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 163 records · Page 9Linked to original sources
PubMed2000

Prospective study of early atropine use in dobutamine stress echocardiography.

AIMS: Dobutamine stress echocardiography is a time-consuming test, often requiring atropine at the end of the protocol to achieve target heart rate (HR). We examined whether earlier administration of atropine in appropriate patients would shorten test time and increase the likelihood of achieving peak HR. METHODS: Two hundred and seventy consecutive patients were randomized prospectively to conventional or early atropine protocols. Of these, 120 patients with an inadequate HR response [mid-30 microg/kg/min HR<100 (age <50) or <90 (age >50); or mid-40 microg/kg/min stage HR<120 (age <50) or <110 (age >50)] were included in the analysis. The remaining patients were used in a model to define which patients are likely to require atropine. RESULTS: The 61 patients receiving early-atropine had decreased test-time relative to the 59 not receiving early-atropine (17:05 vs. 18:24 min:sec, P=0.014) accompanied by a 10% reduction in total dobutamine dose (P=0.008). Their HR at end of 40 microg/kg/min was 123+/-18 vs. 105+/-17 respectively, P<0.0001. Only 7% of the early-atropine group failed to reach target HR vs. 15% not receiving early-atropine. By multivariate analysis, age (P<0.0001), HR at end of 30 microg/kg/min stage (P<0.0001), beta-blocker use (P=0.009) and baseline HR (P=0.04) were predictors of need for atropine. CONCLUSION: Giving atropine early in appropriate patients can reduce test times without an increase in side effects. Our model enables accurate prediction of these patients.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Use of atropine to reduce mucosal eversion during intestinal resection and anastomosis in the dog.

OBJECTIVE: To determine whether atropine altered the degree of mucosal eversion during jejunal resection and anastomosis in the dog. STUDY DESIGN: Part I: Prospective, blinded, randomized, controlled study using a therapeutic dose (0.04 mg/kg systemic) of atropine. Part II: Prospective, unblinded, assigned, controlled study using a pharmacologic (0.04 mg/kg local arterial) dose of atropine. ANIMALS: Part I: Twenty-two young adult female Beagle dogs used during a nonsurvival third-year veterinary student surgical laboratory (small intestinal resection and anastomosis). Part II: Ten young adult female Beagle dogs used immediately after completion of a nonsurvival third-year veterinary student orthopedic surgical laboratory. METHODS: Part I: Dogs were randomly assigned to receive either atropine (0.04 mg/kg), or an equal volume of saline, given intramuscularly (premedication) and again intravenously prior to intestinal resection. Part II: In each dog, atropine (0.04 mg/kg)/saline was alternately given in the proximal/distal jejunum. RESULTS: Part I: There was no clinically or statistically significant difference between systemic atropine and saline solution on the degree of jejunal mucosal eversion after resection. Part II: There was a statistically significant decrease in jejunal mucosal eversion with atropine compared with saline solution when injected into a local jejunal artery. CONCLUSION: Systemic atropine (0.04 mg/kg) does not alter the degree of jejunal mucosal eversion during resection and anastomosis. Jejunal intraarterial atropine (0.04 mg/kg) reduced jejunal mucosal eversion during resection and anastomosis. CLINICAL RELEVANCE: The clinical usefulness and consequences of jejunal arterial atropine administration to reduce mucosal eversion remain to be determined.

Anastomosis, Surgical↗
PubMed1987

Prevention of bradycardic responses to endotracheal suctioning by prior administration of nebulized atropine.

