infusion. METHODS: Study 1: Forty patients were randomly allocated to the control or atropine groups. Induction of anesthesia commenced 3 min following the administration of 0.9% saline or atropine (0.01 mg kg(-1)), using a Diprifuser set to achieve propofol concentration of 6.0 microg mL(-1). The primary end point was the propofol dose per kg at the moment of loss of response to a command. Study 2: Fifteen patients undergoing elective surgery were enrolled. Propofol was administered to all subjects via target-controlled infusion to achieve a propofol concentration at 2.0 microg mL(-1) after intubation. Before and after administration of atropine (0.01 mg kg(-1)), cardiac output (CO) was measured using indocyanine green as an indicator and blood propofol concentration was determined using high-performance liquid chromatography. RESULTS: Study 1: The propofol dose for each group was 2.22+/-0.21 mg kg(-1) for control group and 2.45+/-0.28 mg kg(-1) for atropine, respectively (p=0.014). Study 2: After the administration of atropine, CO was significantly increased from 4.28+/-0.83 to 5.76+/-1.55 l min(-1) (p<0.0001). Propofol concentration was significantly decreased from 2.12+/-0.28 to 1.69+/-0.27 microg mL(-1) (p<0.0001). CONCLUSIONS: Following the administration of atropine, the propofol requirements for the induction of anesthesia were increased and propofol concentrations were decreased during continuous infusion by the administration of atropine.

Adult↗
PubMed1990

A subchronic toxicity study of two inhaled aerosolized atropine sulfate formulations in rats and dogs.

The potential subchronic (21 days) toxicity of inhaled metered aerosol formulations (solution and suspension) of atropine sulfate was investigated in rats and dogs. The doses administered to rats were 0.78 and 2.5 mg/kg/day (solution) or 1.4 and 3.2 mg/kg/day (suspension). In the dog, the daily doses achieved were 0.5 and 1.3 mg/kg/day, regardless of formulation. In both species, sham control animals inhaled air only and vehicle control animals inhaled either placebo solution or placebo suspension. There was no mortality or other evidence of a toxic effect of atropine sulfate. The expected mydriatic effect of atropine sulfate was seen in both species and, similarly, the pupillary light reflex was impaired in rats and dogs receiving either formulation of atropine sulfate at both dose levels. Reduced salivation was also noted and ophthalmologic examinations in both species were unremarkable. In dogs, atropine sulfate (high-dose) caused tachycardia but there was no evidence of an adverse effect on the electrocardiogram or on systolic blood pressure. In both species, atropine sulfate did not alter body weight, food consumption or clinical pathology parameters. Necropsy observations and histopathological findings revealed no effect of atropine sulfate in either species although, in the rat, adrenal gland hypertrophy in both sexes followed inhalation of the suspension at both dose levels. With this possible exception, nothing but the expected pharmacological effects of atropine sulfate were seen in either rats or dogs.

Administration, Inhalation↗
PubMed2002

Delineating potential control mechanisms of mammary protein synthesis utilizing atropine.

Amino acids (AA) and/or somatotropin (ST) were infused into a jugular vein of lactating cows receiving atropine to determine the effect on milk protein secretion. Atropine decreased milk protein yield by 35%. Plasma alpha-amino nitrogen, which was decreased by 31% due to atropine, was restored to control levels upon AA infusion. Plasma ST concentration was not affected by atropine and, upon ST infusion, increased by 236% in treated animals. Amino acids, ST, or the combination of the two were unable to return milk protein to control levels in atropine-treated animals. Plasma insulin concentration decreased by 37% in atropine-treated animals and was not significantly different for cows receiving atropine as well as ST, AA, or both ST and AA. Similarly, glucagon decreased by 36% in atropine-treated animals but was partially restored in cows receiving AA. Overall, the insulin-to-glucagon ratio was not significantly affected by treatment. Plasma glucose concentration was not affected by treatment. These data lend support to the importance of the insulin-to-glucagon ratio in terms of whole-body metabolism, with the exception of the mammary glands, which are glucagon-insensitive and, therefore, sensitive to the observed decrease in circulating insulin concentration.

Amino Acids↗
PubMed1997

Effect of atropine on milk protein yield by dairy cows with different beta-lactoglobulin phenotypes.

