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PubMed1994

Physiological changes, plasma beta-endorphin and cortisol responses to tracheal intubation in neonates.

Physiological, plasma beta-endorphin and cortisol responses to nasotracheal intubation were studied in 20 distressed infants of median age 0.3 days (range 0.1-23 days) randomized into groups given pethidine 1 mg/kg (n = 10) or alfentanil 20 micrograms/kg plus suxamethonium 1.5 mg/kg (n = 10) before intubation. All of the infants were given glycopyrrolate 3-5 micrograms/kg. Hypoxaemia during intubation was found in all 10 infants in the pethidine group and in 7 of 10 infants in the alfentanil-suxamethonium group, its duration being significantly longer in the pethidine group and being associated with the duration of the intubation procedure. Blood pressure increased, but not statistically significantly, in all except 2 patients in the alfentanil-suxamethonium group and bradycardia appeared in 1 patient in each group. Plasma beta-endorphin and cortisol values did not show any statistically significant intra-group or inter-group differences. Newborn infants suffer from hypoxaemia during intubation when awake more and therefore need adequate premedication before elective intubation. One alternative is the combination of glycopyrrolate, alfentanil and suxamethonium described here, although the ideal medication and dosage still remain to be defined.

Alfentanil↗

PubMed1991

Effects of anticholinergic treatment on the cardiac and respiratory systems in dogs sedated with medetomidine.

Alpha 2-adrenergic agonists are often used for sedation and, or, analgesia in dogs, but they are often associated with bradycardia and in some animals with atrioventricular heart block. In this study, atropine or glycopyrrolate either helped to maintain the heart rates or were effective in increasing reduced heart rates of dogs treated with medetomidine. In the process, however, cardiac dysrhythmias often developed. These dysrhythmias were predominantly associated with the combined responses to the medetomidine and the anticholinergic agent because there were no significant changes in respiratory function. A reduced blood oxygen content or increased blood carbon dioxide can contribute to cardiac irritability. Atropine and glycopyrrolate were more effective in preventing bradycardia and had less undesirable side effects when they were given before the administration of medetomidine.

Adrenergic alpha-Agonists↗

PubMed1997

Effect of autonomic blockade on power spectrum of heart rate variability during exercise.

To validate power spectral analysis of heart rate variability (HRV) as an autonomic indicator during exercise, ten males performed four identical progressive cycling tests during infusions of saline, esmolol (beta 1-blocker), glycopyrrolate (muscarinic blocker), or both drugs. Power spectra were constructed from the recorded electrocardiogram by Fourier algorithm and integrated for low-frequency power (LF) and high-frequency power (HF). Four different LF bands (0.004-0.1, 0.004-0.15, 0.05-0.1, and 0.05-0.15 Hz) and two different HF bands (0.1-1.0 and 0.15-1.0 Hz) were evaluated. The parasympathetic index, HF, decreased exponentially with workload and was attenuated by glycopyrrolate and combined treatments with both HF frequency bands measured. Whereas some sympathetic indexes (LF/total power and LF/HF) did reflect expected increases in sympathetic nerve activity associated with progressive increases in work intensity, none of the measured increases responded appropriately to autonomic blockade. It is concluded that HRV is a valid technique for noninvasive measurement of parasympathetic tone during exercise, but its validity as a measure of sympathetic tone during exercise is equivocal.

Adrenergic beta-Antagonists↗

PubMed1998

Primary vagally mediated decelerations in heart rate during tonic rapid eye movement sleep in cats.

