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PubMed1978

Diuretic-induced hypokalaemia, pancuronium neuromuscular blockade and its antagonism by neostigmine.

The effect of hypokalaemia on a neuromuscular blockade induced by pancuronium and its antagonism by neostigmine was studied in the cat anterior tibialis-peroneal nerve preparation using the constant infusion of pancuronium technique. Hypokalaemia was induced by chronic administration of chlorothiazide. The infusion rate of pancuronium required to maintain a 90% depression of twitch tension was reduced from 0.72 +/- 0.06 microgram kg-1 min-1 in the cats with a normal serum concentration of potassium (K+ = 4.4 +/- 0.2 mmol litre-1; n = 7) to 0.41 +/- 0.07 microgram kg-1 min-1 in the hypokalaemic cats (K+ = 2.3 +/- 0.1 mmol litre-1; n = 8). The dose of neostigmine necessary for 50% antagonism of the pancuronium-induced depression of twitch tension (ED50) was 10.0 microgram kg-1 in the cats with a normal potassium concentration and 18.5 microgram kg-1 in hypokalaemic cats. We conclude that hypokalaemia decreases the dose of pancuronium required for neuromuscular blockade and increased the dose of neotigmine required for antagonism of the block.

Animals↗
PubMed1980

The neuromuscular blocking action of ORG NC 45, a new pancuronium derivative, in anaesthetized patients. A pilot study.

The neuromuscular blocking effects of the new monoquaternary analogue of pancuronium, Org NC 45, have been investigated in anaesthetized patients. In different doses administered as a single i.v. bolus or as an initial bolus followed by several small maintenance doses or by a continuous infusion. Org NC 45 appears to be approximately as potent as pancuronium, but has a more rapid onset of action, considerably shorter duration of action and faster recovery rate than pancuronium. It showed no cumulative effects even after 10 maintenance doses were injected in succession. Doses of 0.08 mg kg-1 provided ideal intubating conditions in 90--95 s. Infusions of Org NC 45 provided much smoother control of neuromuscular blockade than did pancuronium. No cardiovascular side-effects were noted even at the greatest dose (0.12 mg kg-1) used. Org NC 45 has clear advantages over pancuronium and represents a potentially valuable addition to the armamentarium of clinically useful muscle relaxants.

Anesthesia, General↗
PubMed1982

Antagonism of org NC 45 (vecuronium) and pancuronium neuromuscular blockade by neostigmine.

The antagonism, by neostigmine, of neuromuscular blockade produced by either Org NC 45 or pancuronium was studied in 29 anaesthetized patients during a continuous infusion of the myoneural blocker. The ED50 of neostigmine (dose which produced a 50% antagonism) when antagonizing Org NC 45 and pancuronium was 0.011 mg kg-1 and 0.010 mg kg-1 respectively. The dose-response relationships for the antagonism of Org NC 45 and pancuronium neuromuscular blockades were not significantly different. The duration of the effect of neostigmine was not different when antagonizing an Org NC 45- or pancuronium-induced blockade. We concluded that Org NC 45 and pancuronium are effectively and equally (independent of pharmacokinetics) antagonized by neostigmine in man.

Adult↗
PubMed1982

Comparison of the effects of Org NC 45 and pancuronium bromide on heart rate and arterial pressure in anaesthetized man.

The effects of Org NC 45 and pancuronium bromide on heart rate and arterial pressure were studied in anaesthetized man. A bolus of either Org NC 45 0.1 mg kg-1 or pancuronium 0.1 mg kg-1 was administered to lightly anaesthetized unstimulated subjects. Following Org NC 45 heart rate decreased in the majority of subjects (mean and SEM 3.78 +/- 1.36), whereas after pancuronium heart rate was increased (mean and SEM 11.91 +/- 1.9). The changes in mean arterial pressure observed were minimal. The effect of endotracheal intubation on mean arterial pressure was then studied. Increase of mean arterial pressure was observed in all subjects. The increase was more marked in those patients who had received pancuronium and was significantly higher than in those patients who had received Org NC 45 (P less than 0.01). We conclude that Org NC 45 is devoid of vagal blocking action, and that the difference in response to the stimulus of endotracheal intubation is a result of the different effects exerted on the sympathetic nervous system by Org NC 45 and pancuronium.

