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At least 181 records · Page 10Linked to original sources
PubMed1997

Residual neuromuscular blockade after cardiac surgery: pancuronium vs rocuronium.

PURPOSE: To determine the incidence of residual neuromuscular blockade after cardiac surgery in patients receiving either rocuronium or pancuronium for muscle relaxation. METHODS: In a prospective, controlled, double-blind study, 20 patients undergoing coronary artery bypass were randomized to receive either rocuronium (n = 10) or pancuronium (n = 10) during surgery. Anaesthesia was induced with sufentanil, benzodiazepine and propofol or ketamine, and maintained with air/O2/sufentanil/isoflurane. Neuromuscular blockade was induced with 0.1 ml.kg-1 from blinded syringes containing recuronium (6 mg.ml-1) (Group R) or pancuronium (1 mg.ml-1) (Group P). Relaxants were administered according to clinical criteria and reversal agents were not given. After surgery, neuromuscular transmission was assessed by train-of-four stimulation of the ulnar nerve/adductor pollicis EMG (Datex Relaxograph). Mean values from three trains of stimuli were recorded and repeated 30 min later if TOF ratio was < 0.7. Time to extubation was recorded. RESULTS: On arrival in the ICU, nine of 10 patients in group R but only three of 10 patients in group P demonstrated four visible responses (P < 0.05). Mean TOF ratio in group P, 0.03 +/- 0.05, was less than in group R, 0.68 +/- 0.34 (P < 0.001). All patients in group P and 4 of 10 patients in group R had TOF ratio < 0.7 (P = 0.01). Time to extubation in group P (median 18, range 6-48 hr) was not statistically different from that in group R (14, 5-44 hr). CONCLUSION: Residual neuromuscular block, TOF ratio < 0.7, is common after cardiac surgery but the incidence is less when pancuronium is replaced by rocuronium.

Aged↗
PubMed1975

The myocardial effects of pancuronium.

The effect of pancuronium on myocardial contractility was studied in three different animal preparations. Pancuronium produced no change in isometric contraction of rabbit atrial or cat papillary muscle but displaced the acetylcholine dose-response curve to the right in the papillary muscle preparations, verifying a muscarinic blocking effect of this drug. In atropinized dogs in vivo pancuronium produced no significant change in the cardiovascular parameters studied. These studies show that pancuronium exerts its cardiovascular effects primarily by blocking muscarinic receptors in the heart.

Acetylcholine↗
PubMed1986

Potentiation of atracurium by pancuronium and d-tubocurarine.

In 60 adult patients undergoing general surgical procedures, the effect of pancuronium or d-tubocurarine "pretreatment" on the injection of a 0.1 mg X kg-1 bolus of atracurium was measured in two separate studies. In study 1, the patients received either 0.5 mg (approximately 0.007 mg X kg-1) or 1.0 mg (approximately 0.015 mg X kg-1) pancuronium, or placebo (saline) three minutes before the injection of atracurium 0.1 mg X kg-1. In study 2, the patients received 0.05 mg X kg-1 or 0.1 mg X kg-1 d-tubocurarine, or a placebo. The degree of neuromuscular blockade was assessed by evoked mechanogram (adductor pollicis muscle) using supramaximal train-of-four stimulation. Patients receiving pancuronium or d-tubocurarine pretreatment (equal to an ED5-ED15 dose) showed significantly greater inhibition of twitch (ED70-ED80) and train-of-four ratio compared with the placebo groups (ED35-ED40). Pretreatment with the larger dose of d-tubocurarine (0.1 mg X kg-1) was associated with significant neuromuscular blockade. It is concluded that pancuronium and d-tubocurarine pretreatments potentiate the clinical action of 0.1 mg X kg-1 atracurium in man by 35-100 per cent.

Adult↗
PubMed1986

Contribution of muscle relaxant to the haemodynamic course of high-dose fentanyl anaesthesia: a comparison of pancuronium, vecuronium and atracurium.

