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PubMed1981

Differential inhibition of plasma cholinesterase variants using the dibutyrate analogue of pancuronium bromide.

A steroid, the dibutyrate analogue of pancuronium bromide (9.8 X 10(-8)M), has been used as differential inhibitor in the study of the plasma cholinesterase variants. Pancuronium dibutyrate numbers have been measured for 190 individuals, and the mean values for six of the known genotypes, E1uE1u, E1uE1f, E1uE1a, E1fE1a, E1aE1a, and E1fE1f, have been calculated. Evidence is presented that a combination of the pancuronium dibutyrate number and the fluoride number give better resolution of the six genotypes than the combination of the pancuronium dibutyrate and the dibucaine number. This new differential inhibitor has real potential for revealing the probable existence of new genotypes.

Cholinesterase Inhibitors↗
PubMed1990

Dose-response characteristics of pancuronium in neonates, infants and children.

This paper presents pharmacodynamic data for pancuronium in neonates, infants, children and adolescents during N2O-O2-fentanyl anaesthesia. Neuromuscular block (NMB) was evaluated by the adductor pollicis electromyogram. Dose-response curves of pancuronium were parallel in all age-groups. ED95 was greatest in children and least in infants (93 vs. 66 micrograms/kg, P less than 0.05). The rate of spontaneous recovery following 95% NMB was comparable in all age-groups, as was the maintenance requirement of pancuronium when related to ED-values. The hourly requirement to maintain NMB greater than 85% was 60-68% of the individual ED95 dose. When administered on this basis, pancuronium is an equally long-acting neuromuscular blocking agent in patients of all ages.

Adolescent↗
PubMedDate not supplied

Response to pancuronium after loss of atracurium-induced neuromuscular blockade.

OBJECTIVE: To describe a previously unreported event in which a patient became refractory to atracurium-induced neuromuscular blockade, but subsequently was adequately paralyzed with a standard dosage of pancuronium. CASE SUMMARY: A previously healthy 17-year-old woman who sustained multiple trauma developed tolerance to an atracurium infusion she was receiving while undergoing mechanical ventilation. On day 3 of neuromuscular blockade, she became unresponsive to atracurium as evidenced by excessive physical movement, increased peak airway pressures, and overbreathing assist control ventilation. Repeat boluses and increases in the atracurium infusion rate to a maximum of 1.27 mg/kg/h failed to provide a desired clinical response. A bolus dose of pancuronium 0.15 mg/kg was administered and the constant infusion was then changed to pancuronium 0.078 mg/kg/h. Within minutes, decreased respirations, peak airway pressures, and agitation were noted. The pancuronium infusion rate was then tapered to 0.045 mg/kg/h over 72 hours and continued to maintain adequate neuromuscular blockade. DISCUSSION: Potential pharmacokinetic and pharmacodynamic causes of loss of neuromuscular blockade in this patient are postulated. Possible explanations for loss of neuromuscular blockade include increased degradation of atracurium and/or a change in acetylcholine receptor physiology. CONCLUSIONS: The development of resistance to a specific neuromuscular blocking agent in the intensive care setting does not necessarily imply cross-tolerance or resistance to alternative agents. Also, loss of respiratory control by one neuromuscular blocking agent may be overcome by changing agents.

Adolescent↗
PubMed1984

Cerebral blood flow and metabolism following pancuronium bromide in newborn lambs.

The purpose of this study was to evaluate cerebral blood flow and metabolism following pancuronium bromide paralysis in healthy newborn lambs. Cerebral blood flow and cerebral metabolic rate for O2 and glucose were measured along with blood pressure and blood gases before and again at 15 and 60 min following pancuronium paralysis in seven newborn lambs. Pancuronium bromide paralysis had no effect on any of these parameters either at 15 or 60 min of paralysis. Total cerebral blood flow, cerebral metabolic rate for O2, and cerebral metabolic rate for glucose were 87 +/- 6 ml/min/100 g, 258 +/- 10 mumol O2/min/100 g, and 53 +/- 10 mmol glucose/min/100 g, respectively. Neither was any change in regional cerebral blood flow noted. In spite of being connected immediately to the ventilator, however, some animals experienced a transient increase (average = 32%) in blood pressure, that was not associated with an increase in end tidal CO2. The data suggest that pancuronium paralysis in healthy awake newborn lambs does not lead to any alteration in cerebral blood flow or metabolism.