Adult↗
PubMed1983

Neuromuscular blocking effects of vecuronium and pancuronium during halothane anaesthesia.

The neuromuscular blocking properties of vecuronium (Org NC 45) and pancuronium were compared in 40 patients during halothane anaesthesia. Onset time was found to be dose-dependent, but no significant difference was found between the two drugs. The duration of action of vecuronium was significantly shorter than pancuronium. Times to 90% recovery of twitch height following vecuronium 0.03 mg kg-1 and 0.057 mg kg-1 were 32.0 min and 44.9 min, respectively, compared with 72.9 min and 124.7 min following equipotent doses of pancuronium (0.042 mg kg-1 and 0.08 mg kg-1). Recovery indices following both doses of vecuronium (10.0 min and 11.8 min) were significantly shorter than after pancuronium (31.0 min and 46.9 min). The reversal times of vecuronium (times from 10% to 90% twitch height recovery) were significantly shorter than those of pancuronium (7.9 min and 7.3 min, respectively, compared with 17.1 min and 17.7 min).

Adult↗
PubMed1985

Neuromuscular blocking effects of atracurium, vecuronium and pancuronium during bolus and infusion administration.

The potencies of atracurium, vecuronium and pancuronium were compared using bolus injections and continuous infusions. The sizes of the bolus injections were based on previously determined cumulative dose-response relationships. Dose requirements for 90% and 50% sustained blockade were estimated by use of continuous infusion, and the corresponding plasma concentrations were measured for vecuronium and pancuronium. The effect of single bolus injections correlated well with the cumulative dose-responses, confirming relative potencies for atracurium, vecuronium and pancuronium of approximately 1:5:4. The maintenance doses (microgram kg-1 h-1) for 90% blockade were: atracurium 382.8, vecuronium 101.9, and pancuronium 36.9, making the relative dose requirements 10.4:2.8:1. The same dose ratio was found for atracurium and vecuronium at 50% blockade. This required about 60% of the doses needed for maintenance of 90% response. The relative potency of vecuronium and pancuronium in plasma was 1.1:1. The 25-75% recovery index was significantly shorter for vecuronium than for atracurium.

Adult↗
PubMed1985

Fade characteristics and onset times following administration of pancuronium, tubocurarine and a mixture of both agents.

The onset characteristics of pancuronium, tubocurarine and a mixture of these two neuromuscular blocking drugs were studied during the induction of neuromuscular blockade, using a train-of-four pattern of stimulation. Four characteristics of onset were defined: train-of-four fade = a reduction in the height of the fourth twitch greater than a reduction in the height of the first twitch; latent onset time = time from injection of neuromuscular blocker to a greater than 5% reduction in the first twitch in the train-of-four; total onset time = time to 90% reduction in twitch height; manifest onset time = time from 5% to 90% reduction in twitch height. Tubocurarine was associated with significantly more fade than either pancuronium or the mixture. During the period of study the fade profile of the mixture was almost identical to that of pancuronium alone. The mixture had the most rapid total onset time (100.3 s), tubocurarine the slowest (135.1 s) and pancuronium was intermediate (124.0 s). The mixture and tubocurarine had similar latent onset times, while the mixture and pancuronium had similar manifest onset times.

Adult↗
PubMed1993

Prolonged paralysis after long-term, high-dose infusion of pancuronium in anaesthetized cats.

We have studied the neuromuscular effects of a 48-h infusion of high-dose pancuronium (400 micrograms kg-1 h-1) in four cats anaesthetized with pentobarbitone, using contraction of tibialis anterior muscles after direct and indirect stimulation. After cessation of the pancuronium infusion, prolonged paralysis existed. The first twitch in the train-of-four stimuli (TOF) reappeared 8-12 h after termination of the pancuronium infusion. Twenty-four hours after termination of the infusion, TOF ratios were less than 0.08 and twitch contraction averaged 39 (SE 8)% of initial values. Twitch contraction after direct stimulation did not differ from initial values. Antagonism of paralysis was accomplished with neostigmine 60 micrograms kg-1 in two animals and neostigmine 90 micrograms kg-1 and 4-aminopyridine 500 micrograms kg-1 in the others. Steady-state plasma concentration of pancuronium (2000 ng ml-1) decreased rapidly after termination of the infusion, but then stabilized at about 130 ng ml-1. These results indicate that prolonged paralysis after long-term administration of high-dose pancuronium is caused primarily by failure of neuromuscular transmission, most likely caused by the persistent plasma concentrations of the drug in the pharmacologically active range.