Endotracheal suctioning can elicit bradycardia and hypotension. We compared the effectiveness of nebulized atropine with that of parenterally administered atropine in preventing these responses. Six mechanically ventilated patients who reproducibly experienced a 20% or greater fall in resting heart rate exclusively with endotracheal suctioning were given three trials: a) inhaled atropine sulfate (0.05 mg/kg); b) inhaled saline aerosol (0.05 ml/kg); and c) atropine sulfate (1 mg, given im or iv). Mean heart rate fell from 114 +/- 10 to 45 +/- 5 beat/min with suctioning after the saline aerosol (p less than .001). Both nebulized and parenteral atropine sulfate prevented the bradycardic response in all six subjects (p less than .001). After nebulized saline, three patients also experienced a greater than or equal to 10 mm Hg fall in systolic BP. Both nebulized and parenteral atropine prevented the hypotensive response. Tachycardia occurred after parenteral atropine in all six patients, while only one episode of tachycardia was seen after nebulized atropine. Both parenteral and nebulized atropine can prevent bradycardia and hypotension elicited by endotracheal suctioning, but nebulized atropine may have a wider margin of safety at the doses used in this study.

Administration, Inhalation↗
PubMed1986

Action of intravenous ethanol and atropine on the secretion of gastric acid, pancreatic enzymes, and bile acids and the motility of the upper gastrointestinal tract in nonalcoholic humans.

To investigate the influence of the cholinergic nerves on the action of i.v. ethanol on interdigestive gastric acid, pancreatic enzyme, and bile acid output, seven healthy volunteers were studied. On each of 4 different days, they swallowed a multilumen intestinal tube system that allowed the measurement of intraluminal pressures and the collection of gastric and duodenal juice. The subjects received an i.v. infusion of either ethanol (600 mg/kg for 30 min followed by 3 mg/kg/min), atropine (5 mu/kg/h), a combination of both drugs, or NaCl. Whereas ethanol did not significantly influence motility, atropine induced motoric quiescence. Ethanol significantly (p less than 0.05) stimulated gastric acid output, by 55%, whereas atropine inhibited it by 91%. When ethanol and atropine were given together, gastric acid output was significantly higher than during atropine use alone. Both ethanol and atropine inhibited pancreatic amylase output--by 47% and by 82%, respectively. The degree of inhibition was 80% when ethanol and atropine were given simultaneously. Atropine but not ethanol significantly reduced bile acid output. The finding that atropine did not completely reverse the stimulating effect of i.v. ethanol on gastric acid secretion suggests that ethanol stimulates gastric acid secretion not only by a cholinergic but also by a noncholinergic mechanism. The observation that atropine did not reverse the inhibiting effect of ethanol suggests, but does not prove, that the effect of ethanol on the pancreas is predominantly mediated by cholinergic nerves.

Adult↗
PubMed1982

A comparison of atropine and glycopyrrolate in anaesthetic practice.

The two anticholinergics, atropine and glycopyrrolate, were used for premedication and as an adjunct to reversal of residual neuromuscular block in a double-blind study. Glycopyrrolate, being about twice as potent as atropine in the clinical situation, was used in half the dosage of atropine. When used for premedication, no difference was found between the drugs concerning patients complaining of dry mouth, but more patients in the glycopyrrolate group had a gastric juice pH greater than 2.5 compared to the atropine group (not statistically different). The reversal mixture consisted of necostigmine 2.5 mg with either atropine 1 mg or glycopyrrolate 0.5 mg. The heart rate response between 2 and 10 min after injecting the reversal mixture was statistically significant (P ranged from 0.0001 to 0.05), the atropine group showing the most marked decrease: 18% in the atropine group had sinus bradycardia compared to 5% in the glycopyrrolate group: 34% in the atropine group exhibited arrhythmias compared to 10% in the glycopyrrolate group, the most common form being a nodal rhythm in both groups. More patients in the atropine group had "excessive" oropharyngeal secretions (more than 2 ml) when extubated (P less than 0.05). The postoperative assessment showed little difference in the two groups, apart from a lower incidence of nausea and vomiting in the atropine group (not statistically different). The study shows that the use of glycopyrrolate was associated with a more stable cardiovascular system, fewer arrhythmias and superior control of oropharyngeal secretions at the time of reversal.

Adolescent↗
PubMed2006

Efficacy of atropine as a chronotropic agent in heart transplant patients undergoing dobutamine stress echocardiography.