To define the role of muscle relaxants in haemodynamic responses to high-dose (75 micrograms X kg-1) fentanyl anaesthesia and to noxius stimuli associated with intubation and sternal spread during coronary artery bypass surgery, we compared haemodynamics between three groups of patients given either pancuronium (0.1 mg X kg-1, n = 11), vecuronium (0.086 mg X kg-1, n = 11) or atracurium (0.43 mg X kg-1, n = 12). Additional doses of the relaxants were given to maintain a 90 per cent neuromuscular block. Patients given pancuronium showed no increases in mean values of heart rate, arterial pressure or cardiac output during the induction of anaesthesia or after intubation, whereas a decrease in these variables was observed in the vecuronium group. The haemodynamics in the atracurium group were intermediate compared with the other two study groups. In spite of a decrease in coronary perfusion pressure, no patient given vecuronium developed myocardial ischaemia. An advantage of vecuronium over pancuronium and atracurium was an attenuation of the blood pressure response to sternotomy. Patients given atracurium had a small increase in pulmonary vascular resistance during sternotomy. Our patients continued their beta-adrenergic antagonist medication until the morning of the day of operation and they were pretreated with a small intravenous dose of diazepam (0.1 mg X kg-1) before induction of anaesthesia. These drugs may have prevented the deleterious haemodynamic effects observed by some investigators after the administration of pancuronium during high-dose fentanyl anaesthesia.

Adult↗
PubMed1994

Reversal of doxacurium and pancuronium neuromuscular blockade with neostigmine in children.

Recovery after doxacurium and pancuronium neuromuscular blockade and their acceleration by neostigmine have not been compared in children. Therefore, 60 paediatric surgical patients aged 2-10 yr (ASA 1-2) were studied. They were randomized to receive doxacurium 30 micrograms.kg-1 or pancuronium 70 micrograms.kg-1 iv during propofol, fentanyl, isoflurane and nitrous oxide anaesthesia. Electromyographic (EMG) responses of the adductor pollicis to train-of-four (TOF) stimulation of the ulnar nerve were recorded every ten seconds using a Datex NMT monitor. Six patients in each relaxant group received neostigmine (0, 5, 10, 20 or 40 micrograms.kg-1) with atropine by random allocation when first twitch height (T1) had recovered to 25% of control. Spontaneous recovery after ten minutes was similar following doxacurium (mean +/- SEM values of 45.0 +/- 3.9 vs 49.5 +/- 10.0% for T1 and 25.2 +/- 3.8 vs 14.8 +/- 3.6% for TOF ratios). Dose-responses to neostigmine were calculated from the log dose vs logit of T1 or TOF ratio after ten minutes. Neostigmine-assisted recovery was not different in the two groups, with ED70 and ED90 doses for T1 of 14.3 +/- 1.8 and 25.7 +/- 2.7 micrograms.kg-1 for doxacurium and 12.5 +/- 1.7 and 25.3 +/- 2.3 micrograms.kg-1 for pancuronium. Time to recovery of TOF ratio to 70% after neostigmine 40 micrograms.kg-1 was 2.3 +/- 1.0 and 4.2 +/- 1.7 min (P = NS) following pancuronium and doxacurium, respectively. Adjusted recovery due to neostigmine alone (spontaneous recovery subtracted from the total) required two to three times higher doses of neostigmine.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia Recovery Period↗
PubMed2000

Train-of-four fade and neuromuscular block in rats: a comparison between pancuronium, vecuronium, and rocuronium.