The objective of this study was to determine the response of individual milk proteins to a reduction in amino acid (AA) availability induced by atropine and to determine whether the response was different in cows with different beta-lactoglobulin (LG) phenotypes. Six cows that were homozygous for the A variant of beta-LG and six cows that were homozygous for the B variant of beta-LG were each given a single subcutaneous injection of saline or 20 mg of atropine. In both groups of cows, atropine decreased milk yield by 30% and reduced the concentration of alpha-lactalbumin (LA) by 25 to 30% at 8 h following injection. Eight hours after atropine injection, yield of beta-LG was 41% lower than it was following saline injection, and yield of beta-casein (CN) after atropine injection declined 16% relative to saline. Concentrations of BSA and the ratio of gamma-CN to beta-CN, which reflects plasmin activity in milk, were significantly increased after administration of atropine. Although the response to atropine tended to be more pronounced in cows that were homozygous for beta-LG B, they were not significantly different from the response of cows that were homozygous for beta-LG B, they were not significantly different from the response of cows that were homozygous for beta-LG A. The differential response of individual proteins to a reduction in AA concentrations in whole blood suggested that susceptibility to restriction in substrate availability differed for individual proteins. The concentration of lactose in plasma did not change, which implied that the integrity of the mammary epithelial barrier was not compromised when AA derived from blood were diminished. The consistent concentration of lactose combined with the minimal increase in total yield of BSA in milk following atropine treatment indicated that the increased concentration in milk of proteins derived from serum was due to the concentrating effect of lower milk volume.

Animals↗
PubMed1992

Influence of atropine on the acute toxicity of isometamidium.

The effectiveness of atropine in blocking the acute toxic effects of the antitrypanosomal drug isometamidium (ISMM) was evaluated in mice and goats using lethality as the primary index. The median lethal dose (LD50) of ISMM in nonatropinized mice was 45.3 mg/kg bodyweight (SE +/- 5.3 mg/kg bodyweight), whereas the LD50 of ISMM in mice pre-treated with atropine was 71.7 mg/kg bodyweight (SE +/- 13.2 mg/kg bodyweight). The increase in LD50 was about 60%. The ratio of the slope of the dose-response curve for ISMM in non-atropinized mice to that in atropinized mice was about 4:1. The results showed that atropine was effective in considerably reducing the lethal effect of ISMM in mice. In contrast, experiments in goats showed markedly different results; atropine was not effective in reducing the lethality of ISMM. It was concluded that in mice atropine has some beneficial action in cases of overdosage or poisoning by ISMM. Treatment with atropine should be attempted as an antidotal measure in humans accidentally poisoned with ISMM.

Animals↗
PubMed2005

Atropine aborts bradycardic effect of endotracheally administered vasopressin.

BACKGROUND: Vasopressin is an alternative drug to adrenaline in intractable ventricular fibrillation. However, vasopressin can cause significant bradycardia, resulting in reduced cardiac output. We investigated whether pre-treatment with atropine abrogates vasopressin-induced bradycardia in a beating-heart canine model. MATERIAL/METHODS: Five adult mongrel dogs received endotracheal vasopressin (1.0 U/kg) with or without endotracheal atropine (0.02 mg/kg) or a placebo (10 ml saline) after being anesthetized and ventilated. Hemodynamic variables and arterial blood gases were determined. Each dog (studied 3 times, one week apart) served as its own control. RESULTS: Endotracheal vasopressin produced early and significant (p<0.05) bradycardia (from 55+/-7 mmHg to 35+/-5 beats/min) compared with controls, starting one minute post-injection and lasting one hour. In contrast, in atropine-pretreated animals the heart rate increased significantly (p<0.05) for as long as one hour post-atropine and vasopressin administration. In addition, animals treated with vasopressin with or without atropine exhibited a significant rise in diastolic blood pressure (from 83+/-5 to 160+/-15 and from 83+/-3 to 108+/-10 mmHg, respectively). Systolic and mean blood pressures also increased significantly compared with controls. Blood gases remained unchanged in all groups. CONCLUSIONS: Endotracheal administration of vasopressin can cause protracted bradycardia. Pretreatment with atropine can abrogate this effect. We suggest that atropine administration be considered when vasopressin is administered during cardio-pulmonary resuscitation. Further studies are warranted to evaluate the effect of vasopressin and atropine in a closed-chest model of cardio-pulmonary resuscitation.