BACKGROUND: After heart transplant (HTX), the heart is completely denervated. While sympathetic reinnervation is likely to occur, there is conflicting evidence regarding parasympathetic reinnervation. Accordingly, it is unclear if atropine is efficacious as a chronotropic agent in HTX patients undergoing dobutamine stress echocardiography (DSE), since cholinergic cardiac stimulation is required for atropine to exert its effect. The purpose of this study was to demonstrate that atropine can sufficiently increase the heart rate (HR) in HTX patients undergoing DSE. METHODS: A retrospective review was performed on 68 HTX patients who underwent DSE as part of their routine annual HTX follow-ups. Dobutamine was administered in the standard fashion of 10, 20, 30, 40, 50 mcg/kg per minute with blood pressure and electrocardiographic monitoring. If target HR was not attained, atropine was administered to aid in achieving 85% of maximum age-predicted HR. RESULTS: Mean patient age was 58 +/- 10 years. Mean period since transplant was 9 +/- 4 years. Forty-seven (69%) patients received dobutamine only, and 21 (31%) required additional atropine to reach target HR. Of the 21 patients who received atropine, 10 (48%) reached target HR. Neither time from transplant, age, gender, resting HR, medications, nor atherosclerotic risk factors predicted responsiveness to atropine. Those responding to dobutamine had a significantly greater resting HR than those receiving additional atropine. CONCLUSIONS: The adjunctive use of atropine in HTX patients during DSE aids in reaching 85% of maximum predicted HR in some patients. Furthermore, resting HR may predict the additional need of atropine during DSE.

Adult↗
PubMed1997

Atropine inhibits gastric distension and pharyngeal receptor mediated lower oesophageal sphincter relaxation.

BACKGROUND: Atropine decreases the frequency of transient lower oesophageal sphincter relaxation (TLOSR) through an unknown mechanism. Gastric distension and pharyngeal receptor excitation are two possible sources for the afferent stimulus responsible for TLOSR. AIMS: To determine whether atropine affects gastric distension induced TLOSR and pharyngeal receptor mediated lower oesophageal sphincter (LOS) relaxation. METHODS: Oesophageal manometry and pH recordings were performed in 10 healthy volunteers on two separate days in the postprandial setting, following either atropine (15 micrograms/kg intravenous bolus and 4 micrograms/kg/h as a maintenance dose) or placebo. Pharyngeal receptor mediated LOS relaxation was studied in nine subjects by rapid injection of minute amounts of water (0.05, 0.1, 0.2, 0.3, and 0.4 ml) in the pharynx before and after atropine. Gastric distension mediated TLOSR was studied in eight subjects by insufflating the stomach with 300, 600 and 900 ml of CO2 before and after atropine. RESULTS: Atropine reduced the frequency of spontaneous gastro-oesophageal reflux and TLOSR compared with placebo (p < 0.05). Pharyngeal stimulation resulted in bolus volume dependent LOS relaxation. Atropine decreased the frequency and amplitude of pharyngeal receptor mediated LOS relaxation at bolus volumes of 0.05, 0.1, and 0.2 ml. Gastric distension resulted in intermittent episodes of TLOSR. The frequency of gastric distension induced TLOSR was significantly decreased by atropine. CONCLUSION: (1) Atropine reduces the frequency of spontaneous reflux and TLOSR in normal subjects; and (2) gastric distension induced TLOSR and pharyngeal receptor mediated LOS relaxation is inhibited by atropine.

Adult↗
PubMed1981

Atropine and exercise-induced bronchoconstriction.

Six asthmatic children were studied to determine whether supplemental, parenteral atropine would increase the effects of bronchodilation and protection against exercise-induced bronchoconstriction after maximal effects had been achieved by inhalation. First, we determined the amount of inhaled atropine sulfate that would give maximal bronchodilation for each patient at rest. This quantity of atropine was designated as "A." Then all subjects exercised for five sessions with the following pre-exercise treatments in a random order: (a) inhaled distilled water plus intramuscular (IM) saline solution; (b) inhaled A dose of atropine plus IM saline solution; (c) inhaled distilled water plus 0.35 mg IM atropine; (d) inhaled A dose of atropine plus 0.35 mg IM atropine; and (e) inhaled double the A dose plus IM saline solution. The results showed that the combination of inhaled and IM atropine had the greatest bronchodilation effect and the greatest protection against exercise-induced bronchoconstriction. Atropine inhalation alone (A dose) or IM injection (0.35 mg) was not as effective in bronchodilation or in alleviation of exercise-induced bronchoconstriction. Doubling the dose of inhalation (2A) did not increase the effects of the A dose. These results support the hypothesis that inhaled atropine does not reach all the airways where cholinergic receptors are present.

