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The efficacy of atropine or glycopyrrolate in doses of 10 or 20 micrograms kg-1 and 5 or 10 micrograms kg-1, respectively, has been compared when administered to block the muscarinic effects of edrophonium 0.5 mg kg-1 administered for the reversal of neuromuscular blockade. Both doses of atropine and the higher dose of glycopyrrolate prevented any edrophonium-induced decreases in heart rate; glycopyrrolate at this dose was associated with tachycardia. Atropine and edrophonium could be safely administered together in a mixture. The control of oropharyngeal secretions was adequate even with the lower doses of both anticholinergic agents. Atropine 10 micrograms kg-1 appears to be a better anticholinergic agent for use with edrophonium.

Atropine and glycopyrrolate were compared when given in a mixture with neostigmine for the reversal of non-depolarising neuromuscular block in children. Glycopyrrolate was an effective antimuscarinic agent and could be safely used as an alternative to atropine, although the advantages in this age group were not as marked as have been observed in adults.

Atropine and glycopyrrolate (glycopyrronium bromide), a quaternary ammonium drug, were evaluated in volunteers following intramuscular administration with respect to effects on various end-organs with cholinergic innervation. Glycopyrrolate appears to be five to six times more potent than atropine in its antisialogogue effect and also exhibits a selective, though prolonged, effect on salivary secretion and sweat gland activity. It has minimal cardiovascular, ocular and central nervous system effects.

Neuromuscular block was antagonized using pyridostigmine 250 micrograms kg-1 in two groups of 50 patients; one group received atropine 20 micrograms kg-1 and the other glycopyrrolate 10 micrograms kg-1 with the anticholinesterase drug. Atropine was associated with a greater initial tachycardia than was glycopyrrolate. The subsequent bradycardia was also greater in this group, although the decreases in heart rate were smaller than those generally observed following mixtures of atropine and neostigmine. Arrhythmias were transient and required no treatment in either group. Better control of secretions was achieved with glycopyrrolate.

Heart rate and rhythm were studied in conscious children and children under nitrous oxide and halothane anaesthesia following intravenous administration of atropine or glycopyrrolate. Both drugs produced a similar increase in heart rate when the potency of glycopyrrolate is considered twice that of atropine. There is no difference in the response of anaesthetised and awake children. Junctional rhythm is the main dysrhythmia observed which appears to occur more frequently in anaesthetised children. The administration of both drugs is safe in paediatric patients.

The frequency and nature of the oculocardiac reflex and its prevention by atropine or glycopyrrolate (i.m. and i.v.) has been studied in 160 children undergoing surgery for the correction of squint. Ninety per cent of those given no anticholinergic premedication exhibited the reflex. This was decreased to about 50% in those receiving the drugs i.m. Glycopyrrolate 7.5 micrograms kg-1 and atropine 15 micrograms kg-1 i.v. were effective in most instances, the latter being slightly better. However, glycopyrrolate was associated with tachycardia of smaller magnitude. The reflex was observed more often following traction on the medial rectus muscle.

Atropine, glycopyrrolate and hyoscine were compared in a mixture with neostigmine for the reversal of neuromuscular block in patients undergoing closed mitral valvotomy. Both atropine and glycopyrrolate were effective in counteracting the muscarinic effects of neostigmine. Glycopyrrolate was, associated with less initial increase in heart rate, a factor of importance in patients with mitral stenosis. The incidence of significant dysrhythmias was low in this small series. The control of secretions was better with glycopyrrolate. Administration of hyoscine was associated with unacceptable falls in heart rate and is not recommended.

The effects of glycopyrrolate in doses of 5, 10 and 15 microgram/kg and atropine 10, 20 and 30 microgram/kg on heat rate and rhythm was studied in anesthetised patients. Both drugs produced a dose-related increase in heart rate. Glycopyrrolate was approximately twice as potent as atropine in increasing heart rate. The average time taken to achieve peak effect was 2-6 and 3-7 minutes for atropine and glycopyrrolate respectively, and this was significantly different. The smallest doses of both drugs were generally associated with supraventricular dysrhythmias, whereas these were mainly ventricular following the highest dose of both drugs.