Animals↗
PubMed1986

Cardiovascular effects of d-tubocurarine and pancuronium in newborn lambs during normoxia and hypoxia.

Nondepolarizing muscle relaxants are administered to hypoxic neonates (including those with severe cyanotic congenital heart disease) to reduce oxygen consumption. However, it is unknown whether paralysis actually reduces oxygen consumption or whether the drugs used affect the cardiovascular system of neonates. Therefore, we studied the effects of d-tubocurarine and pancuronium induced muscle paralysis on oxygen consumption, cardiac output, and tissue oxygen delivery in healthy normoxic and hypoxic 1- to 3-day-old lambs. We measured intravascular pressures, cardiac output and its distribution (microspheres), and blood gases and pH during: 1) spontaneous respiration with room air (control); 2) spontaneous respiration with a Pao2 of 27-33 mm Hg (hypoxia); 3) mechanical ventilation with room air; 4) mechanical ventilation with room air and paralysis with d-tubocurarine (0.3 mg/kg) or pancuronium (0.1 mg/kg); and 5) mechanical ventilation with hypoxia and paralysis. Mechanical ventilation, with or without muscle paralysis, had no effect on the oxygen delivery or oxygen consumption of normoxic animals. Hypoxia and spontaneous ventilation had no effect on oxygen consumption, but hypoxia, paralysis, and mechanical ventilation reduced it 35% (p less than 0.002 d-tubocurarine) and 50% (p less than 0.001 pancuronium). Cardiac output was unaffected by oxygenation, mechanical ventilation, or muscle paralysis. However, blood flow to the brain and heart increased during hypoxia, which maintained normal oxygen delivery to these organs. During hypoxia and spontaneous ventilation, mean pulmonary arterial pressures increased 34% (d-tubocurarine) and 54% (pancuronium) above control; during hypoxia, muscle paralysis, and mechanical ventilation, it increased 81%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Antagonism of pancuronium and its metabolites by neostigmine in cats.

Antagonism by neostigmine of neuromuscular blockade produced by pancuronium or its metabolites was studied in the cat anterior or tibialis muscle-peroneal nerve preparation using constant infusions of muscle relaxants. The ED50 of neostigmine (dose which caused a 50% antagonism) was 16, 11, 29, and 26 micrograms/kg for pancuronium, 3-hydroxypancuronium, 17-hydroxypancuronium, and 3, 17-hydroxypancuronium, respectively. Times of onset of neostigmine action were shorter when antagonizing 17-hydroxypancuronium neuromuscular blockade. Duration of neostigmine action when antagonizing 17- or 3, 17-hydroxypancuronium blockade was shorter than with pancuronium or 3-hydroxypancuronium. We conclude that more neostigmine is required to antagonize 17- or 3,17-hydroxypancuronium neuromuscular blockade than is required to antagonize pancuronium. Conversely, less neostigmine was required to antagonize 3-hydroxypancuronium blockade.

Animals↗
PubMedDate not supplied

Pancuronium reduces halothane requirement in man.

We studied the contribution of pancuronium to anesthetic requirement in man by comparing MAC for halothane alone in 18 patients, with that after intravenous administration of pancuronium, 0.1 mg/kg, in 17 patients. In each group, movement was observed in limbs isolated from the circulation by tourniquet. In patients receiving pancuronium, halothane MAC was 0.55%, whereas the control value was 0.73%. Thus pancuronium reduces halothane MAC by 25%.