Adolescent↗
PubMed2000

Reducing the progression of myopia with atropine: a long term cohort study of Olmsted County students.

BACKGROUND: Myopia is an important public health problem because it is common and is associated with increased risk for chorioretinal degeneration, retinal detachment, and other vision- threatening abnormalities. In animals, ocular elongation and myopia progression can be lessened with atropine treatment. This study provides information about progression of myopia and atropine therapy for myopia in humans. METHODS: A total of 214 residents of Olmsted County, Minnesota (118 girls and 96 boys, median age, 11 years; range 6 to 15 years) received atropine for myopia from 1967 through 1974. Control subjects were matched by age, sex, refractive error, and date of baseline examination to 194 of those receiving atropine. Duration of treatment with atropine ranged from 18 weeks to 11.5 years (median 3.5 years). RESULTS: Median followup from initial to last refraction in the atropine group (11.7 years) was similar to that in the control group (12.4 years). Photophobia and blurred vision were frequently reported, but no serious adverse effects were associated with atropine therapy. Mean myopia progression during atropine treatment adjusted for age and refractive error (0.05 diopters per year) was significantly less than that among control subjects (0.36 diopters per year)(P<.001). Final refractions standardized to the age of 20 years showed a greater mean level of myopia in the control group (3.78 diopters) than in the atropine group (2.79 diopters) (P<.001). CONCLUSIONS: The data support the view that atropine therapy is associated with decreased progression of myopia and that beneficial effects remain after treatment has been discontinued.

Adolescent↗
PubMed1992

[The effects of diazepam premedication upon atropine-induced hemodynamic changes].

Positive or negative chronotropic effects of atropine and their magnitude are known to be determined primarily by patient's age, atropine dose, anesthetic agents or techniques, and preanesthetic medication. The aim of the present study is to investigate the effects of oral diazepam upon the hemodynamic responses to intravenous atropine in awake patients. Diazepam group (n = 26) received oral diazepam, 10 mg, whereas control group (n = 20) received no premedication. The direction and magnitude of heart rate and blood pressure responses to atropine were similar between the two groups. Heart rate significantly decreased from baseline values following atropine, 2.5 micrograms.kg-1, returned to baseline values following cumulative atropine doses, 5 micrograms.kg-1, then significantly increased from baseline values following cumulative atropine dose, 10 micrograms.kg-1 in both groups. Mean blood pressure significantly decreased from baseline values following cumulative atropine dose, 2.5 and 5 micrograms.kg-1, and returned to baseline following cumulative atropine dose, 10 micrograms.kg-1, in both groups. It is concluded that oral diazepam, 10 mg, as a premedicant does not alter the hemodynamic responses to intravenous atropine in humans.

Administration, Oral↗
PubMed1992

[Atropine in the premedication of patients at risk. Its effect on hemodynamics and salivation during intubation anesthesia using succinylcholine].

Should atropine be administered for premedication? This question continues to be controversial; in particular, the combined administration of atropine and succinylcholine has been investigated with conflicting results by numerous researchers. The present study was carried out to assess the effect of premedication with atropine on hemodynamic variables and salivation in patients assigned to ASA class II and III. METHODS. Eighty ASA class II or III patients received pethidine 1.0 mg/kg and promethazine 0.5 mg/kg i.m. 30 min prior to induction of anesthesia and atropine, either 0.01 mg/kg i.v. 10 min or 0.01 mg/kg i.m. 30 min prior to a standardized anesthetic induction with alcuronium (precurarizing dose), thiopental, and succinylcholine. In the control groups (20 patients each), no atropine was given. Systolic, diastolic, and mean arterial pressures (MAP) were measured. The ECG was monitored for arrhythmias. Salivation was assessed semiquantitatively using swabs positioned within the pharyngeal space. RESULTS. Ten minutes after the administration of atropine i.v., a significant increase in heart rate (HR) was observed; this did not occur within 30 min after administration of atropine i.m. At the time of tracheal intubation, HR was significantly increased in both i.v. atropine risk groups. After atropine i.m., an increase in heart rate during intubation was observed in ASA class II patients only. No increase in heart rate occurred in the control groups during tracheal intubation. Neither i.m. nor i.v. atropine had any significant effect on blood pressure. Arrhythmias occurred in a few cases with both routes of administration; several instances of marked tachycardia were recorded.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