Glycopyrrolate and atropine were studied in doses of 5, 10, or 15 microgram/kg and 10, 20, or 30 microgram/kg, respectively, given intravenously either before or in a mixture with neostigmine, 50 microgram/kg, at the time of reversal of neuromuscular block. When given first, both anticholinergic drugs produced a dose-related increase in heart rate; following the administration of neostigmine the heart rates decreased. When administered in a mixture with neostigmine, the 20- and 30-microgram/kg doses, but not the 10-microgram/kg dose of atropine were associated with an initial increase in heart rate. This was, however, absent with all the doses of glycopyrrolate. The 5-microgram/kg dose of glycopyrrolate and 10-microgram/kg dose of atropine given either before or in a mixture with neostigmine were associated with unacceptable decreases in heart rate and needed further anticholinergic drug administration. The 10-microgram/kg dose of glycopyrrolate, when administered in a mixture with neostigmine, was associated with the most stable heart rates. Increasing the dose to 15 microgram/kg was not associated with undue tachycardia and is not hazardous. Atropine, 20 microgram/kg, necessitated a further administration of atropine in nearly a third of patients in this group due to bradycardia (heart rate of 50 beats/min or less) and would be considered inadequate. Increasing the dose to 30 microgram/kg prevented bradycardia but was accompanied by significant initial tachycardia and a higher incidence of dysrhythmias when administered before neostigmine. The frequency of dysrhythmias was otherwise similar. It is recommended that anticholinergic drugs be administered in a mixture with neostigmine. Glycopyrrolate, administered in this way in a dose of 10 microgram/kg, is associated with stable heart rates.

The effect of premedication with the cholinergic blocking drugs, atropine and glycopyrronium, was investigated in two groups, each of twenty patients, with regard to their effects on cardiac rate and rhythm during induction of anaesthesia and tracheal intubation. Another similar group of twenty patients was given no anticholinergic premedication. The incidence of dysrhythmias was 35% in the atropine group and 10% in the glycopyrronium group but there were no dysrhythmias in patients given no anticholinergic drug. The average rises in arterial pressure were similar in all three groups. Atropine administration led to a greater initial rise in heart rate before the induction of anaesthesia, although the average heart rates were similar in the three groups at the time of intubation and cuff inflation. The routine use of anticholinergic premedication seems to be unnecessary since the antisialogogue effect does not make any difference to the course of anaesthesia. However, if the antisialogogue action is important, glycopyrronium offers an advantage over atropine.

Glycopyrrolate, a new anticholinergic agent, was evaluated and compared with atropine. Glycopyrrolate 0.2 mg to neostigmine 1.0 mg was found to be safe and effective. The heart rates remained more stable with glycopyrrolate, and the frequency of arrhythmia, which was both transient and of no consequence, was similar in the two groups. The antisialogogue action of glycopyrrolate was superior to that of atropine.

A randomised prospective study was carried out in children undergoing surgery for squint correction, to determine the value of controlled ventilation as a prophylaxis against the occurrence of the oculocardiac reflex. One hundred patients anaesthetised with nitrous oxide/oxygen and halothane were randomly assigned to either ventilated or spontaneously breathing groups of 50 each. Half the patients in each group received glycopyrronium 7.5 micrograms/kg intravenously at the time of induction of anaesthesia. Heart rate, rhythm, blood pressure and end tidal CO2 concentration were monitored throughout. A positive oculocardiac reflex, defined as a fall in heart rate of 20% or more and/or the occurrence of dysrhythmias, was observed in 72% of spontaneously breathing patients and in 100% of ventilated patients not receiving prophylactic intravenous glycopyrronium. The incidence of a positive reflex in patients receiving glycopyrronium was 10% (4 and 16% respectively in spontaneously breathing and ventilated patients). It is concluded that controlled ventilation is of no value as a preventive measure against the occurrence of the oculocardiac reflex in patients undergoing squint surgery and that prophylaxis is safely achieved with the use of intravenous glycopyrronium.