Adult↗
PubMed1993

Hemodynamic and pharmacodynamic comparison of doxacurium and pipecuronium with pancuronium during induction of cardiac anesthesia: does the benefit justify the cost?

We compared the pharmacodynamic effects and hospital costs of three long-acting neuromuscular blocking drugs in a prospective, randomized, double-blind manner. Each neuromuscular blocking drug was administered with fentanyl (50 micrograms/kg) for intravenous induction of anesthesia for coronary artery bypass surgery. Each patient received twice the 95% effective dose (ED95) of either pancuronium (0.14 mg/kg, n = 10), pipecuronium (0.10 mg/kg, n = 10), or doxacurium (0.05 mg/kg, n = 10). Hemodynamic measurements were recorded at baseline, 5 min after completion of anesthetic induction, immediately after endotracheal intubation, and 5 min after intubation. Only small hemodynamic differences between neuromuscular blocking drugs were observed. Doxacurium (but not pancuronium or pipecuronium) significantly decreased mean arterial blood pressure (from 94 +/- 4 mm Hg before induction to 83 +/- 3 mm Hg 5 min after intubation); nevertheless, there were no significant between-group differences at any time. Pancuronium increased heart rate (from 68 +/- 4 beats/min before induction to 76 +/- 5 beats/min 5 min after intubation); however, pancuronium differed significantly from doxacurium and pipecuronium only 5 min after induction and 5 min after intubation. Central venous pressure, pulmonary artery occlusion pressure, cardiac index, and systemic and pulmonary vascular resistance indices did not change. Electrocardiographic abnormalities were observed in two pipecuronium patients: ST segment depression in one and premature ventricular contractions in another. No other electrocardiographic changes were observed. There were no significant between-group differences in the need for hemodynamic interventions.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Intravenous↗
PubMed1993

Accelerated onset and delayed recovery of neuromuscular block induced by mivacurium preceded by pancuronium in children.

The goal of this study was to describe a technique which could shorten the time from mivacurium administration to peak neuromuscular block (NMB) after administration of the maximum recommended dose of mivacurium. Forty-eight pediatric patients were randomized into three groups and studied during nitrous oxide-alfentanil-thiopental anesthesia. Every patient received two blinded injections 3 min apart: either 15 micrograms/kg of pancuronium in 1 mL of saline followed by 170 or 200 micrograms/kg of mivacurium or saline followed by 200 micrograms/kg of mivacurium. Intravenous induction of anesthesia followed the first injection. Thenar electromyogram response to supramaximum train-of-four stimulation of the ulnar nerve at 10-s intervals was used for neuromuscular monitoring. Pretreatment with pancuronium significantly shortened the time to NMB and prolonged spontaneous recovery from NMB in comparison to the temporal course of NMB after administration of 200 micrograms/kg of mivacurium. Time from injection to 90% NMB averaged 116 (SEM 11) s after administration of 200 micrograms/kg of mivacurium, and 71 (7) s and 94 (11) s when 200 micrograms/kg or 170 micrograms/kg of mivacurium, respectively, was preceded by pancuronium (P = 0.0095). Mean times from injection to recovery of neuromuscular function to > 25% of baseline (T25) and to train-of-four ratio of 0.75 were 9.1 (0.7) and 15.8 (1.2) min, respectively, after administration of 200 micrograms/kg of mivacurium alone. T25 and train-of-four of 0.75 occurred significantly later at 21.9 (1.8) and 35.0 (2.8) min, respectively (P = 0.0001), when 200 micrograms/kg of mivacurium was preceded by 15 micrograms/kg of pancuronium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1978

Pancuronium bromide.

