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PubMed1999

Metabolic and clinical responses to different types of premedication in children.

The metabolic and clinical responses to intravenously administered atropine+meperidine (pethidine), glycopyrrolate+meperidine, diazepam and placebo were examined in 76 healthy children. After atropine+meperidine and glycopyrrolate+meperidine administration, a significant antisialogogue effect, tachycardia and elevation in systolic blood pressure were observed. Diazepam decreased oxygen consumption (VO2) whereas atropine+meperidine increased both VO2 and energy expenditure (EE). The maximal effect of diazepam on VO2 was found 10 min after drug administration (mean difference from baseline -10.0%) and maximal effect of atropine+meperidine on VO2 and EE after 5 min (mean difference from baseline +6.0% and +3.3%, respectively). It is concluded that intravenous administration of meperidine with atropine or glycopyrrolate is followed by profound anticholinergic effects and such combinations do not appear to be suitable for clinical purposes. Although statistically significant, the alterations in VO2 and EE after diazepam and atropine+meperidine premedication can be considered clinically insignificant because they were of short duration and the measured changes represented only a fraction of fluctuation seen in normal values.

Carbon Dioxide↗

PubMed2005

Evaluation of induction by use of a combination of oxymorphone and diazepam or hydromorphone and diazepam and maintenance of anesthesia by use of isoflurane in dogs with experimentally induced hypovolemia.

OBJECTIVE: To compare induction with hydromorphone and diazepam (HydroD) or oxymorphone and diazepam (OxyD) followed by maintenance with isoflurane in dogs with induced hypovolemia. ANIMALS: 6 healthy mixed-breed dogs. PROCEDURE: The study used a crossover design. Measurements were obtained in normovolemic dogs during isoflurane. Hypovolemia was induced (blood loss of 30 mL/kg) and measurements repeated following recovery from anesthesia, after HydroD (hydromorphone, 0.1 mg/kg; diazepam, 0.2 mg/kg; i.v.) or OxyD (oxymorphone, 0.05 mg/kg; diazepam, 0.2 mg/kg; i.v.), after another dose of the same opioid, during administration of isoflurane (end-tidal concentration, 0.9%), and after glycopyrrolate (0.01 mg/kg, i.v.). Significant changes were identified. RESULTS: Induction effect was evident within 1 minute. All dogs were intubated after the second dose of opioid. No significant differences were found between inductions. The HydroD decreased heart rate (mean +/- SEM, -41 +/- 9.8 beats/min), whereas both inductions increased stroke index (0.4 +/- 0.09 mL/kg/beat) and caused moderate respiratory depression. Cardiac index was decreased (-30.2 +/- 6.04 mL/kg/min) and there was minor metabolic acidosis during isoflurane following HydroD, compared with values for anesthetized normovolemic dogs. Glycopyrrolate increased heart rate (50 +/- 8.6 beats/min) and decreased systolic blood pressure (-23.2 +/- 4.87 mm Hg) in dogs induced with HydroD and decreased stroke index (-0.3 +/- 0.08 mL/kg/beat) for both inductions. CONCLUSIONS AND CLINICAL RELEVANCE: Similar effects were detected after administration of HydroD or OxyD in hypovolemic dogs. Either combination should be safe for use in hypovolemic dogs. Administration of glycopyrrolate was not beneficial.

Adjuvants, Anesthesia↗

PubMed2006

The effect of acute xerostomia on vocal function.

OBJECTIVE: To evaluate whether xerostomia can affect vocal function in an experimental model. DESIGN: Randomized controlled study. SETTING: Academic center. SUBJECTS: Twenty healthy young men. INTERVENTIONS: Glycopyrrolate was administered to induce acute xerostomia in 10 men, and saline was administered to 10 men who served as controls. MAIN OUTCOME MEASURES: Whole salivary flow rate and dry mouth scale were time-serially measured, and subjective and objective vocal functions were checked before and after treatment. The salivary and vocal functions were compared between groups. RESULTS: Significant salivary hypofunction and symptoms developed within 90 minutes after the administration of glycopyrrolate. Vocal effort and phonation threshold pressure significantly increased (P<.005) and voice range profiles decreased in the xerostomia group (P = .003) but not in the control group. Other voice parameters were comparable between groups (P>.05). High correlations were also found between salivary and vocal parameters. CONCLUSION: Our findings suggest that vocal function can be affected by xerostomia.