The parasympatholytic effects of atropine sulfate and glycopyrrolate in rats and rabbits.

Nine groups of rats (n = 5 per group) received an intramuscular (IM) injection of one of the following drugs or drug combinations: saline, atropine (0.05 mg/kg), glycopyrrolate (0.5 mg/kg), ketamine:xylazine (85:15 mg/kg), ketamine:detomidine (60:10 mg/kg), atropine:ketamine:xylazine (0.05: 85:15 mg/kg), glycopyrrolate: ketamine:xylazine (0.5:85:15 mg/kg), atropine:ketamine:detomidine (0.05: 60:10 mg/kg) or glycopyrrolate: ketamine:detomidine (0.5:60:10). Similarly six groups of rabbits (n = 5) received an IM injection of either saline, atropine (0.2 mg/kg), atropine (2 mg/kg), glycopyrrolate (0.1 mg/kg), ketamine:xylazine (35:10 mg/kg) or glycopyrrolate:ketamine:xylazine (0.1:35:10 mg/kg). In rats, atropine sulfate (0.05 mg/kg) and glycopyrrolate (0.5 mg/kg) produced an increase in heart rate for 30 and 240 min, respectively. In rabbits atropine sulfate at either 0.2 or 2.0 mg/kg did not induce a significant increase in heart rate, but glycopyrrolate (0.1 mg/kg) elevated the heart rate above saline treated animals for over 50 min. Both atropine and glycopyrrolate provided protection against a decrease in heart rate in rats anesthetized with ketamine: xylazine (85:15 mg/kg) or ketamine: detomidine (60:10 mg/kg); however, glycopyrrolate was significantly more effective in maintaining the heart rate within the normal range. Glycopprrolate also prevented a decrease in heart rate in rabbits anesthetized with ketamine:xylazine (35:5 mg/kg). Neither glycopyrrolate nor atropine influenced respiration rate, core body temperature or systolic blood pressure when used alone or when combined with the injectable anesthetic. Glycopyrrolate is an effective anticholinergic agent in rabbits and rodents and more useful as a preanesthetic agent than atropine sulfate in these animals.

Animals↗
PubMed1993

[A comparison of the two anticholinergic agents atropine and glycopyrrolate during antagonism of a muscle relaxation with pyridostigmine].

Central, peripheral and cardiac side-effects of both anticholinergic drugs atropine and glycopyrrolate were compared during the antagonism of muscle relaxation with pyridostigmine. In a randomized, double-blind fashion 50 patients were given 10 micrograms/kg of atropine and 50 were given 5 micrograms/kg of glycopyrrolate with 125 micrograms/kg pyridostigmine intravenously. Continuous Holter ECG-monitoring over 3 hours was performed. The procedure was divided into the following phases: control (5 minutes before application of antagonists), phase I (application of antagonists and the following 5 minutes), phase II (subsequent 30 minutes), phase III (until 3 hours had passed). The first 32 minutes were subdivided into periods of 4 minutes. Analysed were: 1st: The number of patients with supraventricular, junctional and ventricular beats, 2nd: The mean heart rate per period, 3rd: The incidence of central-anticholinergic syndromes and the peripheral antimuscarinic side-effects. Supraventricular beats were found after atropine in 42 patients and after glycopyrrolate in 18 patients (p < 0.001). The differences mainly occurred during phase I (atropine 15 vs. glycopyrrolate 4 p < 0.05) and III (atropine 38 vs. glycopyrrolate 18, p < 0.01). Junctional beats were found after both drugs (atropine 7 vs. glycopyrrolate 10), above all during phase III. Ventricular beats were observed after atropine (21) and glycopyrrolate (18). Atropine as well as glycopyrrolate caused an increased heart rate within the first 4 minutes (atropine 47% vs. glycopyrrolate 27%, p < 0.01). During phase III after atropine, the heart rate decreased below the control value (p < 0.05). None of the patients showed central anticholinergic syndromes after either drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