Rapid eye movement (REM) sleep results in profound state-dependent alterations in heart rate. The present study describes a novel phenomenon of a primary deceleration in heart rate that is not preceded or followed by increases in heart rate or arterial blood pressure and occurs primarily during tonic REM sleep. The goals were to characterize the primary decelerations and to provide insights on the underlying central and peripheral autonomic mechanisms. Cats were chronically implanted with electrodes to record electroencephalogram, pontogeniculooccipital wave activity in lateral geniculate nucleus, hippocampal theta rhythm, electromyogram, electrooculogram, respiration (diaphragm), and electrocardiogram. Arterial blood pressure was monitored from a carotid artery catheter. R-R interval fluctuations were continuously tracked using customized software. The muscarinic blocking agent glycopyrrolate (0.1 mg/kg i.v.) and the beta-adrenergic blocking agent atenolol (0.3 mg/kg i.v.) were administered in alternating sequence with a 90- to 120-min interval. Glycopyrrolate immediately eliminated the decelerations during REM sleep. Atenolol alone had no effect on their frequency. These findings suggest that a change in the centrally induced pattern of autonomic activity to the heart is responsible for the primary decelerations, namely, a bursting of cardiac vagal efferent fiber activity.

Adrenergic beta-Antagonists↗

PubMed2004

Local heating of human skin causes hyperemia without mediation by muscarinic cholinergic receptors or prostanoids.

Local changes in surface temperature have a powerful influence on the perfusion of human skin. Heating increases local skin blood flow, but the mechanisms and mediators of this response (thermal hyperemia response) are incompletely elucidated. In the present study, we examined the possible dependence of the thermal hyperemia response on stimulation of muscarinic cholinergic receptors and on production of vasodilator prostanoids. In 13 male healthy subjects aged 20-30 yr, a temperature-controlled chamber was positioned on the volar face of one forearm and used to raise surface temperature from 34 to 41 degrees C. The time course of the resulting thermal hyperemia response was recorded with a laser-Doppler imager. In one experiment, each of eight subjects received an intravenous bolus of the antimuscarinic agent glycopyrrolate (4 microg/kg) on one visit and saline on the other. The thermal hyperemia response was determined within the hour after the injections. Glycopyrrolate effectively inhibited the skin vasodilation induced by iontophoresis of acetylcholine but did not influence the thermal hyperemia response. In a second experiment, conducted in five other subjects, 1 g of the cyclooxygenase inhibitor aspirin administered orally totally abolished the vasodilation induced in the skin by anodal current but also failed to modify the thermal hyperemia response. The present study excludes the stimulation of muscarinic receptors and the production of vasodilator prostaglandins as essential and nonredundant mechanisms for the vasodilation induced by local heating in human forearm skin.

Acetylcholine↗

PubMed1995

Vagal modulation of epicardial coronary artery size in dogs. A two-dimensional intravascular ultrasound study.

BACKGROUND: Because the role of tonic vagus nerve activity in regulating conduit coronary artery size remains undefined, we investigated the response of epicardial coronary artery size to changes in resting vagal tone resulting from vagotomy and muscarinic receptor blockade. METHODS AND RESULTS: Using intravascular ultrasound to measure left circumflex coronary artery cross-sectional area continuously, we examined the effects of vagotomy on left circumflex cross-sectional area in nine dogs. Lumen area decreased 20% from 8.70 +/- 2.81 to 6.92 +/- 1.97 mm2 after right vagotomy, 17% to 7.19 +/- 2.80 mm2 after left vagotomy (both P < .05 versus baseline), and 38% to 5.42 +/- 2.00 mm2 after bilateral vagotomy (P < .05 versus unilateral vagotomy). Vasoconstriction occurred despite increases in heart rate and an unchanged rate-pressure product. In six additional dogs, after acetylcholine (100 micrograms/kg i.v.), lumen area increased by 18%, although heart rate, blood pressure, and rate-pressure product were unchanged. Vasodilation was prevented by prior muscarinic blockade with glycopyrrolate. With glycopyrrolate administration and heart rate control by pacing, lumen area decreased by 26% (P = .011). When stellate stimulation was performed in a third group of eight dogs with heart rate, blood pressure, and rate-pressure product controlled by a combination of pacing and exsanguination, there was no change in coronary area, thus precluding reflex sympathetic activation as a contributor to the vasoconstriction produced by vagal withdrawal. CONCLUSIONS: Vagus nerve activity maintains tonic dilation of the left circumflex coronary artery by muscarinic receptor activation. Each vagus nerve contributes approximately equally to the tonically dilated state. Vagotomy-induced vasoconstriction occurs independently of local metabolic factors and coronary distending pressure and is a result of cholinergic withdrawal rather than reflex sympathetic activation.