Adult↗

PubMed1994

Muscarinic antagonists in the treatment of acquired pendular and downbeat nystagmus: a double-blind, randomized trial of three intravenous drugs.

We performed a double-blind, randomized trial of intravenous scopolamine, benztropine, and glycopyrrolate in 7 patients with acquired nystagmus and oscillopsia. Five patients had pendular nystagmus and 2, downbeat nystagmus. We recorded eye movements with a magnetic search coil technique and tested visual acuity and motion perception before and after administration of each drug. Scopolamine reduced nystagmus in all patients. Benztropine was moderately effective and glycopyrrolate had a negligible impact. Visual acuity improved only with scopolamine; motion discrimination and oscillopsia improved significantly with scopolamine and benztropine. Pendular and downbeat nystagmus respond to intravenous antagonists of central muscarinic receptors.

Adult↗

PubMed1980

Modification of chronotropic response to anticholinergics by halogenated anaesthetics in children.

Cardiac rate and rhythm changes were studied in 40 children after intravenous injection of atropine or glycopyrrolate following induction of anaesthesia with halothane and enflurane. Premedication was standardized in all groups and ventilation controlled to achieve normal end tidal carbon dioxide. Heart rate increased in all cases following anticholinergic medication and the increase in heart rate was significantly higher in children receiving halothane anaesthesia as compared to those given enflurane. There was no significant difference between atropine and glycopyrrolate groups. There was no difference in frequency of occurrence of junctional tachycardia, which was the only arrhythmia observed, in the four groups studied. Our findings suggest that, in clinical situations where development of marked tachycardia is a concern, the combination of enflurane and anticholinergic drugs offers an advantage over the combination of halothane and anticholinergic drugs in paediatric patients.

Age Factors↗

PubMed1986

Nausea and vomiting after strabismus surgery in preschool children.

The incidence of nausea and vomiting after strabismus surgery was studied in 64 children aged one to six years. Incidence was determined in the post-anaesthesia recovery room (PARR), in the same day surgery (SDS) unit, and at home on days one and two after the operation. After induction of anaesthesia, the children received an intravenous injection of droperidol (50 micrograms . kg-1) or saline in a double-blind randomized fashion, and an intravenous injection of glycopyrrolate (7.5 micrograms . kg-1) or atropine (10 micrograms . kg-1) in an open randomized fashion. The incidence of emetic symptoms was highest in the SDS unit and at home on day one. Droperidol slightly but significantly delayed awakening and was not, at least in this particular age group, associated with any difference in postoperative sickness. Despite theoretical advantages, glycopyrrolate offered no significant benefit over atropine as far as postoperative emesis was concerned.

Anesthesia, General↗

PubMedDate not supplied

The dose-response relationship for memory impairment by anticholinergic drugs.

Twelve stabilized chronic schizophrenic outpatients receiving maintenance treatment with fluphenazine decanoate plus anticholinergic antiparkinsonian drugs underwent two challenge sessions receiving, in random sequence and double-blind, injections of either benztropine or glycopyrrolate (a peripherally active anticholinergic agent that penetrates the CNS poorly, used as an active placebo). Performance on free recall testing was significantly worse after benztropine than after glycopyrrolate. It has previously been shown that routine clinical doses of anticholinergic antiparkinsonian drugs impair verbal learning relative to a drug-free baseline. Our results suggest that memory impairment continues to further increase as anticholinergic drugs are pushed to the upper limit of the acceptable clinical range.

Adult↗

PubMed1995

No antidepressant effect of biperiden compared with placebo in depression: a double-blind 6-week clinical trial.

Depression may result from an increased ratio of cholinergic to aminergic central neurotransmission. The effect of centrally active anticholinergic agents on depressive ratings in depressed patients, however, has not been well studied. In a previous open label 4-week clinical trial, Kasper et al. (1981) reported that biperiden (Akineton) had antidepressant effects in depressed patients. We compared the effects of placebo and biperiden in a randomized, double-blind, parallel-design 6-week study. All patients received placebo for the first week and then received either biperiden (< or = 12 mg/day) or a peripherally acting anticholinergic agent, glycopyrrolate (Robinul, 1 mg/day) for 4 weeks. All patients received placebo during week 6. Both groups significantly improved, but biperiden did not demonstrate any significant benefit compared with glycopyrrolate. In a subgroup of patients receiving biperiden, the percentage of rapid eye movement sleep was significantly decreased only in the first week of biperiden compared with the initial placebo week, suggesting that tolerance to the central effects of biperiden developed. Further studies would be needed to determine whether anticholinergic agents possess antidepressant properties.