4-Aminopyridine↗
PubMed1998

Duration of the pharmacodynamic interaction between pancuronium and mivacurium.

The aim of this study was to determine for how long the duration of action of increments of mivacurium can be influenced by previous pancuronium administration. Fifteen patients, ASA I or II, undergoing general anaesthesia for major abdominal surgery were investigated. The post-tetanic count (PTC) was measured at the adductor pollicis muscle. Pancuronium 0.1 mg kg-1 was injected first. At recovery of the 10th response of the PTC (PTC10), a second dose of pancuronium was injected (0.02 mg kg-1). On recovery to PTC10, a bolus of mivacurium (0.04 mg kg-1) was given and regularly repeated at recovery of PTC10 until the end of surgery. The mean duration of the second dose of pancuronium was 53 min (SD 13 min) and of the first dose of mivacurium, 66 min (SD 14 min) (P < 0.01). The duration of action of further mivacurium boluses decreased significantly until the fifth dose. It took 222 minutes (95% confidence interval 190, 253 min) after the second pancuronium dose before the duration of action of mivacurium returned to normal values and became constant and predictable.

Abdomen↗
PubMed1997

Decreased mivacurium constant infusion requirements with defasciculating doses of pancuronium.

This study was designed to verify a technique in which the pharmacologic profile of mivacurium infusions could be altered by small doses of pancuronium to reduce the infusion requirement without altering the subsequent recovery kinetics. Thirty ASA physical status I or II patients were randomized into two groups in a blinded fashion. One group was administered pancuronium 10 micrograms/kg followed by pancuronium 2.5 micrograms.kg-1.h-1 thereafter. The control group was given identical volumes of saline. Subsequently, all patients were given an initial bolus of mivacurium, and anesthesia was maintained using a nitrous oxide/ alfentanil technique. When the thenar electromyogram response to supramaximal train-of-four stimulation returned to 5% of baseline, a mivacurium infusion was begun in both groups, and the infusion rate required to maintain the electromyographic response at 1%-10% of baseline was determined. At the conclusion of the procedure, the infusion was terminated and the recovery profile ascertained. The mivacurium infusion requirement for the group receiving the pancuronium supplementation was 2.77 +/- 1.38 micrograms.kg-1.min-1 (mean +/- SD), which represented a 49% decrease compared with the group that used mivacurium alone which required an infusion rate of 5.43 +/- 1.85 micrograms.kg-1.min-1. No statistically significant difference was found in the recovery profiles of the two groups when the infusion was terminated. We conclude that the addition of a small amount of pancuronium decreased the required mivacurium infusion rate by nearly 50% without affecting the spontaneous recovery when terminating the infusion.

Adult↗
PubMed1983

Recovery of neuromuscular function in the perfused rat diaphragm after succinylcholine and pancuronium blockade.

The recovery of the rat diaphragm from neuromuscular blockade was studied in order to separate the contributions of drug binding and tissue washout. The in vitro rat diaphragm preparation was perfused with a cholinesterase-free solution via the phrenic vein and stimulated electrically via the phrenic nerve. Muscle paralysis was induced by infusion of a depolarizing blocker succinylcholine or by the nondepolarizing blocker pancuronium. The time for recovery from 25-75% recovery averaged 1.0 +/- 0.1 min for pancuronium and 0.8 +/- 0.1 min for succinylcholine at the fast (1.9 ml/min) perfusion rate. This was prolonged to 2.0 +/- 0.3 min for pancuronium and 1.4 +/- 0.1 min for succinylcholine at the slower (0.76 ml/min) rate. More sensitive paired tests of recovery utilizing recovery time and rate demonstrated no drug difference in three comparisons and a 44% longer recovery time for pancuronium only at the lower perfusion rate. In general, recovery times were similar for both drugs. The rapid recovery from pancuronium blockade in this mammalian system as perfusion rate was increased suggests that recovery from this drug is not impaired by drug binding but is strongly dependent on organ perfusion.