Administration, Inhalation↗
PubMed2006

[The effects of continuous infusion of landiolol on heart rate changes after neostigmine-atropine administration during recovery from general anesthesia].

BACKGROUND: On reversal of muscle relaxants when neostigmine-atropine mixture is used, heart rate changes occurr. We examined whether landiolol attenuate the initial increases in heart rate after intravenous injections of a neostigmine-atropine mixture. METHODS: Twenty-four patients were assigned to one of two groups (n=12 each): control group and landiolol group. Anesthesia was induced with propofol and was maintained with isoflurane-nitrous oxide-pentazocine. A mixture of neostigmine 2 mg and atropine 1 mg was injected intravenously over 30s in the control group. In the landiolol group, 0.125 mg x kg)-1) x min(-1) of landiolol for 1 minute was administered immediately after neostigmine-atropine injection. Blood pressure and heart rate were measured noninvasively. RESULTS: Heart rate was significantly increased after neostigmine-atropine administration compared with that at pre-administration in both groups. At 2 and 3 minutes after neostigmine-atropine administration, heart rate in the landiolol group was significantly lower than that in the control group. The maximum increase in heart rate after the neostigmine-atropine injections was significantly less in the landiolol group than that in the control group. Blood pressure showed no significant changes in both groups during the observation period. CONCLUSIONS: Landiolol was useful for heart rate control after neostigmine-atropine administration during recovery from general anesthesia.

Adrenergic beta-Antagonists↗
PubMed1990

[Atropine resistance and its significance in the selection of the method of surgical treatment of duodenal ulcer].

Medical vagotomy with atropine allows two types of patients with duodenal ulcer to be distinguished--atropine-resistant and atropine-sensitive. A complicated course of the disease, high values of nocturnal gastric secretion before the operation, and positive Hollander's insulin test after vagotomy are encountered most frequently in atropine-resistant patients. The values of gastrin are significantly higher in these patients than in atropine sensitive patients. In 3-year follow-up periods, recurrence of the ulcer after vagotomy was revealed in 6.5% of atropine-resistant patients but in none of the atropine sensitive patients. Medical vagotomy with consideration for atropine sensitivity may be a reliable prognostic criterion in the choice of the operative intervention in patients with duodenal ulcer.

Atropine↗
PubMed1989

Inhibitory effects of atropine on growth hormone release in normal subjects and acromegaly.

Growth hormone (GH) secretion is mediated by hypothalamic factors, mainly growth hormone releasing factor (GRF) and somatostatin (SS). The hypothalamic hormones, under direct neurotransmitter control, stimulate GH secretion through different central mechanisms. Atropine, an anticholinergic agent, can cross the blood-brain barrier and inhibit GH secretion stimulated by exercise and sleep in normal persons. In order to study the inhibiting effect of atropine on GH release and whether glucose can be replaced by atropine, normal persons and acromegaly patients were observed during exercise, after atropine, and 100 g glucose loading. The results confirmed that GH secretion increases after exercise and that this GH elevation can be inhibited by atropine in normal subjects. But in acromegaly patients high basal GH levels can not be inhibited by 100 g glucose loading or 0.6 mg atropine during the active phase of the disease. Blood sugar levels remained unchanged during the atropine test. It is suggested that the atropine test can be used as a GH inhibitory test in acromegaly patients with overt diabetes.

Acromegaly↗
PubMed1986

[Immunologic and pharmacologic activity of atropine-protein conjugates].

The immunological (production of specific antibodies to hapten) and pharmacological activity of bovine serum albumin conjugates with different chemical modifications of atropine was investigated. Mice and rabbits treated with atropine-protein conjugates (1-10 mg/kg) have produced a considerable number of specific serum antibodies to hapten during primary and secondary immune response. Mice treated with atropine-protein conjugates (25 and 50 mg/kg) have produced undetectable amounts of specific serum antibodies. The study of pharmacological activity in mice has revealed peripheral activity of atropine-protein conjugates. There was a correlation between the pharmacological activity of atropine-protein conjugates (25-50 mg/kg) and the activity of atropine (5 mg/kg), however the pharmacological effect of atropine-protein conjugates was somewhat longer. The results suggest that atropine-protein conjugates are both immunologically and pharmacologically active compounds.