Adult↗

PubMed1993

Protection by tacrine and some adjuncts against the depressant effects of soman in guinea-pig atrium.

1. The negative inotropic effects of soman have been reported previously. It was suggested that the depression in atrial force of contraction was a consequence of continuous muscarinic receptor activation by excessive acetylcholine (ACh) accumulation and also possibly through direct interactions at the receptor-associated K+ channels by organophosphate (OP). 2. In this study, the protective effects of tacrine (THA), an antimuscarinic as well as a K+ channel blocker, against soman in guinea-pig atrium were investigated. 3. It was found that tacrine could antagonize the negative inotropic effects of soman. This antagonism occurred in a concentration dependent manner, with effective concentrations (ECs) for tacrine ranging from 1.7 to 12.1 microM when the atrium was equilibrated with 0.05-10 microM soman. 4. Inclusion of an oxime HI-6 (100 microM) in the regimen improved the efficacy of tacrine against soman (1 microM) by 16.1 fold. 5. Addition of a potent antimuscarinic, either atropine or glycopyrrolate with tacrine also improved tacrine's efficacy against soman significantly. 6. Atropine, at equivalent concentration, appeared to be the most effective of the three. At 0.1 microM concentration, atropine was 4.25 and 3.47 times more potent than HI-6 and glycopyrrolate respectively in enhancing THA efficacy. 7. Our results suggested that the immediate suppression of the muscarinic manifestations and the reactivation of the enzyme acetylcholinesterase for the removal of excess ACh are both critical in maintaining the mechanical functions of a heart during acute OP poisoning. The blockade of K+ channels by tacrine may also contribute to countering the depressant effects of soman.

Animals↗

PubMed2005

PM-induced cardiac oxidative stress and dysfunction are mediated by autonomic stimulation.

Epidemiological studies show that increases in particulate air pollution (PM) are associated with increases in cardiopulmonary morbidity and mortality. However, the mechanism(s) underlying the cardiac effects of PM remain unknown. We used pharmacological strategies to determine whether oxidants are implicated in PM-dependent cardiac dysfunction and whether PM-induced increase in autonomic stimulation on the heart mediates cardiac oxidative stress and toxicity. Adult Sprague-Dawley rats were exposed to either intratracheal instillation of urban air particles (UAP 750 microg) or to inhalation of concentrated ambient particles (CAPs mass concentration 700+/-180 microg/m3) for 5 h. Oxidative stress and cardiac function were evaluated 30 min after UAP instillation or immediately after exposure to CAPs. Instillation of UAP led to significant increases in heart oxidants measured as organ chemiluminescence (UAP: 38+/-5 cps/cm2, sham: 10+/-1 cps/cm2) or thiobarbituric acid reactive substances (TBARS, UAP: 76+/-10, Sham 30+/-6 pmol/mg protein). Heart rate increased immediately after exposure (UAP: 390+/-20 bpm, sham: 350+/-10 bpm) and returned to basal levels over the next 30 min. Heart rate variability (SDNN) was unchanged immediately after exposure, but significantly increased during the recovery phase (UAP: 3.4+/-0.2, Sham: 2.4+/-0.3). To determine the role of ROS in the development of cardiac malfunction, rats were treated with 50 mg/kg N-acetylcysteine (NAC) 1 h prior to UAP instillation or CAPs inhalation. NAC prevented changes in heart rate and SDNN in UAP-exposed rats (340+/-8 and 2.9+/-0.3, respectively). To investigate the role of the autonomic nervous system in PM-induced oxidative stress, rats were given 5 mg/kg atenolol (beta-1 receptor antagonist), 0.30 mg/kg glycopyrrolate (muscarinic receptor antagonist) or saline immediately before exposure to CAPs aerosols. Both atenolol and glycopyrrolate effectively prevented CAPs-induced cardiac oxidative stress (CL(ATEN): 11+/-1 cps/cm2, CL(GLYCO): 10+/-1 cps/cm2, TBARS(ATEN): 40+/-6 pmol/mg protein, TBARS(GLYCO): 38+/-6 pmol/mg protein). These data indicate that PM exposure increases cardiac oxidants via autonomic signals and the resulting oxidative stress is associated with significant functional alterations in the heart.