Effect of low-dose atropine administration on dobutamine dose requirement in horses anesthetized with detomidine and halothane.

OBJECTIVE: To determine whether a low dose of atropine is associated with decreased requirement for cardiovascular supportive treatment in horses given detomidine prior to maintenance of general anesthesia with halothane. ANIMALS: 3 groups of 10 healthy horses. PROCEDURE: Detomidine (20 micrograms/kg of body weight, i.m.) was administered to all 30 horses. Then, 10 horses received atropine (0.006 mg/kg, i.v.) 1 hour after detomidine administration, 10 horses received atropine (0.012 mg/kg, i.m.) at the time of detomidine administration, and 10 horses served as a control group. Heart rate was measured prior to detomidine administration and at fixed intervals throughout anesthesia. The dobutamine infusion rate necessary to maintain mean arterial blood pressure between 70 and 80 mm of Hg was recorded. Systemic blood pressures, end-tidal halothane, end-tidal CO2, and arterial blood gas tensions were measured at fixed intervals. RESULTS: Mean heart rate was higher among horses receiving atropine i.v. or i.m., compared with that in control horses. Horses that received atropine i.v. had higher systemic arterial blood pressure and required a lower dobutamine infusion rate than did horses of the other groups. CONCLUSION: Detomidine-treated, halothane-anesthetized horses given atropine i.v. required less dobutamine, compared with horses receiving or not receiving atropine i.m. Complications, such as colic and dysrhythmias, from use of higher doses of atropine, were not observed at this lower dose of atropine. CLINICAL RELEVANCE: i.v. administration of a low dose of atropine prior to induction of general anesthesia may result in improved blood pressure in horses that have received detomidine before anesthesia with halothane.

Adjuvants, Anesthesia↗
PubMed1982

Plasma pharmacokinetics of intravenously administered atropine in normal human subjects.

The pharmacokinetics of atropine (dl-hyoscyamine) was studied in six normal volunteers following a single 1-mg intravenous dose of atropine. Atropine plasma levels were collected for 24 hours and analyzed by radioimmunoassay. Pulse rates were monitored and compared with predose values in each subject. Atropine plasma concentrations were fitted by least-squares regression analysis. The observed maximal increase in pulse rate, at 12 to 16 minutes after the dose, correlated with the maximum predicted tissue levels of atropine based on the computer fit of the plasma atropine concentration-time data. No correlation between the time of maximum response and atropine plasma concentrations was observed. The average half-life of atropine was 4.125 hours. This data may be used to design a multiple-dosing regimen for intravenous atropine in patients.

Adult↗
PubMed1989

Atropine absorption after intramuscular administration with 2-pralidoxime chloride by two automatic injector devices.

Compared with manual intramuscular injection, automatic injector delivery substantially enhances drug absorption rate. We examined the effect of two types of automatic injector delivery of two drugs which are components of the standard antidote to anticholinesterase poisoning and which have been previously shown to have a reduced absorption rate when mixed together in a manual injection. In crossover experiments one week apart, 20 nonsmoking healthy young male humans (ages 20-30) were studied after citrated atropine (6.9 mumol/0.7 mL) and pralidoxime chloride (3.5 mmol/2.0 mL; PAMCL) were injected sequentially into a single intramuscular site by either a multichambered autoinjector or a device which delivers the drugs into two separate intramuscular sites (MARK I). Atropine absorption was assessed by the appearance of atropine in the serum and by changes in heart rate, salivary secretion, pupil diameters, and near vision accommodation. Atropine absorption was significantly greater in the first 30 min following injection with the MARK I. The results of this study suggest that: (1) the MARK I device produces a faster absorption of atropine, probably through some combination of its broader dispersal of atropine in the muscle site and its separation of atropine from the PAMCL; (2) salivary secretion may be the most convenient and sensitive marker of atropine action; and (3) the 6.9- mumol (2-mg) dose of atropine delivered by either autoinjector gives near maximal antisialogogue activity in normal male humans.