Acetylcholine↗

PubMed2003

Aging and secretory reserve capacity of major salivary glands.

A loss of acinar cells occurs with aging, while salivary production remains age-stable in healthy adults. It is hypothesized that a secretory reserve exists to preserve function despite a loss of acinar cells in normal aging. The purpose of this double-blind, placebo-controlled, crossover study was to determine age-related differences in salivary response to an anti-sialogogue (glycopyrrolate). Thirty-six healthy subjects (18 young--20-38 yrs; 18 older--60-77 yrs) received 4.0 microg/kg i.v. glycopyrrolate. Parotid and submandibular/sublingual saliva samples and xerostomia questionnaire responses were collected. Variables calculated for each subject were: times to initial and maximum suppression and xerostomic complaint; time to recovery; and durations of suppression and complaint. Salivary function was more adversely affected in older persons. There were no consistent age-associated questionnaire response differences. These findings suggest that salivary gland output is more adversely affected by an anti-sialogogue in healthy older vs. younger adults, supporting the secretory reserve hypothesis of salivary function.

Adult↗

PubMed2006

Multiple centrally acting antidotes protect against severe organophosphate toxicity.

BACKGROUND: Accumulation of acetylcholine in the central nervous system is believed to account for the rapid lethality of organophosphate pesticides and chemical nerve agents. Diazepam is known to supplement atropine therapy, but its specific mechanism of action is uncertain. OBJECTIVES: To test four centrally acting agents for early antidotal efficacy in severe dichlorvos poisoning in the murine model. METHODS: The up-and-down method was used to dose four candidate antidotes: diazepam, xylazine, morphine, and ketamine. Antidotes were administered subcutaneously to unsedated adult Sprague-Dawley rats who were pretreated with 3 mg/kg intraperitoneal glycopyrrolate. All animals received 20 mg/kg of dichlorvos subcutaneously 5 minutes later. A blinded observer adjudicated the outcomes of 10-minute mortality and survival time. RESULTS: All animals pretreated with either no antidote (8/8 deaths) or glycopyrrolate alone (8/8) died within 10 minutes of dichlorvos injection. Pretreatment with diazepam (3/9 deaths), or xylazine (3/9), decreased lethality substantially (Fisher p = 0.007; median effective doses, 0.12 mg/kg and 3.0 mg/kg, respectively). Intermediate doses of morphine (3.1 to 5.5 mg/kg) resulted in survival, but higher doses did not, presumably because of excessive respiratory depression (7/11 deaths; p = 0.09). Ketamine (7/8 deaths) was ineffective as an antidote. Survival times also were prolonged in the diazepam and xylazine groups (log-rank p < 0.001) and, to a lesser degree, the morphine group (p = 0.07). CONCLUSIONS: Doses of diazepam, xylazine, and morphine below those used for deep sedation protect against severe dichlorvos poisoning, implying that several distinct central mechanisms are each sufficient to avert lethality. These findings suggest new possibilities for prophylaxis or therapy.

Animals↗

PubMed1984

Analysis of the specificity of physostigmine stimulation of adrenocorticotropin in man.

Five normal men were given infusions of saline and three doses (6, 12, and 18 micrograms/kg) of physostigmine, a centrally acting anticholinesterase, after pretreatment with glycopyrrolate, a peripheral cholinergic antagonist. There was no increase in basal ACTH or cortisol concentrations in any of the subjects after saline or the two smaller doses of physostigmine. However, each subject had a marked increase in ACTH and cortisol levels after the largest dose of physostigmine. These changes were preceded in each subject by the occurrence of noxious side effects and were accompanied by a rise in PRL levels in four of the subjects. Four subjects who received physostigmine (12 micrograms/kg) without glycopyrrolate pretreatment also experienced noxious side effects; these symptoms were followed by elevations in ACTH, cortisol, and PRL levels. These findings suggest that physostigmine stimulates ACTH and cortisol secretion through a stress-mediated effect rather than through a specific cholinergic mechanism. Consequently, physostigmine is not a reliable tool for investigating the cholinergic regulation of ACTH and cortisol.