Acetylcholine↗

PubMed1982

Direct measurement of the anticholinergic activity of a series of pharmacological compounds on the canine and rabbit urinary bladder.

Antimuscarinic therapy is used widely in the treatment of urine storage failure. Examples of antimuscarinic agents used clinically include atropine, propantheline bromide and glycopyrrolate. Other agents used in clinical urology that are believed to act at least in part by antimuscarinic activity include oxybutynin, imipramine and dicyclomine, These studies were designed to determine the relative potency of a variety of agents to compete directly for muscarinic cholinergic receptors isolated from the canine and rabbit urinary bladder. Radio-ligand binding assays for muscarinic receptors were performed with 10 nM 3H-QNB and various concentrations of the drugs under study. Of the agents tested, propantheline bromide, atropine, and glycopyrrolate were the potent muscarinic antagonists/unit of concentration. Oxybutynin and dicyclomine hydrochloride were 30 to 50 times less potent than atropine. Chlorpromazine and desmethylimipramine were approximately 500 times less potent than atropine. As expected, agents such as guanethidine, tranylcypramine and hexamethonium possessed little antimuscarinic activity.

Animals↗

PubMed1999

A survey of current usage of anticholinergic drugs in paediatric anaesthesia in Finland.

BACKGROUND: The aim of this survey was to obtain information about the current use of anticholinergic preanaesthetic medication in children. It was carried out as a follow-up study of the previous survey amongst Finnish anaesthesiologists in 1990. METHODS: A questionnaire was send to all members of the Finnish Society of Anaesthesiologists. Data from anaesthesiologists taking care of at least three paediatric anaesthesias/week (n= 183) were analyzed. RESULTS: In 1998 only one-third of the Finnish anaesthesiologists routinely used anticholinergics before paediatric anaesthesia. The main indications for routine anticholinergic premedication were ENT surgery (66%), eye surgery (71%) and endoscopic procedures (67%). Anticholinergic drugs were administered principally via the intravenous route (90%) briefly before induction of anaesthesia, and glycopyrrolate was the most frequently used (66%). CONCLUSION: During the last eight years in Finland the routine use of anticholinergic premedication has decreased. As in 1990 the anticholinergic prophylaxis is directed to ENT and eye surgery, endoscopic procedures and to children younger than 1 year. Use of glycopyrrolate has gained popularity at the expense of atropine and scopolamine.

Atropine↗

PubMed2001

Time domain, geometrical and frequency domain analysis of cardiac vagal outflow: effects of various respiratory patterns.

The purpose of this study was to compare the applicability of four different measures of heart rate variability (HRV) in the assessment of cardiac vagal outflow, with special reference to the effect of breathing pattern. The anticholinergic effects of an intravenous glycopyrrolate infusion (5 microg x kg(-1) x h(-1) for 2 h) during spontaneous and controlled (15 min(-1)) breathing rate were investigated in eight volunteers, and the effects of different fixed breathing rates (6-15-24 min(-1)) and hyperventilation in 12 subjects. Cardiac vagal activity was assessed by ECG recordings in which the following measures of HRV were computed: the high-frequency (HF) spectral component, the instantaneous RR interval (RRI) variability (SD1) analysed from the Poincaré plots, the percentage of differences between successive RRIs greater than 50 ms (pNN50), and the square root of the mean squared differences of successive RRIs (RMSSD). On average, glycopyrrolate reduced the HF spectral component by 99.8%, SD1 by 91.3%, pNN50 by 100% and RMSSD by 97.0%. The change of breathing pattern from controlled to spontaneous decreased significantly the HF component and pNN50, but did not affect SD1 or RMSSD. Rapid breathing rate (24 min(-1)) decreased the HF component, but had no effects on the other measures. A controlled breathing rate is needed for a reliable assessment of cardiac vagal outflow by the spectral analysis technique. The quantitative geometrical analysis of short-term RRI variability from the Poincaré plots and the time domain measure RMSSD were not significantly affected by changes in the breathing rate, suggesting that these indices are more suitable for the measurement of cardiac vagal outflow during the 'free-running' ambulatory conditions.