PURPOSE: To clarify the relationship between neuromuscular block and train-of-four fade and to investigate the causes of these drug-dependent differences, we compared the neuromuscular block and TOF fade after pancuronium, vecuronium and rocuronium. METHODS: In 24 anesthetized rats, the sciatic nerve was stimulated, and the twitch of left tibialis anterior muscle was recorded. After T1 (first twitch response) was kept constant at 95% block by administration of pancuronium, vecuronium, or rocuronium (n=8, in each), the TOF fade was measured when T1 block was decreased to 40% and 20%. In addition, using 24 phrenic nerve-diaphragm preparations, the fade was measured when the T1 block increased to 20% and 40% by titrating of either one of the three drugs (n=8, in each). RESULTS: In in vivo experiments, the fade produced by pancuronium was greater than that by vecuronium or rocuronium when T1 block was at 40% (81 +/- 9 vs 63 +/- 15 and 63 +/- 6%, respectively) and at 20% (66 +/- 13 vs 34 +/- 17 and 40 +/- 6%, respectively). In contrast, in in vitro experiments, the differences did not reach significant levels among the three drugs either at 20% (32 +/- 19 vs 33 +/- 10 and 32 +/- 17%) or 40% of block (62 +/- 29 vs 65 +/- 14 and 55 +/- 14%). CONCLUSIONS: For vecuronium and rocuronium, the results were similar in vivo and in vitro. For pancuronium, fade was greater in vivo. These results suggest that different neuromuscular blocking agent have different relationships between the fade and the block. In vitro results might not be the same as in vivo, possibly due to pharmacokinetic differences.

Acetylcholine↗
PubMed1989

Intravenous administration of d-tubocurarine and pancuronium in fetal limbs.

The purpose of this study was to assess the effects of intravenous administration of d-tubocurarine and pancuronium in fetal lambs. Eighteen experiments were performed in seven chronically instrumented pregnant ewes between 0.8 and 0.9 of timed gestation. Each fetus received 6 ml of study drug intravenously at 1.2 ml/min over 5 minutes (d-tubocurarine 3.0 mg/kg, pancuronium 0.5 mg/kg, or saline solution control). Pancuronium (n = 7) significantly increased both fetal heart rate and mean arterial pressure. d-Tubocurarine (n = 5) significantly decreased both fetal heart rate and mean arterial pressure. Saline solution control (n = 6) did not significantly alter fetal heart rate or mean arterial pressure. The present study suggests that pancuronium is preferable to d-tubocurarine for those intrauterine procedures when an increase in fetal heart rate is desired.

Animals↗
PubMed1994

Cholinesterase inhibition by vecuronium and pancuronium in human airways.

Vecuronium (100 microM) but not pancuronium (100 microM) increased the sensitivity of human isolated bronchial preparations (HBP) to exogenous acetylcholine (ACh). The pD2 values obtained from concentration-dependent contractions were: control, 4.59 +/- 0.29 vecuronium, 5.86 +/- 0.31. Vecuronium or pancuronium (100 microM) significantly decreased (50%) the neostigmine contractions in HBP. In addition, vecuronium was more potent than pancuronium in preventing exogenous ACh degradation. These results suggest that vecuronium and pancuronium may have physiological effects in human airways by inhibiting both the tissue cholinesterases and muscarinic (M3) receptors.

Bronchi↗
PubMed1987

Direct evidence that pancuronium and gallamine enhance the release of norepinephrine from the atrial sympathetic nerve by inhibiting prejunctional muscarinic receptors.

The effect of different non-depolarizing muscle relaxants (gallamine, pancuronium, vecuronium, D-tubocurarine) on [3H]norepinephrine release in response to electrical stimulation was studied in isolated guinea-pig atrium. High pressure liquid chromatography combined with electrochemical and radiochemical detection revealed that the released radioactivity was mainly in the form of [3H]norepinephrine release. Oxotremorine, a pure muscarinic agonist, reduced the release of tritium. Gallamine and pancuronium, like atropine, prevented the inhibitory effect of oxotremorine. D-Tubocurarine and vecuronium had no such effect. These findings indicate that gallamine and pancuronium exert a presynaptic antimuscarinic, atropine-like effect, by inhibiting muscarinic receptors located on the axon terminals of sympathetic neurons thereby enhancing norepinephrine release. It is suggested that this phenomenon might play some role in tachycardia observed during surgical anaesthesia when gallamine or pancuronium have been administered.