Animals↗
PubMed1983

The cardiovascular effects of vecuronium (ORG NC45) and pancuronium in patients undergoing coronary artery bypass grafting.

Vecuronium is a new nondepolarizing muscle relaxant which has been shown to cause no significant cardiovascular effects. Utilizing invasive monitoring in patients undergoing coronary artery bypass grafting, the authors compared the cardiovascular effects of vecuronium (0.28 mg/kg) in seven anesthetized patients with those of pancuronium (0.1 mg/kg) in five anesthetized patients. This dose of pancuronium represents three times its ED90 (dose producing a 90% depression of evoked twitch tension), while the vecuronium dose represents twelve times its ED90. This relatively large dose of vecuronium was chosen deliberately in an attempt to manifest any possible cardiovascular effects. Following administration of vecuronium, cardiac output increased 9% and systemic vascular resistance decreased 12%, while pancuronium produced a significantly greater 17% increase in cardiac output without change in systemic vascular resistance. Heart rate and systemic mean arterial pressure did not change following vecuronium, while increasing 22% and 24%, respectively, following pancuronium. The authors conclude that large doses of vecuronium have minimal cardiovascular effects and thus offer an advantage over pancuronium in patients anesthetized for coronary artery surgery.

Adrenergic beta-Antagonists↗
PubMed1983

The effects of hypercarbia and hypocarbia on pancuronium and vecuronium neuromuscular blockades in anesthetized humans.

To determine the effects of hypercarbia and hypocarbia on a pancuronium or vecuronium neuromuscular blockade, 54 patients were anesthetized with halothane and 60% nitrous oxide in oxygen. In 30 patients, end-tidal PCO2 was maintained at either 25 mmHg (3.5 kPa, N = 10), 41 mmHg (5.5 kPa, N = 10), or 56 mmHg (7.5 kPa, N = 10). Five patients in each group then were given pancuronium or vecuronium 0.022 mg/kg iv. Neither maximal depressions of twitch tension nor recovery indexes (time for spontaneous recovery of twitch tension from 25 to 75% of control) were altered by hypercarbia or hypocarbia. The remaining 24 patients were divided into three equal groups. Either pancuronium (N = 8) or vecuronium (N = 8) was administered iv as continuous infusion at a rate sufficient to produce a 50% depression of twitch tension. In the remaining eight patients, no muscle relaxant was given. After twitch tension was stable, half of the patients in each group had hypercarbia induced, which depressed twitch tension in all three groups. The patients who received vecuronium had a significantly larger decrease in twitch tension than those who received pancuronium or no muscle relaxant. Conversely, in the remaining patients, hypocarbia produced a significant increase in twitch tension. There was no difference in the magnitude of the increases in twitch tension among the three groups. The authors conclude that pre-muscle relaxant administration-induced hypercarbia or hypocarbia has no effect on a subsequent neuromuscular blockade from pancuronium or vecuronium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Recovery times following edrophonium and neostigmine reversal of pancuronium, atracurium, and vecuronium steady-state infusions.

The ability of edrophonium and neostigmine to antagonize nondepolarizing neuromuscular blockade produced by steady-state infusions of atracurium, pancuronium, and vecuronium was studied in 71 adult patients anesthetized with nitrous oxide and halothane. Infusion rates of blocking drugs were adjusted so that single twitch depression as measured by the evoked integrated EMG of the hypothenar muscles was kept at 10% of control. Two minutes after the termination of the infusion either edrophonium (0.75 mg/kg) or neostigmine (0.05 mg/kg) was administered. Single twitch depression and train-of-four (T4/T1) fade was recorded during the recovery period. T4/T1 fade ratios observed at 20 min postreversal were 0.80 (atracurium-edrophonium); 0.76 (vecuronium-edrophonium); 0.44 (pancuronium-edrophonium); 0.95 (atracurium-neostigmine); 0.89 (vecuronium-neostigmine); and 0.68 (pancuronium-neostigmine). Under conditions of this study neostigmine produced more rapid and complete recovery than did edrophonium. Although edrophonium produced adequate antagonism of atracurium if 20-30 min were allowed to elapse, edrophonium reversal of pancuronium was rarely acceptable even at 30 min. Increasing the dose of edrophonium to 1.0 mg/kg produced single twitch values of 0.90 at 5 min postreversal but did not increase the rate of recovery of the train-of-four fade ratio. Neostigmine reversal of pancuronium, on the other hand, generally produced T4/T1 ratios of greater than 0.70 in 20-30 min. Although the pattern of recovery seen after reversal of vecuronium was in general quite similar to that seen after atracurium, two patients in the vecuronium-edrophonium group showed delayed recovery and also failed to respond significantly to subsequent doses of neostigmine.(ABSTRACT TRUNCATED AT 250 WORDS)