Animals↗
PubMed1986

Effects of atropine on thermoregulatory responses to exercise in different environments.

The thermoregulatory effects of atropine (2 mg im) were examined in six heat-acclimated subjects during exercise in three environments, which provided different evaporative capacities, but similar heat stress as indicated by the wet bulb, globe temperature index (WBGT). Subjects walked in environments of Ta = 42.3 degrees C, Tdp = 14.6 degrees C, WBGT = 29.1 degrees C (HD); Ta = 33.9 degrees C, Tdp = 23.5 degrees C, WBGT = 28.9 degrees C (WM); Ta = 30.4 degrees C, Tdp = 23.8 degrees C, WBGT = 27.4 degrees C, (WW) after atropine and saline injections. In comparison to saline, atropine elevated rectal temperature (Tre) (p less than 0.05) in HD. Additionally, atropine elevated (p less than 0.01) mean skin temperature (Tsk), and heart rate (HR) in all three environments relative to saline. Whole body sweating rate (msw) was 45% lower (p less than 0.01) in each environment after atropine relative to saline. Exercise time was reduced from saline values (p less than 0.05) by 26.5 min in the HD after atropine. Within the atropine treatments, Tre was higher (p less than 0.05) in HD (0.6 degrees C) than WW, and HR was higher (p less than 0.05) in HD (23 b X min-1) and WM (14 b X min-1) than WW. Tsk was higher (p less than 0.01) in WM than WW (1.2 degrees C) and in HD than WM (1.5 degrees C). Exercise time was 26.5 min longer (p less than 0.05) in WW than HD in the atropine experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1979

[The effect of atropine on the pancreas].

The literature relating to the effect of atropine on exocrine pancreatic secretion in man and animals is critically reviewed. In most species basal secretion of volume, bicarbonate, and enzyme secretion are reduced by atropine, thus indicating some neural control of basal pancreatic secretion. The literature is replete with conflicting findings on the effect of atropine on pancreatic response to exogenous hormones. In well controlled studies atropine had no effect on the action of cholecystokinin-pancreozymin (CCK) or caerulein on the pancreas. Atropine either moderately depressed or did not alter the volume and bicarbonate response to secretin but constantly reduced enzyme secretion. With respect to pancreatic response to a meal, and to intestinal instillation of aminoacids, fat or HCL, all studies agree that pancreatic secretion is depressed by atropine. The recent finding that atropine did not alter the response of a transplanted denervated pancreas to intestinal stimulants suggests that atropine acts on the pancreas by interrupting an enteropancreatic vago-vagal reflex and not by blocking the action of hormones on the pancreas or by interfering with cholinergic facilitation of gastrointestinal hormone release.

Anesthesia↗
PubMed1981

Studies on the hypotensive response to atropine in hypertensive rats.

The hypotensive effect of atropine sulfate was evaluated in conscious, unanesthetized hypertensive rats (spontaneously hypertensive rats and Sprague-Dawley rats made hypertensive by s.c. implantation of deoxycorticosterone acetate, tablets) and their respective normotensive controls. In all animals, atropine (5-50 mg/kg i.v.) caused an immediate and dose-dependent decrease in blood pressure. However, the hypotensive response was of greater magnitude and of longer duration in the hypertensive rats. Pretreatment of the animals with phentolamine prevented the hypotension by atropine. Plasma concentrations of atropine were determined by radioimmunoassay and were identical in both hypertensive and normotensive rats. Atropine blocked the pressor responses to norepinephrine and shifted the dose-response curve for norepinephrine to the right to a similar extent in spontaneously hypertensive and Wistar-Kyoto rats. Thus, atropine acts as a competitive antagonist of norepinephrine and this action underlies its hypotensive effect. The greater responsiveness of hypertensive rats is not due to a difference in pharmacokinetic handling of atropine nor to a greater degree of blockade of the norepinephrine pressor response in vivo, but may result from the altered sympathetic tone in the hypertensive rats. Atropine may, in addition to its action on alpha adrenergic receptors, affect other systems such as calcium handling. It is speculated that an effect on this system may contribute to the longer duration of response seen in hypertensive rats.