Adrenergic Fibers↗
PubMed1991

Hemodynamic responses to pancuronium and vecuronium during high-dose fentanyl anesthesia for coronary artery bypass grafting.

The hemodynamic and electrocardiographic (ECG) effects of pancuronium and vecuronium were compared during high-dose fentanyl anesthesia for coronary artery bypass grafting (CABG) surgery. Forty-eight morphine-scopolamine premedicated patients scheduled for elective CABG were anesthetized with fentanyl (100 micrograms/kg) in divided doses, and either of two muscle relaxants, pancuronium (n = 26; 0.10 mg/kg) or vecuronium (n = 22; 0.09 mg/kg). Hemodynamic data, blood gas samples, and ECG tracings were obtained at the following intervals: (1) control; (2) prior to intubation; (3) 1 minute after intubation; (4) prior to sternotomy; and (5) 1 minute after sternotomy. In the pancuronium group, heart rate (HR), cardiac index (CI), and rate-pressure product (RPP) were increased after induction of anesthesia and following intubation. Eleven patients (42.3%) displayed ischemic ST segment changes. Four patients in this group developed tachycardia and hypertension to an extent requiring pharmacological intervention. Vecuronium-treated patients displayed no increases in HR, MAP, and RPP, and a decrease in CI. Only one patient (5.6%) developed evidence of ischemic ECG changes. Four patients in the vecuronium group, all receiving preoperative beta-blocker therapy, became hypotensive and bradycardic after the induction of anesthesia. The present investigation confirms the increased incidence of myocardial ischemia during high-dose fentanyl-pancuronium anesthesia. Although vecuronium was associated with fewer myocardial ischemic changes, the occurrence of bradycardia and hypotension in some patients receiving preoperative beta-adrenergic blocking drugs remains a concern.

Anesthesia, Intravenous↗
PubMed1979

Pancuronium inactivates alamethicin-induced conductance in artificial membranes.

The effect of pancuronium on alamethicin-induced currents was studied in negatively charged lipid bilayer membranes. Pancuronium induces inactivation of the alamethicin-induced current. Inactivation is only observed if this compound is added to the compartment containing alamethicin. Moreover, the process of inactivation is reduced or abolished if pancuronium is added to the alamethicin-free side of the membrane. The time needed to recover from inactivation is greatly reduced if the aqueous solution in the alamethicin-free compartment is stirred. These data suggest that pancuronium permeates through the membrane when the alamethicin-induced conductance is "turned on," binds to the other membrane surface, and changes the surface potential.

Alamethicin↗
PubMed1998

Neurophysiological monitoring of pharmacological manipulation in acute organophosphate (OP) poisoning. The effects of pralidoxime, magnesium sulphate and pancuronium.