Adrenocorticotropic Hormone↗

PubMed1994

Comparison of transesophageal atrial pacing with anticholinergic drugs for the treatment of intraoperative bradycardia.

We compared the effectiveness of atropine, glycopyrrolate, and a transesophageal atrial pacing (TAP) stethoscope for treating intraoperative bradycardia in 64 unpremedicated patients receiving a standardized sufentanil/N2O/vecuronium anesthetic. Patients were allocated randomly to receive either atropine, 5 micrograms/kg (Group 1), glycopyrrolate, 2.5 micrograms/kg (Group 2), or transesophageal atrial pacing (Group 3) after the onset of bradycardia, defined as a heart rate of < or = 50 beats/min (or < or = 60 beats/min with concurrent hypotension). Bradycardia occurred in 15 patients of each treatment group. The time required for the heart rate to increase to > or = 70 beats/min was 270 (range 30-490), 270 (70-465), and 12 (2-30) s in Groups 1, 2, and 3, respectively. Although all patients in Group 3 responded to pacing at 150% of the threshold current, 10 patients in Group 1 and 8 patients in Group 2 required a second dose of anticholinergic medication before a heart rate response was observed. One patient in Group 2 required three doses, and another who did not respond even after four doses was treated with the TAP device. Bradycardia subsequently recurred in five patients in Group 1 and four patients in Group 2. Temporary recurrence of bradycardia occurred in seven patients in Group 3 due to outward migration of the pacing stethoscope. However, heart rates were more consistently maintained in paced patients. There were no significant differences in postoperative side effects between the three groups, or when compared with patients who did not receive treatment for bradycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed2002

Sialorrhea - therapeutic drug options.

OBJECTIVE: To review the efficacy and safety of various drug treatments for sialorrhea. Pharmacotherapy for drug-induced sialorrhea is not addressed. DATA SOURCES: Clinical studies were identified using PubMed (1966-October 2001). Key search terms included sialorrhea and drug therapy. DATA SYNTHESIS: Sialorrhea is a social and physical detriment to patients. Drug treatment, although not necessarily the treatment of choice for all patients, can offer some symptom relief. CONCLUSIONS: Literature has documented that benztropine, glycopyrrolate, and scopolamine can reduce the incidence of sialorrhea. Although the literature evaluating the therapeutic options has limitations (e.g., small sample size, inconsistent outcome measurements), glycopyrrolate may have an advantage over the other agents due to fewer adverse effects.

Adolescent↗

PubMed2005

Effects of antitussive agents administered before bronchoalveolar lavage in horses.

OBJECTIVE: To determine whether treatment of horses with antitussive agents before bronchoalveolar lavage (BAL) reduces the frequency and intensity of the cough reflex during BAL. ANIMALS: 8 healthy horses. PROCEDURE: Standard BAL was performed on each horse weekly for 6 weeks. Detomidine was used as a general sedative, and various antitussive agents were evaluated for their suitability to suppress undesirable coughing. Treatments administered prior to BAL consisted of saline (0.9% NaCl) solution (control treatment), codeine, butorphanol tartrate, glycopyrrolate, lidocaine hydrochloride (final concentration, 0.33%), and lidocaine hydrochloride at a final concentration of 0.66% (lidocaine 0.66%). Frequency and intensity of coughing were digitally recorded throughout the BAL procedure. The volume of BAL fluid collected was measured, and the fluid was cytologically examined to assess potential effects of the medications on composition. RESULTS: Coughing frequency was significantly reduced after intratracheal administration of lidocaine 0.66%. Moreover, intratracheal administration of lidocaine 0.66% or IV administration of butorphanol resulted in a significant reduction in the intensity of coughing episodes. All other treatments failed to significantly suppress coughing frequency and intensity, compared with results for the saline treatment. Glycopyrrolate caused obvious adverse clinical effects. Treatments did not influence the volume of BAL fluid collected nor composition of the fluid. CONCLUSIONS AND CLINICAL RELEVANCE: Intratracheal administration of lidocaine (final concentration, 0.66%) proved to be the most reliable method to reduce frequency and intensity of coughing in horses during BAL.