Atracurium↗
PubMed1989

The incidence of myocardial ischemia during anesthesia for coronary artery bypass surgery in patients receiving pancuronium or vecuronium.

This study was performed to compare the incidence of prebypass myocardial ischemia in patients receiving fentanyl and enflurane for anesthesia along with either pancuronium or vecuronium. Ninety-eight patients with normal left ventricular function were randomly allocated to receive either pancuronium 0.15 mg.kg-1 or vecuronium 0.15 mg.kg-1 in a double-blind manner after fentanyl 40 micrograms.kg-1 for induction of anesthesia for elective coronary artery bypass grafting (CABG). Premedication included diazepam 0.15 mg.kg-1 po, morphine 0.10 mg.kg-1, and scopolamine 0.005 mg.kg-1 im. Two lead Holter monitor recordings (leads V6 and V9) from the time of arrival in the operating suite to institution of cardiopulmonary bypass were analyzed for ischemia by a cardiologist blinded to the choice of muscle relaxant. Intraoperatively, heart rates greater than 90 beats.min-1 and systolic blood pressure +/- 20% of ward values were treated with propranolol, enflurane, or phenylephrine. Nitroglycerin was infused for ECG signs of ischemia or pulmonary hypertension. After induction of anesthesia the heart rate and cardiac index were consistently decreased in patients receiving vecuronium and also lower in these patients compared with those receiving pancuronium. Thirty-two per cent of patients receiving pancuronium received propranolol for heart rates greater than 90 beats.min-1 versus 7% of those who received vecuronium (P approximately 0.01). Eight patients developed 13 episodes of ischemia after administration of the muscle relaxant: four who received pancuronium (n = 44; 9%) and four receiving vecuronium (n = 54; 7%). Four episodes occurred at induction or tracheal intubation, two in each group. There were four perioperative myocardial infarctions as determined by ECG and CPK-MB levels, two in each group.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1992

Pancuronium increases the duration of electroencephalogram burst suppression in dogs anesthetized with isoflurane.

Earlier studies have demonstrated both a decrease as well as no effect on halothane MAC after administration of nondepolarizing neuromuscular relaxants. To clarify further the relationship between neuromuscular blocking agents and anesthetic potency, the authors studied the effect of pancuronium on steady-state electroencephalogram (EEG) burst suppression produced by isoflurane in dogs. Anesthesia was induced using isoflurane and oxygen via mask without the administration of other drugs. The trachea was intubated, and isoflurane was administered at a concentration sufficient to produce EEG burst suppression. Thereafter, end-tidal isoflurane concentration, temperature, and end-tidal PCO2 were meticulously maintained at constant values. Dogs in group 1 (n = 6) received pancuronium 0.1 mg.kg-1. The percent of the EEG that was isoelectric increased from 21 +/- 9% (mean +/- SD) to 35 +/- 11% (P less than 0.01). After the return of single-twitch response to train-of-four stimulation, neostigmine 0.05 mg.kg-1 and glycopyrrolate 0.01 mg.kg-1 were administered. This resulted in a reduction in EEG isoelectricity to 19 +/- 8% (P less than 0.01), similar to the value before pancuronium administration. In group 2 dogs (n = 6), the percent isoelectricity of the EEG prior to pancuronium was 25 +/- 10%. After administration of pancuronium 0.02, 0.04, and 0.2 mg.kg-1 sequentially, the percent isoelectricity of the EEG was 29 +/- 11, 37 +/- 15, and 43 +/- 9%, respectively. This represents a dose-related increase in isoelectricity for the 0.04- and 0.2-mg.kg-1 doses (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed2004

Up-regulation of acetylcholine receptors during subchronic infusion of pancuronium is caused by a posttranscriptional mechanism related to disuse.