OBJECTIVES: The neuromuscular transmission failure in acute organophosphate (OP) poisoning occurs because of the irreversible inactivation of the enzyme acetylcholinesterase located in the neuromuscular junction, and is distinguished neuroelectrophysiologically by single electrical stimulus-induced repetitive responses and either a decremental or a decrement-increment response upon high-rate repetitive nerve stimulation (RNS). Understandably, the administration of pharmacological agents with actions at different sites in the neuromuscular junction would alter the neuroelectrophysiological findings in acute OP poisoning. METHODS: The effect of several pharmacological agents including pralidoxime (10 patients), magnesium sulphate (4 patients) and pancuronium (7 patients) on the neuroelectrophysiological abnormalities was studied in 21 patients with acute OP poisoning. RESULTS: Pralidoxime administration produced neurophysiological amelioration in 11 out of 15 occasions. In those cases where it produced a beneficial effect, pralidoxime administration was continued and its neuroelectrophysiological effects were studied daily. The efficacy of pralidoxime administration was demonstrated by neuroelectrophysiological testing for a maximum of 6 days after poisoning. Three types of neuroelectrophysiological responses to pralidoxime were noted: (i) lack of neuroelectrophysiological improvement (two patients); (ii) initial improvement with subsequent lack of improvement (two patients); and (iii) initial improvement with subsequent normalisation of neuromuscular transmission (5 patients). Normalisation of the electrodiagnostic tests and the failure of pralidoxime to ameliorate the neuromuscular transmission abnormalities were neuroelectrophysiological indications for the discontinuation of pralidoxime treatment. The administration of magnesium sulphate (MgSO4.7H2O, 4 g intravenous) resulted in a decrease in the CMAP amplitude, loss of the repetitive response and conversion of the decrement-increment response at high-rate RNS to an incremental response. Repetitive responses and the decremental response at high-rate RNS also disappeared after the administration of pancuronium (0.5 mg intravenous) to 6 patients. However, in one case where pancuronium administration was preceded by pralidoxime, there occurred a dramatic worsening of the neuromuscular transmission defect. CONCLUSIONS: While the administration of all 3 agents-- pralidoxime, magnesium sulphate and pancuronium-- resulted in the reversion of the neuroelectrophysiological defects, only pralidoxime is contended to be therapeutically useful. The therapeutic benefit due to its administration is limited by a short duration of action, and hence it is recommended that it should be administered for a longer period of time under neuroelectrophysiolgical guidance.

Acute Disease↗
PubMed2001

Open channel and competitive block of nicotinic receptors by pancuronium and atracurium.

Mouse myotubes were used to investigate effects of the nondepolarizing neuromuscular blocking drugs pancuronium and atracurium on embryonic-type nicotinic acetylcholine receptor channels. Experiments were performed using patch-clamp techniques in combination with devices for ultra-fast solution exchange at outside--out patches. Application of 0.1 mM acetylcholine resulted in a fast current transient. When the peak amplitude was achieved, the current decayed monoexponentially due to desensitization. After application of drugs (pancuronium or atracurium), two different mechanisms of block were observed: (1) open channel block of embryonic-type nicotinic acetylcholine receptor channels after coapplication of blocker and acetylcholine, characterized by decrease of the time constant of current decay; (2) competitive block of embryonic-type nicotinic acetylcholine receptor channels by pancuronium or atracurium after preincubation of outside-out patches with the respective blocker. Different affinities of pancuronium (K(B) approximately 0.01 microM) and atracurium (K(B) approximately 1 microM) to embryonic-type nicotinic acetylcholine receptor channels were observed.

Acetylcholine↗
PubMed2000

Prelude to pancuronium and vecuronium.

The discovery of the neuromuscular blocking activity of malouetine isolated from Malouetia bequaertiana Woodson by Quevauviller and Lainé in 1960 stimulated interest in aminosteroids as potential neuromuscular blockers. Alauddin (a pharmacist) and Martin-Smith (a medicinal chemist) began research in this area, which was then taken up by pharmaceutical companies. Pure pancuronium was synthesised in 1964 by Savage and his co-workers, directed by Hewett. Pharmacologists headed by Buckett discovered that pancuronium was far more potent than d-tubocurarine and had minimal side-effects. Buckett quickly recognised the value of pancuronium, and his persistence resulted in successful clinical trials, followed by the commercial launch of pancuronium in 1968. Vecuronium was synthesised, tested and the studies published by Buckett, Hewett and Savage in 1973, but this was before anaesthetists called for a 'clean muscle relaxant' and, furthermore, it was unstable in aqueous solution. Hence, it was only promoted for clinical trials six years later.

History, 20th Century↗
PubMed1976

Pancuronium bromide: an indirect sympathomimetic agent.