Pancuronium bromide is a nondepolarizing muscle relaxant approved to induce skeletal muscle relaxation during anesthesia and to facilitate the management of patients undergoing mechanical ventilation. The use of pancuronium bromide during surgery led to the appreciation that it has advantages over drugs previously used for muscle relaxation. Patients in whom pancuronium bromide is of value are (1) hypoxemic patients resisting mechanical ventilation and so cardiovascularly unstable that use of sedatives is precluded, (2) patients with bronchospasm unresponsive to conventional therapy, (3) patients with severe tetanus or poisoning where muscle spasm prohibits adequate ventilation, (4) patients with status epilepticus unable to maintain their own ventilation, (5) shivering patients in whom metabolic demands for oxygen should be reduced, and (6) patients requiring tracheal intubation in whom succinylcholine administration is contraindicated. Without concomitant sedation, use of pancuronium bromide is associated with psychological risks. Other risks are undetected ventilator disconnection, tachyarrythmias, prolonged paralysis and drug interactions.

Animals↗
PubMed1999

Effect of atracurium or pancuronium on the anemic fetus during and directly after intravascular intrauterine transfusion. A double blind randomized study.

BACKGROUND: To determine the effect of atracurium or pancuronium on onset and duration of fetal paralysis, movements and heart rate parameters directly after transfusion, using computer analyzed fetal heart rate recording (c-FHR). METHODS: Double blind randomized study of 23 RhD alloimmunized pregnant women requiring an intravascular intrauterine fetal blood transfusion (IUT) between 24 and 36 weeks. Atracurium was injected in 11 fetuses at 17 IUT's and pancuronium in 12 fetuses at 19 IUT's. For statistical analysis the Mann-Whitney test was used. RESULTS: No statistical differences were found in fetal heart rate and movements between both groups before transfusion. The fetal movements returned more rapidly in the atracurium group when compared to the pancuronium-group (median 24 vs. 57 min, range 6-55 vs. 4-220; (p<0.02). Fetal movements did not hamper the procedure in any case. The atracurium group showed significantly more fetal movements (p<0.01), more accelerations (0<0.05) but no significant reduction of fetal heart rate variability directly after transfusion which was in direct contrast to the pancuronium group. CONCLUSIONS: Neuromuscular blockade with atracurium produces sufficient paralysis for intrauterine transfusion with minimal disturbance of the parameters used to monitor fetal wellbeing after the procedure. Although the routine use of fetal paralysis during IUT may be questionable, we believe that when it is necessary the use of atracurium is the better choice.

Anemia↗
PubMed1992

[A case of suicide by an intravenous injection of pancuronium].

A 25-year-old male anesthesiologist was found dead in his room with an intravenous drip line connected with his leg. There were several empty ampules of pancuronium, midazolam and buprenorphine around him. Pancuronium and midazolam in the blood and urine samples collected at postmortem examination were detected by spectrofluorometry and ECD-gas chromatography, respectively. The concentrations of pancuronium and midazolam were 0.3 micrograms/g and 0.12 micrograms/g in the blood, respectively; 0.9 micrograms/g and 0.05 micrograms/g in the urine, respectively. The cause of death was determined to be asphyxia due to respiratory muscle paralysis caused by pancuronium.

Adult↗
PubMed1979

Influence of gallamine, pancuronium, d-tubocurarine and succinylcholine on adrenergic neurotransmission.

The influence of gallamine, pancuronium, d-tubocurarine and succinylcholine on adrenergic neurotransmission was studied in the isolated saphenous vein of the dog. Pancuronium increased the response of vascular smooth muscle to adrenergic nerve stimulation and to exogenous norepinephrine; gallamine, d-tubocurarine and succinylcholine had no effect. The relaxation caused by small doses of acetylcholine added during sympathetic nerve stimulation (prejunctional effect), was inhibited by pancuronium and by gallamine. In vein strips, charged with (3H) norepinephrine, acetylcholine inhibits the catecholamine-efflux evoked by sympathetic nerve stimulation. That inhibition was abolished by gallamine. This confirms that gallamine inhibits the prejunctional effect of acetylcholine on adrenergic neurotransmission. When extrapolated to the intact organism, this means that gallamine and pancuronium will augment the release of norepinephrine by acting as muscarinic antagonists also at prejunctional receptor sites in tissues exposed to combined sympathetic and vagal nerve activity. This mechanism would explain in part the cardiovascular effects of these muscle relaxants.