Adult↗

PubMed2003

Effect of cardiac vagal outflow on complexity and fractal correlation properties of heart rate dynamics.

1. Cardiac vagal outflow is the major factor determining the magnitude of heart rate (HR) variability analysed by traditional time and frequency domain methods. New analysis techniques, such as fractal and complexity methods, have been developed to probe non-linear features in HR behaviour that may not be detectable by traditional methods. 2. We investigated the effects of vagal blockade (glycopyrrolate i.v. 5 microg kg-1 h-1 for 2 h, n = 8 vs. unmedicated control group, n = 8) and various breathing patterns (n = 12) on two non-linear measures of HR variability--detrended fluctuation analysis (DFA) and approximate entropy (ApEn)--in healthy male volunteers. 3. Glycopyrrolate decreased the mean (+/-SD) ApEn from 1.46 +/- 0.18 to 0.85 +/- 0.24 (P = 0.001 in comparison with the control group), and increased the short-term (alpha 1) and intermediate-term (alpha 2) fractal scaling exponents of DFA, alpha 1 from 0.96 +/- 0.19 to 1.43 +/- 0.29 (P = 0.003) and alpha 2 from 1.13 +/- 0.10 to 1.34 +/- 0.14 (P < 0.001). 4. Decrease in fixed respiration rate from 15 to 6 breaths min-1 increased alpha 1 from 0.83 +/- 0.25 to 1.18 +/- 0.27 (P < 0.001), but decreased alpha 2 from 0.88 +/- 0.09 to 0.45 +/- 0.17 (P < 0.001) and ApEn from 1.26 +/- 0.12 to 1.10 +/- 0.14 (P = 0.028). Rapid breathing (24 min-1) had no influence on these non-linear measures of HR variability. Hyperventilation (15 min-1, tidal volume increased voluntarily by 0.5 l) decreased alpha 1 from 0.83 +/- 0.25 to 0.66 +/- 0.28 (P = 0.002) but did not affect alpha 2 or ApEn. 5. To conclude, vagal blockade alters the fractal scaling properties of R-R intervals (alpha 1, alpha 2) and reduces the complexity (ApEn) of HR behaviour. Both the fractal and complexity measures of HR variability can also be influenced by changes in the breathing pattern.

Adolescent↗

PubMed1997

The effects of reversal of neuromuscular blockade on autonomic control in the perioperative period.

Impaired parasympathetic control of heart rate is associated with increased incidence of cardiac dysrhythmias and ischemia. Anticholinergic drugs suppress parasympathetic control and could be detrimental in the early postoperative period in high-risk patients. In this double-blind randomized trial, 30 ASA physical status I and II patients undergoing minor surgery received either atropine 20 micrograms/kg and neostigmine 50 micrograms/kg (Group A), glycopyrrolate 8 micrograms/kg and neostigmine 50 micrograms/kg (Group G), or placebo (Group P) for reversal of neuromuscular blockade. Two indices of parasympathetic modulation of heart rate, spontaneous baroreflex sensitivity, and high-frequency heart rate variability, were assessed. At 2 h after reversal, Group A showed persisting impairment of baroreflex sensitivity with respect to Group P (7.12 +/- 0.86 vs 12.71 +/- 1.38 ms/mm Hg, P = 0.022) as well as decreased high-frequency heart rate variability (280.8 +/- 30.1 vs 569.2 +/- 115.2 ms2/Hz, P = 0.015). Groups A and G showed a borderline decrease in normalized high-frequency variability at 2 h (P = 0.05 for Groups A and G versus Group P). Anticholinergic drugs with neostigmine cause impairment of parasympathetic control of heart rate which persists into the early postoperative period. The effects of glycopyrrolate appear to be of shorter duration; this drug may thus be preferable in patients at risk of cardiovascular complications.

Adolescent↗

PubMed1985

The cerebral effects of pancuronium and atracurium in halothane-anesthetized dogs.