Animals↗

PubMed1990

Trimeprazine as oral premedication in children.

The effect of oral trimeprazine alone or in combination with either atropine or glycopyrrolate or pethidine as oral premedication in children was studied. The effects of different drug combinations were evaluated in respect of pre-operative sedation, salivary secretion, induction characteristic, postoperative sedation and postoperative vomiting. The study concludes that trimeprazine in combination with either atropine or glycopyrrolate is mostly effective, safe and satisfactory as oral premedication in children. Trimeprazine along with pethidine can be recommended for all purpose oral medication both in pre- and post-operative period.

Administration, Oral↗

PubMed1989

Cardiovascular and respiratory effects of medetomidine in dogs and influence of anticholinergics.

A total of 10 laboratory beagles was used to determine the cardiovascular and respiratory effects of medetomidine. The effects of atropine sulphate and glycopyrrolate on heart rate were also observed. Xylazine was included as a positive control. Medetomidine induced initial hypertension followed by a longer lasting hypotensive period. Evident bradycardia with second degree atrioventricular blocks and decrease in respiratory frequency was observed. Atropine sulphate and glycopyrrolate transiently abolished the bradycardic effect of medetomidine. Xylazine exhibited a similar cardiovascular and respiratory pattern to medetomidine.

Animals↗

PubMed1986

Anticholinergics and human brain stem auditory evoked potentials.

The effect of premedication with morphine and anticholinergic drugs on absolute and interpeak latencies of brain stem auditory evoked potentials was studied in thirty patients. Two commonly used anticholinergics, glycopyrrolate and scopolamine, given in combination with morphine were studied. Patients premedicated with morphine alone served as a control group. No significant change in either absolute or interpeak latencies was noted in patients premedicated with either morphine alone or morphine and glycopyrrolate. Results in patients premedicated with morphine and scopolamine are inconclusive because of large intersubject variability.

Adolescent↗

PubMed1993

Alpha 2-adrenergic receptor agonist effects on supraventricular and ventricular automaticity in dogs with complete atrioventricular block.

Complete atrioventricular block was induced in 26 pentobarbital-anesthetized dogs to determine the effects of the alpha 2-adrenergic receptor agonists, xylazine and medetomidine, on supraventricular and ventricular automaticity. Prazosin and atipamezole, alpha-adrenoceptor antagonists, were administered to isolate alpha 1- or alpha 2-adrenoceptor effects. Six dogs served as controls and were given glycopyrrolate (0.1 mg/kg of body weight, IV) and esmolol (50 to 75 micrograms/kg/min, IV) to induce parasympathetic and beta 1-adrenergic blockade, respectively. Eight dogs were given sequentially increasing doses of xylazine (n = 5), 0.000257 mg (10(-9)M) to 25.7 mg (10(-4)M) and medetomidine (n = 3), 0.000237 mg (10(-9)M) to 2.37 mg (10(-5)M) after parasympathetic and beta 1-adrenergic blockade. Twelve dogs were given xylazine (n = 6, 1.1 mg/kg, IV) or medetomidine (n = 6, 0.05 mg/kg, IV) after parasympathetic and beta 1-adrenergic blockade. Three dogs given xylazine and 3 dogs given medetomidine were administered prazosin (0.1 mg/kg, IV) followed by atipamezole (0.3 mg/kg, IV). The order of prazosin and atipamezole was reversed in the remaining 3 dogs given either xylazine or medetomidine. Complete atrioventricular block and administration of glycopyrrolate and esmolol resulted in stable supraventricular and ventricular rates over a 4-hour period. Increasing concentration of xylazine or medetomidine did not cause significant changes in supraventricular or ventricular rate. Xylazine and medetomidine, in the presence of the alpha-adrenoceptor antagonists, prazosin (alpha 1) and atipamezole (alpha 2), did not cause significant changes in supraventricular or ventricular rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗

PubMed1995

Dose-response relationships for edrophonium antagonism of mivacurium-induced neuromuscular block during N2O-enflurane-alfentanil anaesthesia.