Glycopyrronium 10 micrograms/kg has been compared with atropine 20 micrograms/kg in a mixture with neostigmine 50 micrograms/kg administered for antagonism of residual nondepolarising neuromuscular block in patients over 65 years of age. The initial peak increase in heart rate was less after glycopyrronium, but there were no differences beyond the first two minutes. The incidence of dysrhythmias was less after glycopyrronium but the difference was not significant. The control of secretions was superior with glycopyrronium. It is suggested that the dosage of anticholinergic agents given with neostigmine could be reduced in elderly patients in comparison to that in younger patients.

The effects on cardiovascular changes during induction of anaesthesia and intubation of routine premedication with three different anticholinergic drugs, atropine, hyoscine, and glycopyrronium, were compared in a double blind trial. Administration of both atropine and hyoscine, whether intramuscularly or orally, was found to be associated with a high incidence of dysrhythmias. With glycopyrronium the incidence was much lower, but control patients receiving no anticholinergic premedication had no dysrhythmias. The heart rates and blood pressures were similar in all the groups during intubation and cuff inflation. A single dose of suxamethonium was not associated with any bradycardia. The need for routine anticholinergic drug administration should be reconsidered. However, if necessary, glycopyrronium appears to have an obvious advantage over atropine and hyoscine.

Glycopyrrolate, a quaternary ammonium anticholinergic compound, and atropine were evaluated in combination with neostigmine for antagonism of non-depolarizing neuromuscular block. A total of 641 patients were investigated in a "true-to-life" situation. The patients receiving glycopyrrolate with neostigmine had smaller changes in heart rate than those who received atropine. This was particularly apparent in patients with cardiovascular disease.

Intravenous administration of glycopyrronium in doses up to 0.2 mg, was associated with minimal changes in cardiac rate and rhythm. Sinus arrhythmia, nodal rhythm and occasional atrial ectopics were the dysrhythmias observed. There were no accompanying changes in blood pressure.

Intermittent doses of suxamethonium have been known to result in bradycardia changes in cardiac rhythm. In order to assess the efficacy of a newer quaternary ammonium antimuscarinic, glycopyrrolate, on the cardia effects of intermittent suxamethonium, 28 patients received this drug intravenously just before induction of anesthesia. For comparison, 28 other patients were given atropine. In the atropine series, three patients developed bradycardia while none of those of the glycopyrrolate series did so. In addition, more patients had cardiac arrhythmias in the atropine group. Although no statistically significant differences were seen, clinically, glycopyrrolate seems to afford better protection against the cardiac changes resulting from intermittently administered suxamethonium.

1. Glycopyrronium was evaluated by intramuscular, intravenous and oral routes in six adult volunteers for its efficacy as an antisialogogue as also for its action on other aspects of cholinergic activity. 2. It was found to be an effective antisialogogue of long duration of action by all three routes. When given orally the effects were delayed in onset and persisted for too long. Intramuscular and intravenous routes were useful. The intramuscular absorption of the drug is rapid and consistent. 3. Sweat gland activity was affected in a similar fashion but less consistently and other parameters were mostly unaffected. 4. Glycopyrronium 0.2 mg intramuscularly was found to be the optimal dose. Larger doses produced subjective discomfort out of proportion to a further reduction in salivary secretion. 5. Intravenous administration causes no changes in cardiovascular stability.

This is a review of glycopyrrolate whose function in clinical practice is compared with that of atropine.

Atropine 15 micrograms/kg and glycopyrrolate 5 or 10 microgram/kg were studied as anticholinergic premedicants in groups of 20 children each. A control group of 20 children did not receive anticholinergic premedication. Both atropine and the higher dose of glycopyrrolate produced significant increases in heart rate prior to induction of anaesthesia. The subsequent increase during the process of induction was less than in those who had not received an anticholinergic drug or glycopyrrolate 5 micrograms/kg. Dysrhythmias during induction of anaesthesia occurred slightly less frequently in the patients given atropine or the higher dose of glycopyrrolate. Although the incidence was similar in these two groups, ventricular ectopic beats occurred less frequently following the use of glycopyrrolate. The control of secretions was also superior with this anticholinergic premedicant.