Adrenal Medulla↗
PubMed1982

Inhibition of gallstone formation by sphincterotomy in the prairie dog: reversal by atropine.

Sphincterotomy has previously been shown to decrease gallbladder volume and gallbladder bile stasis while inhibiting gallstone formation in the prairie dog. We tested the possibility that atropine administration might reverse the effects of sphincterotomy on gallbladder mechanical function and gallbladder bile stasis and thereby reverse the inhibition of gallstone formation seen after sphincterotomy. Sixteen prairie dogs underwent sphincterotomy and were placed on a high cholesterol diet known to consistently induce gallstone formation. After 6 wk, in addition to the lithogenic diet, 8 animals were administered atropine. A control group of 8 animals was continued on the lithogenic diet. At death, animals that had undergone sphincterotomy and received atropine had a larger mean gallbladder volume (2.7 +/- 0.4 ml) than sphincterotomized control animals (0.66 +/- 0.2 ml, p less than 0.005), more total lipid stored in the gallbladder (176.1 +/- 33.9 mumol, sphincterotomy and atropine vs. 42.8 +/- 17.3 mumol, sphincterotomy, p less than 0.005), and a larger fraction of administered radiolabeled bile salt stored in the gallbladder (51.5 /- 7.3%, sphincterotomy and atropine vs. 24.5 +/- 10.7 sphincterotomy, p less than 0.05). The ratio of the fraction of [3H]cholic acid in the gallbladder (given 1 day before death) to the fraction of [14C]cholic acid in the gallbladder (given 4 days earlier) was lower for animals that underwent sphincterotomy and received atropine (0.63 +/- 0.04) than for sphincterotomized control animals (1.0 +/- 0.15, p less than 0.05), indicating a return of gallbladder bile stasis in the atropine-treated group. Confirming our previous work, only 1 of 8 animals that underwent sphincterotomy had gallstones. In contrast, 8 of 8 atropine-treated animals formed stones (p less than 0.005). Gallbladder bile of both groups were equally supersaturated with cholesterol. These findings provide direct support for the role of gallbladder bile stasis in the pathogenesis of cholesterol gallstone formation in this model.

Ampulla of Vater↗
PubMedDate not supplied

Analysis of cardiovascular and respiratory effects of various doses of soman in guinea-pigs: efficacy of atropine treatment.

The acute cardiovascular and respiratory effects of poisoning by high soman doses and its therapy by atropine, as well as the underlying mechanisms, are not well known as yet. Therefore, it was the purpose of this study to analyze the circulatory and respiratory functions in soman-poisoned and atropine-treated guinea-pigs. Female Pirbright-white guinea-pigs were anaesthetized with urethane (1.8 g/kg) and the arteria carotis, vena jugularis and trachea were cannulated. After base line measurements, soman (32, 80 or 160 micrograms/kg, i.v.; i.e. 2, 5 or 10 x LD50, respectively) or saline were injected and 2 min later, atropine (10 mg/kg, i.v.) or saline were applied. Respiratory and circulatory parameters were recorded for 60 minutes or until death of the animals. Poisoning by soman resulted in a rapid respiratory arrest, followed by circulatory failure and death after a few minutes. Atropine treatment restored circulatory parameters after soman (2 x LD50) and improved respiration to about 80% of base line values. All animals survived the 60 minutes period. After soman (5 x LD50), atropine improved respiratory parameters only slightly and circulatory parameters markedly. Only 2 of the 8 guinea-pigs survived. Atropine was almost completely ineffective after soman (10 x LD50), despite of a transitory improvement of circulation, and all animals died within a few minutes. In control animals, atropine did not impair respiration or circulation. The results of this study suggest that the soman-induced respiratory depression is primarily caused at the central nervous level and that a significant peripheral neuromuscular block develops only at very high soman doses. The circulatory disturbances are mainly the result of bradycardia due to peripheral muscarinic stimulation. Atropine has a high therapeutic effect in the restoration of circulatory function and may even improve respiration at high soman doses.