Acetylcholine↗
PubMed1989

Pancuronium, gallamine, and d-tubocurarine compared: is speed of onset inversely related to drug potency?

The relative potency and speed of onset of action of pancuronium, gallamine, and d-tubocurarine was studied in 55 adult female patients receiving nitrous oxide/oxygen-narcotic anesthesia. The integrated electromyogram of the adductor pollicis muscle was monitored using a cumulative dose-response technique; train-of-four stimuli were administered at 0.05 Hz. The measured ED95 values for pancuronium and gallamine were 0.069 and 2.38 mg/kg, respectively. In three separate groups, pancuronium 0.07 mg/kg, gallamine 2.4 mg/kg, or d-tubocurarine 0.45 mg/kg were given as a single bolus and the speed of onset and time to maximum effect determined. Peak twitch depression was essentially identical in all groups (92.7 +/- 1.4 [SE] vs. 93.3 +/- 1.1 vs. 93.7 +/- 1.1%, respectively). The rate of onset of neuromuscular blockade in these three groups was, however, quite different. After administration of pancuronium (n = 10) the times to 5%, 20%, 50%, and 80% twitch depression were 68 +/- 5, 97 +/- 6, 141 +/- 8, and 222 +/- 18 s. The comparable times following gallamine (n = 10) were 29 +/- 2, 42 +/- 3, 66 +/- 5, and 136 +/- 14 s; d-tubocurarine (n = 10) was intermediate in speed with onset times of 40 +/- 4, 63 +/- 6, 99 +/- 11, and 178 +/- 25 s. It appears that the onset times of different nondepolarizing blocking agents (even when given in equipotent doses) may vary by clinically appreciable amounts. The results of this study support the hypothesis that nondepolarizing neuromuscular blocking agents of low potency may have a more rapid onset of action than that seen with agents of high potency.

Adult↗
PubMed1985

[Circulatory effects of vecuronium as well as pancuronium under different conditions of anesthesia].

The cardiovascular effects of equipotent doses (1,25 X ED95) of vecuronium (70 micrograms/kg iv) and pancuronium (80 micrograms/kg iv) were studied in 16 patients scheduled for elective coronary artery bypass surgery during steady-state conditions of isoflurane (0,4-0,5 vol% end-tidal)-nitrous oxide anaesthesia. All patients were chronically treated with oral beta receptor-blocking agents. Vecuronium did not cause any significant cardiovascular changes whereas pancuronium produced increases in heart rate (13%), cardiac index (15%) and mean arterial pressure (4%) while systemic vascular resistance decreased (8%). In a second part of this study we analysed whether the magnitude of the vagolytic effects of pancuronium is influenced by the anaesthetic procedure and/or by preoperative beta-blocker therapy. A group of 8 patients who were pretreated with beta-receptor blockers and received fentanyl (7 micrograms/kg) during the anaesthetic procedure showed low control values of heart rate (HR), cardiac index (CI), mean arterial pressure (MAP) and the rate-pressure product (RPP) which were due to both, the antisympathetic effects of beta-blocker therapy and the central vagomimetic properties of fentanyl. The administration of pancuronium (80 micrograms/kg) caused the greatest percentage increases in HR (20%), CI (22%), MAP (8%) and RPP (31%) in this group of patients. In contrast, patients (n = 8) anaesthetized with isoflurane-nitrous oxide who were not on preoperative beta-receptor blocker medication, demonstrated higher haemodynamic control values and less increases in HR (10%), CI (10%) and RPP (15%), MAP did not change. The clinical significance of these findings is discussed.

Adrenergic beta-Antagonists↗
PubMed1986

Does intravenous infusion of nitroglycerin potentiate pancuronium- and vecuronium-induced neuromuscular blockade?