In the dog, pancuronium 0.2 mg/kg increased left ventricular systolic pressure and systemic arterial pressure, but did not change central venous pressure. Repeated doses produced diminishing responses and eventually no change in arterial pressure. After tachyphylaxis was established, a pressor response to pancuronium could be induced by an i.v. infusion of noradrenaline. Desipramine, a noradrenaline blocking agent, prevented the restoration of the pressor effect of noradrenaline. Guanethidine and reserpine abollished the restoration of the pressor response to pancuronium by noradrenaline. These findings are consistent with the hypothesis that pancuronium acts on the postganglionic nerve endings and causes release of noradrenaline.

Animals↗
PubMed1978

Plasma concentrations of pancuronium during predetermined intensities of neuromuscular blockade.

The plasma concentrations of pancuronium were monitored during i.v. infusions of the relaxant in dogs. Pancuronium was administered at rates which maintained the degree of neuromuscular blockade at three predetermined levels. The concentrations of the drug in the blood were consistent for any one animal but showed considerable overlap for the three levels of paralysis between animals. Concentrations obtained during infusion and which maintained the twitch response at 20% and 80% of control were compared, in the same dogs, with concentrations obtained during recovery from a bolus injection of pancuronium. When the infusion maintained the twitch response at 20% of the control value, the mean plasma concentration of pancuronium was 0.152 microgram ml-1. That measured after the bolus injection was 0.156 microgram ml-1. The concentrations at 80% of control were 0.094 microgram ml-1 and 0.083 microgram ml-1 respectively. The agreement between these results suggests a relationship between the plasma concentration of the relaxant and its effect during the termination of the action after a large bolus injection of the drug. As this occurs chiefly during the postdistribution equilibrium, the relatively slow decrease in plasma concentration would appear to become the rate-limiting factor in recovery from paralysis.

Animals↗
PubMed1980

Inhibition of neuronal uptake of noradrenaline in the isolated perfused rat heart by pancuronium and its homologues, Org. 6368, Org. 7268 and NC 45.

The cardiovascular effects of pancuronium may be caused partly by an interaction of this drug with the sympathetic nervous system. We examined one possible mechanism of interaction, the effect on the re-uptake processes for noradrenaline. Pancuronium and its closely related steroidal homologues, Org. 6368, Org. 7268 and NC 45, were studied at a high concentration (500 mumol litre-1) for inhibition of the uptake of tritiated noradrenaline into neuronal sites (Uptake1) and extraneuronal sites (Uptake2) in the isolated perfused rat heart. All drugs tested caused almost total inhibition of Uptake1. The bis-quaternary steroids pancuronium and Org. 6368 were selective for Uptake1 inhibition, the mono-quaternary steriods Org. 7268 and NC45 also produced significant inhibition of Uptake2. Uptake1 inhibition was investigated in detail using lesser concentrations of the compounds. All four steroids were found to cause a concentration-dependent inhibition of Uptake1. It seems likely, therefore, that inhibition of neuronal uptake of noradrenaline plays a significant role in the aetiology of the chronotropic actions of pancuronium in the rat.

Animals↗
PubMed1981

Recovery from pancuronium blockade in the neonatal intensive care unit.

Neuromuscular blockade with pancuronium and its antagonism was evaluated in 33 critically ill infants. The evoked contraction of the adductor pollicis from indirect stimulation of the ulnar nerve was measured. The neuromuscular blockade recovered spontaneously from pancuronium in seven infants, 23 required one or more doses of atropine 0.02 ng kg-1 and neostigmine 0.06 mgkg-1. In three infants the blockade failed to reverse. Immature infants less than 32 weeks did not show any significant different in their requirement for pancuronium compared with mature infants. Age and birth weight of the infant, dose of pancuronium and duration of its administration did not affect the requirements for reversal. Train-of-four and tetanus; twitch ratios were lower (P less than 0.05) in infants less than 32 weeks of developmental age reflecting immaturity of neuromuscular transmission.

Critical Care↗