Pancuronium decreases the minimal alveolar anesthetic concentration (MAC) of halothane in humans, while atracurium has a metabolite, laudanosine, which is a known cerebral stimulant. To determine if these muscle relaxants significantly alter cerebral function, their effects on cerebral metabolic rate (CMRo2), cerebral blood flow (CBF), intracranial pressure (ICP), EEG, and the cerebral energy state were studied in halothane-anesthetized dogs. Group A dogs (n = 6) were maintained at 0.86% end-expired (1.0 MAC) halothane. Thereafter, a sequence of 1) pancuronium 0.1 mg . kg-1; 2) reversal of neuromuscular blockade with neostigmine plus glycopyrrolate; and 3) pancuronium 0.2 mg . kg-1 produced no changes in CMRo2, CBF, ICP, or EEG. Group B dogs (n = 6) also were maintained at 0.86% end-expired halothane and received the following in sequence: 1) atracurium 0.5 mg . kg-1; 2) reversal of neuromuscular blockade with neostigmine plus glycopyrrolate; 3) atracurium 1.0 mg . kg-1; and 4) atracurium 2.5 mg . kg-1. There were no changes in CMRo2, CBF, or ICP; EEG evidence of cerebral arousal occurred in only one dog with the final dose of atracurium. Group C dogs (n = 6) received tetracaine spinal anesthesia and the minimal halothane concentration (mean +/- SE = 0.69 +/- 0.03% end-expired) that would maintain an "anesthetic" EEG pattern. Each Group C dog received the following in sequence: 1) atracurium 1.0 mg . kg-1, and 2) atracurium 2.5 mg . kg-1. EEG evidence of cerebral arousal occurred in all six Group C dogs. Arousal was not accompanied by significant increases in CBF, CMRo2, or ICP.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗

PubMedDate not supplied

Autonomic and cardiovascular effects of neuromuscular blockade antagonism in the dog.

Autonomic and cardiovascular changes were studied when neuromuscular blockade was antagonized in 96 dogs with one of eight anticholinesterase-antimuscarinic drug combinations. Neostigmine (50 or 100 micrograms/kg) was administered before or after atropine (40 micrograms/kg) or glycopyrrolate (10 micrograms/kg). The high dose of neostigmine (100 micrograms/kg) caused bradyarrhythmias, salivation, and signs of bronchosecretion when used with either antimuscarinic agent and irrespective of the administration sequence. The heart rate increased, but not significantly, when atropine was injected before either dose of neostigmine. This did not occur when this administration sequence was reversed. Arrhythmias and cardiovascular and autonomic changes did not occur when glycopyrrolate was injected before or after neostigmine at 50 micrograms/kg.

Animals↗

PubMed2003

Early death due to severe organophosphate poisoning is a centrally mediated process.

OBJECTIVE: To distinguish whether early death from severe organophosphate (OP) poisoning with dichlorvos is mediated through peripheral or central nervous system (CNS) actions. METHODS: Wistar rats (n = 72) were randomized to pretreatment with either: normal saline (controls), peripheral anticholinergics (glycopyrrolate [low, medium, or high dose] or nebulized ipratropium bromide), or CNS + peripherally acting anticholinergics (diphenhydramine, nebulized atropine, or injected atropine). All treatments were given prior to a subcutaneous injection of 25 mg/kg dichlorvos (n = 8 per group). Survival was assessed at 10 minutes (early death) and 24 hours (delayed death). Kaplan-Meier (95% confidence intervals [95% CIs]) and chi-squared analysis was then performed to determine differences between treatments. RESULTS: Regardless of treatment, all animals exhibited profound nicotinic effects (fasciculations) without obvious seizures within 2 minutes of poisoning. In rats pretreated with peripherally acting agents, the fasciculations were rapidly followed by reduced motor activity, sedation, and death. Mortality at 10 minutes for saline controls, glycopyrrolate, and ipratropium was 88%, 96%, and 100%, respectively. The single control animal surviving beyond 10 minutes went on to develop peripheral cholinergic manifestations, including hypersalivation, urination, and defecation. Only one of 24 animals treated with injected atropine, nebulized atropine, or diphenhydramine died during the early phase of poisoning; all others survived to 24 hours (p < 0.01). CONCLUSIONS: Death in acute, severe OP poisoning is prevented by pretreatment with anticholinergic agents that cross the blood-brain barrier, but not by agents with only peripheral actions. Early death due to OP poisoning appears to be a centrally mediated process.

Animals↗