Animals↗
PubMed1993

[Emesis and the oculocardiac reflex. Drug prophylaxis with droperidol and atropine in children undergoing strabismus surgery].

Although droperidol is often used to prevent emesis, vomiting is still common in children undergoing strabismus surgery. METHODS. One hundred children aged 3 to 12 years admitted for strabismus surgery were enrolled in a randomised, double-blind study to investigate the influence of the timing of the administration of droperidol (75 micrograms/kg i.v.) and the effect of atropine (10 micrograms/kg i.v.) on postoperative vomiting and the occurrence of the oculocardiac reflex (OCR). Each child was prospectively assigned to one of the following groups: Group A: atropine and droperidol before the beginning of surgery (n = 25); Group B: atropine before the beginning, droperidol after completion of surgery (n = 25); Group C: no atropine, droperidol before the beginning of surgery (n = 25); Group D: no atropine, droperidol after completion of surgery (n = 25). After oral premedication with 0.4 mg/kg midazolam, anaesthesia was induced via a face mask by inhalation of halothane, nitrous oxide, and oxygen and 1 mg/kg succinylcholine was given to facilitate tracheal intubation. Gastric contents were aspirated by a gastric tube at the end of the operation. Vomiting and retching were recorded for 24 h; recovery from anaesthesia was assessed by a modified Steward score. RESULTS. The four groups were comparable regarding age, sex, body weight, duration of anaesthesia, and number of repaired eye muscles. Patients receiving droperidol before and after the end of surgery had a similar incidence of vomiting (groups A and C 60% vs. groups B and D 50%). There was no significant difference in the number of patients vomiting between groups A and B (58%) and groups C and D (52%). The incidence of the OCR was lower in the patients premedicated with atropine (18% vs. 60%, P < 0.01). There was no statistical relationship between the occurrence of the OCR and post-operative emesis. Younger children (3 to 6 years) vomited more often than older ones (7 to 12 years). The incidence of the OCR was higher in patients with more than two eye muscles repaired than in others. Recovery scores were slightly lower in patients with droperidol after completion of surgery; postoperative recovery times did not differ significantly between the study groups. CONCLUSIONS. The timing of the administration of droperidol (75 micrograms/kg) had no influence on postoperative vomiting. The application of atropine (10 micrograms/kg) prior to surgery did not influence vomiting after strabismus surgery. Atropine (10 micrograms/kg) reduced the incidence of the OCR significantly. There was no statistical relationship between the occurrence of the OCR and postoperative vomiting.

Atropine↗
PubMed1993

Atropine reduces experimental myopia and eye enlargement via a nonaccommodative mechanism.

PURPOSE: To determine whether the muscarinic antagonist atropine effectively reduces or prevents experimentally induced myopia via a nonaccommodative mechanism. METHODS: Chicks were monocularly deprived (MD) of pattern vision by placement of a translucent occluder over the left eye. In two of the three MD groups, chicks received a series of intravitreal injections of atropine (n = 8) or saline vehicle (n = 8) with MD. Control groups (n = 8) of chicks were employed to assess the effects of MD, intravitreal injections, and drug effects. RESULTS: In sham-injected or saline-injected MD chicks, 8 days of MD produced -18.5 D and -20.9 D of experimental myopia, respectively. In atropine-injected MD chicks, 8 days of MD produced only -2.8 D of experimental myopia. This significant reduction in experimentally induced myopia in atropine-injected MD chicks was associated with a marked reduction in the relative axial elongation of the deprived eye (0.21 mm) when compared to saline-injected or sham-injected MD chicks (1.04 mm and 1.00 mm). This reduction in axial length in atropine-injected MD chicks was predominantly the result of a reduction in vitreous chamber elongation, although a reduction in anterior segment depth also was observed. Mean equatorial diameter was significantly reduced in atropine-injected MD chicks compared to saline-injected and sham-injected MD chicks, although to a lesser extent. Control experiments demonstrated that intravitreally injected atropine did not reduce carbachol-induced accommodation or light-induced pupil constriction in the skeletal intraocular muscles of the chick eye. CONCLUSIONS: These findings demonstrate that chronic administration of the muscarinic antagonist atropine prevents experimentally induced myopia in chick via a nonaccommodative mechanism.

Accommodation, Ocular↗