The purpose of this study was to determine the dose-response relationships for edrophonium antagonism of mivacurium-induced neuromuscular block. Seventy-five ASA I or II adults were given mivarcurium 0.15 mg x kg(-1) followed by an infusion (7 micrograms x kg(-1) x min(-1) during alfentanil-propofol-N2O-enflurane anaesthesia. Train-of-four stimulation (TOF) was applied to the ulnar nerve every 20 sec and the response of the adductor policis was recorded (Relaxograph NMT-100, Datex, Helsinki, Finland). Mivacurium infusion was modified at five-minute intervals in order to keep the height of the first twitch in TOF(T1) at 5% of its control value. At the end of surgery, edrophonium (0.0, 0.125, 0.25, 0.5, or 1.0 mg x kg(-1) combined glycopyrrolate (0.0, 0.0012, 0.0025, 0.005, or 0.01 mg x kg(-1) were administered by random allocation. Edrophonium doses of 0.25, 0.5 and 1.0 mg x kg(-1) were different from placebo with regard to time to attain a TOF ratio (fourth twitch in TOF/T1) = 0.7 (13.8 +/- 4.5, 11.1 +/- 3.5, 11.4 +/- 3.0 vs 19.7 +/- 4.7 min P< 0.05). Doses of 0.5 and 1.0 mg x kg(-1) permitted faster recovery time of T1 from 10 to 95% (T10-95) than did placebo (7.5 +/- 3.8, 8.9 +/- 3.5 vs 14.5 +/- 5.0 min P<0.05). Edrophonium 0.5 mg x kg(-1) was different from placebo with regard to recovery time of T1 from 25 to 75% (T25-75) (3.3 +/- 2.0 vs 6.7 +/- 2.0 min P<0.05). Only edrophonium 0.5 mg x kg(-1) provided faster recovery than placebo with regard to all three indices. It is concluded that edrophonium 0.5 + glycopyrrolate 0.005 mg x kg(-1) allow the fastest recovery from a mivacurium-induced block during enflurane-N2O anaesthesia.

Adolescent↗

PubMed1980

Synergism of the toxicity of physostigmine and neostigmine by lithium or by a reserpine-like agent (Ro4-1284).

A single sublethal i.p. dose of lithium chloride (300 mg/kg or 7.1 meq/kg) followed 12 h later by an otherwise sublethal s.c. dose of physostigmine sulfate (1.0 mg/kg) resulted in 90% mortality among male rats following a pronounced cholinergic syndrome, including convulsions. This confirms a previous report of a lethal synergism of physostigmine after subacute dosing with lithium. Mortality could be completely prevented by 1.0 mg/kg of atropine sulfate given 30 min before physostigmine, but was incompletely, if at all, reduced by selective peripheral cholinergic blockers, methylatropine bromide (0.5, 1.5 mg/kg) or glycopyrrolate (1 mg/kg). This suggested a predominantly central site for the toxic interaction. However, a similar synergism of lethality caused by neostigmine methylsulfate (0.3 mg/kg, s.c.) after treatment with lithium, which could be eliminated by methylatropine or glycopyrrolate, indicates that lithium may also produce lethal synergism of a cholinesterase (ChE) inhibitor that does not act centrally. Ro4-1284, an agent that has reserpine-like actions, was tested in combination with physostigmine or neostigmine; it showed synergism of toxicity nearly the same as in the case of lithium plus the cholinergic agents. These findings support the hypothesis that lithium causes the toxic synergism via a reduction of adrenergic activity, leading to an imbalance between adrenergic and cholinergic influences and a consequent failure to tolerate the effects of the ChE inhibitors. A potential hazard for the clinical use of physostigmine and neostigmine, concurrently with lithium or reserpine-like agents, it suggested.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