Accommodation, Ocular↗
PubMed1997

Atropine reduces but does not eliminate the age-related decline in perfusion outflow facility in monkeys.

Accommodative amplitude and outflow facility decline with age in rhesus monkeys and humans. In monkeys, there is an age-related reduction in ciliary muscle (CM) mobility due to stiffening of its posterior and outer attachments. Since the CM inserts into the trabecular meshwork (TM) and CM contraction deforms the TM so as to increase outflow facility, we asked whether the age-related decline in outflow facility observed in anesthetized monkeys is consequent to the age-related reduction in CM mobility. One eye of 19 pentobarbital-anesthetized rhesus monkeys aged 4-24 years underwent 2-level constant pressure perfusion of the anterior chamber (AC) for 40 min to measure baseline total outflow facility. Both eyes then received 100 micrograms of atropine, given topically to the central cornea. The AC of the second eye was cannulated 40 min after atropine treatment. Facility was measured simultaneously in both eyes for 40 min beginning 45 min after atropine treatment. Baseline facility declined with age by -0.0160 +/- 0.0059 microliters min-1 mmHg-1 yr-1 (P = 0.009). The average facility at baseline was approximately 50% higher in the youngest (ages 4-10 years) compared to the oldest (ages 21-25 years) animals (P < or = 0.03). Following atropine facility decreased by approximately 25% in the youngest monkeys (N.S.), but not at all in the oldest animals when compared to baseline. Thus, the age-related facility decline persisted after atropine in both eyes, but was not as dramatic as prior to atropine (-0.0092 +/- 0.0050 [P < or = 0.09] and -0.0078 +/- 0.0044 [P < or = 0.10] microliter min-1 mmHg-1 yr-1 respectively). Apparently, atropine inhibits facility-relevant anesthetic-induced ciliary muscle tone to a greater extent in younger than in older monkeys, presumably because stiffening of the posterior and outer attachments of the CM in the older animals has already reduced its ability to move and thereby deform the TM. The inability of atropine to completely eliminate the age-related facility decline indicates the presence of atropine-independent, facility-relevant age-dependent changes in the TM itself, such as loss of cells or build-up of extracellular material.

Aging↗
PubMed1977

Kinetics of atropine inhibition of pentagastrin-stimulated H+, electrolyte, and pepsin secretion in the dog.

The effects of atropine on pentagastrin-stimulated gastric secretion of water, H, Cl, Na, K, and pepsin were determined by kinetic analysis of dose-response studies in 5 dogs with esophagostomy and gastric cannula. First a dose-response study was done using 7 doses of pentagastrin (1-6 mug/kg hr), each dose given by I.V. infusion for 4 hr at a separate time. The same series of doses was used with atropine sulfate 10 mug/kg hr as background. Atropine inhibited pentagastrin-stimulated secretion competively with a dose ratio change of 20. In a third set of studies pentagastrin was infused alone for 4 hrs in the dose of 1.5 mug/kg hr and then with each of 7 doses of atropine (0.625-40 mug/kg hr), each dose used separately. Atropine competitively inhibited water, H, Cl, and K secretion, with Ki (dose of atropine giving 50% inhibition) of 1.0 mug/kg hr. Pepsin secretion was much more strongly inhibited than acid secretion by atropine with Ki 0.27 mug/kg hr and the inhibition was uncompetitive. Calculated maximal inhibition of H+ secretion by atropine was 89% and of pepsin 95%. Furthermore the shape of the response to pentagastrin was altered by atropine so that the peak response was delayed to the third and fourth hour of pentagastrin infusion.

Animals↗