OBJECTIVE: Contrasting with the classic theory that competitive block of the acetylcholine receptor induces up-regulation of the receptor, recent studies show that irreversible block of acetylcholine receptors with alpha-bungarotoxin decreases acetylcholine receptor number within hours. This study investigated the early effects of competitive acetylcholine receptor block with the reversible, competitive muscle relaxant, pancuronium. DESIGN: Prospective, randomized, placebo-controlled experimental study. SUBJECTS: Healthy adult Sprague-Dawley rats. SETTING: Animal laboratory in a university hospital. INTERVENTIONS: After internal review board approval, Sprague-Dawley rats were anesthetized and received pancuronium at a rate to completely suppress neuromuscular twitch. The control group received saline. Infusion times were 0, 3, 6, or 12 hrs (n = 8 per group). One sciatic nerve was stimulated to induce muscle twitch, and the other nerve remained unstimulated. Total acetylcholine receptor expression, as well as expression of messenger RNA of the five subunits, was assayed. MEASUREMENTS AND MAIN RESULTS: There were no differences in acetylcholine receptor number between groups at time points 0, 3, and 6 hrs. At 12 hrs, acetylcholine receptor numbers in both the stimulated (35.2 +/- 4.8 fmol acetylcholine receptor/mg protein) and nonstimulated (38.3 +/- 4.8) pancuronium group, as well as the nonstimulated control saline group (37.5 +/- 4.6), were significantly increased compared with stimulated controls (27.6 +/- 4.0). Pancuronium did not potentiate the acetylcholine receptor up-regulation of the nonstimulated control group at 12 hrs. There were no changes in messenger RNA expression between groups. CONCLUSIONS: Infusion of the reversible competitive inhibitor pancuronium up to 12 hrs does not reduce acetylcholine receptor number and therefore contrasts with the irreversible acetylcholine receptor blocker alpha-bungarotoxin. This study documents that 12 hrs of disuse per se leads to an increased expression of the acetylcholine receptor number by a posttranscriptional mechanism that can be prevented by nerve-evoked muscle contraction.

Animals↗
PubMed2004

Chromosome instability in T-cells cultured in the presence of pancuronium or fentanyl.

BACKGROUND: Genomic instability is recognized as a cause of cellular apoptosis and certain drugs that exhibit a proapoptotic effect are also able to induce chromosome damage. Since we found in recent experiments that drugs such as pancuronium and fentanyl exerted an apoptogenic effect on T cells, we studied the capacity of those agents to promote chromosome instability, i.e. chromosome aberrations (CA) and telomeric associations (tas) in peripheral blood lymphocytes. METHODS: Lymphocytes from healthy donors were cultured with pancuronium or fentanyl, using two different concentrations for each drug: 20 and 200 ng/ml for pancuronium and 10 and 30 ng/ml for fentanyl, respectively. Cells were exposed to each concentration of these drugs either for 24 or 48 h. The higher concentration chosen was the same at which we detected the proapoptotic effect in our previous works. Cytogenetic analysis was performed by means of a standard technique and chromosome aberrations or telomeric associations were blindly evaluated by two independent observers. RESULTS: The chromosome aberrations we observed in treated cells were not significantly different from control lymphocytes. However, an unusual rate of telomeric associations (P < 0.001) was detected in cells exposed to both pancuronium and fentanyl, at each concentration tested and at each exposure time of the study. CONCLUSIONS: Fentanyl and pancuronium do not have a direct clastogenic effect on T cultures, but at the same concentrations at which we demonstrated their apoptogenic power, these drugs are able to increase genomic instability through inducing an elevated rate of telomeric associations. Such a capacity could exploit in peripheral T cells the same mitochondrion-mediated signal pathway of apoptosis death.

Adult↗