The dose requirement for 95% depression of twitch tension and the time course of the neuromuscular blocking effects of the ED95 of pancuronium bromide and vecuronium bromide were studied during intravenous infusion of glucose, 5%, and nitroglycerin, 1 microgram X kg-1 X min-1, in 20 cats anesthetized with pentobarbital. Nitroglycerin administered continuously starting 1 hr before the administration of the ED95 and maintained during at least five maintenance doses of either pancuronium or vecuronium did not significantly potentiate the action of the neuromuscular blocking drugs, nor did it alter their time course of action. A tendency for a decrease (statistically not significant) rather than an increase in the duration of action of maintenance doses of both pancuronium and vecuronium was apparent during the treatment with nitroglycerin. These findings indicate a lack of interaction between pancuronium or vecuronium and nitroglycerin, provided that moderate doses are used.

Animals↗
PubMed1985

[Vecuronium: onset of effect and intubation conditions in comparison to pancuronium and suxamethonium].

The onset of neuromuscular blockade following the i.v. injection of vecuronium and pancuronium 0.05, 0.08 or 0.1 mg/kg and suxamethonium 0.5 or 1.0 mg/kg was studied in 304 patients during induction of anaesthesia by means of the compound action potential derived from the adductor pollicis muscle, which was indirectly stimulated via the ulnar nerve. The intubation conditions 1-5 min after injection were assessed using a scoring system related to ease of laryngoscopy, movement of vocal cords and coughing, and reflex movements of extremities. Development of motor blockade was time- and dose-dependent. After administration of 0.1 mg/kg vecuronium, the actual maximum effect (more than 90% block) was established within 4 min; after 0.1 mg/kg pancuronium within 6 min and after 1.0 mg/kg suxamethonium within 2 min. Intubation conditions improved with time. After 0.1 mg/kg vecuronium atraumatic intubation was possible within 2 min and after 0.1 mg/kg pancuronium within 4 min. Following 1.0 mg/kg suxamethonium, optimum intubation conditions were achieved within 1 min. Although suxamethonium acts the fastest and tracheal intubation can be achieved within 0.5-1.0 min, its use involves certain side effects and disadvantages. Vecuronium acts considerably faster than pancuronium and good or excellent intubation conditions are present within 2 min. Suxamethonium is no longer the muscle relaxant of choice for intubation except for crash intubation, e.g., in patients with a full stomach.

Adult↗
PubMed1988

Structure:action relationships among some desacetoxy analogues of pancuronium and vecuronium in the anesthetized cat.

The hypothesis that the neuromuscular blocking potency of pancuronium and vecuronium depends on the two acetylcholine moieties present at positions 3 and 17 was tested in cats by examining the neuromuscular profile of several desacetoxy analogues. Blockade of sciatic nerve-induced contraction of the tibialis and soleus muscles, as well as the effects on vagal-induced bradycardia and on sympathetically induced contractions of the nictitating membrane, were studied. The bis-desacetoxy analogue of pancuronium (ORG 7931) was one-fifth as potent as the parent compound as a neuromuscular blocking drug and as a vagolytic agent, but the neuromuscular block was faster in onset and shorter in duration than that produced by pancuronium. The desacetoxy analogues of vecuronium (ORG 8730 and ORG 8764) also were less potent neuromuscular blocking drugs, and, in addition, produced more vagal block than did vecuronium itself. The neuromuscular block produced by these desacetoxy analogues was of more rapid onset and shorter duration than that produced by vecuronium. The results thus showed that the greater neuromuscular blocking potency of pancuronium and vecuronium is lost after removal of one or both of the acetylcholine moieties. An analysis of the relationship between neuromuscular blocking dose and duration of action revealed that it was reciprocal, and it is suggested that a nondepolarizing equivalent of suxamethonium, when discovered, may necessarily be a drug of relatively low potency.

Animals↗