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At least 19 recordsLinked to original sources
PubMed1979

The neuromuscular and autonomic blocking activities of pancuronium, Org NC 45, and other pancuronium analogues, in the cat.

Twenty-six mono- or bis-quaternary salts of 3,17-dioxy-2 beta, 16 beta-dipiperidino-5 alpha-androstanes (including pancuronium) and one 17-desoxy congener were tested for neuromuscular blocking and autonomic blocking activities in the chloralose-anaesthetized cat. The 17 beta-acetoxy series, all the members of which contain an acetylcholine-like fragment in the steroidal D-ring, was most selective for effecting neuromuscular blockade. The salient member of this series is 3 alpha, 17 beta-diacetoxy-2 beta, 16 beta-dipiperidino-5 alpha-androstane 16 beta-N-monomethobromide (Org NC 45) which is highly selective in blocking neuromuscular transmission in that a dose approximately sixty times greater than the neuromuscular blocking dose was required to block responses to vagal stimulation. In contrast, in doses sufficient to produce neuromuscular block, pancuronium simultaneously blocked responses to vagal stimulation. Moreover, pancuronium and Org NC 45 exhibited the same order of neuromuscular blocking activity and therefore the latter potentially represents a useful addition to the armamentarium of neuromuscular blocking agents currently in clinical use.

Androstanes↗
PubMed1990

[Hemodynamics and myocardial energy balance in coronary surgery patients during high-dose fentanyl-pancuronium anesthesia and modified neurolept-pancuronium anesthesia].

In 8 patients with coronary artery disease (CAD) classed as NYHA II or III, anesthesia was induced with high-dose fentanyl (0.05 mg/kg) and pancuronium (0.1 mg/kg). The patients were ventilated normally with the aid of a mask (O2: air 1:1, tidal volume 10 ml/kg with a rate of 10/min) for 5 min and then intubated. In 8 further patients with CAD NYHA class II or III, anesthesia was induced with 0.02 mg/kg flunitrazepam, N2O/O2 1:1 and isoflurane 0.5 vol%; they were relaxed with pancuronium (0.1 mg/kg) in combination with a bolus of 0.005 mg/kg fentanyl. These patients were also ventilated normally for 5 min and then intubated. Measurements of cardiovascular dynamics included cardiac output (CO), heart rate (HR), arterial pressure (AP), pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP), right atrial pressure (RAP), myocardial blood flow (MBF), and arterial and coronary sinus oxygen and lactate contents. Cardiac index (CI), stroke volume index (SVI), total peripheral resistance (TPR), myocardial oxygen consumption (MVO2), coronary vascular resistance (CVR), coronary perfusion pressure (CPP), myocardial oxygen content difference (AVDO2cor) and myocardial lactate extraction rate (LE) were calculated from standard formulas. Measurements and an electrocardiogram were taken before anesthesia, after induction of anesthesia and after intubation. The hemodynamic parameters HR, AP, CI, CPP were relatively stable in patients anesthetized with high-dose fentanyl and pancuronium, whereas we found greater decreases in these parameters with the balanced anesthesia technique. Determinants of myocardial oxygen demand were higher in the high-dose fentanyl group; therefore, myocardial blood flow and oxygen consumption did not decrease to the same extent as in the balanced anesthesia group.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1978

The comparative potency and pharmacokinetics of pancuronium and its metabolites in anesthetized man.

To determine the potency of pancuronium and its metabolites, 3-OH-, 17-OH- and 3,17-OH-pancuronium, cumulative dose-response curves were determined in five anesthetized patients with each drug. Pancuronium (ED50 = 0.041 mg/kg) was 2 times more potent than 3-OH-pancuronium (ED50 = 0.082 mg/kg), 50 times more potent than 17-OH-pancuronium (ED50 = 2.0 mg/kg) and 54 times more potent than 3,17-OH--pancuronium (ED50 = 2.15 mg/kg). In 21 other patients, one equipotent dose of either pancuronium or one of its metabolites was given as an i.v. bolus. Onset time and duration of neuromuscular blockade from 3-OH- and 3,17-OH-pancuronium did not differ significantly from that of pancuronium; 17-OH-pancuronium had a shorter duration of action than did pancuronium. Although pancuronium tended to have a slightly longer elimination half-life, the pharmacokinetics of the four drugs did not differ significantly. The elimination half-lifes were 110, 68, 73 and 71 min for pancuronium and its 3-OH, 17-OH and 3,17-OH derivatives, respectively. We conclude that although pancuronium is more potent than its 3-OH, 17-OH and 3,17-OH metabolites, the pharmacokinetics of these three metabolites do not differ from each other and from that of pancuronium.

Dose-Response Relationship, Drug↗
PubMed1975

The effect of pancuronium on myocardial contraction and catecholamine metabolism.

The effects of pancuronium bromide infusion on the uptake and release of [14C] noradrenaline (14C-NA) by the isolated, perfused rat heart and on the chronotropic and inotropic activity of the isolated heart were evaluated. Hearts were removed from animals under light ether anaesthesia, transferred to a modified Langendorff perfusing apparatus and perfused with Krebs-Ringer bicarbonate solution at a rate of 5 ml min-1. The effect of pancuronium on the uptake of noradrenaline was determined by perfusing hearts for 5 min with perfusate containing various concentrations of pancuronium and 200 ng ml-1 of 14C-NA. After 5 min pancuronium-treated hearts contained less 14C-NA. The degree of reduced uptake increased with increasing concentrations of pancuronium. In addition, the combination of pancuronium perfusion and electrical stimulation (15 mA for 10 ms at 4 Hz) blocked the 50 min uptake of 14C-NA by the heart to a greater degree than either factor separately. The release of noradrenaline was determined after perfusing hearts with 14C-NA followed by perfusion with solution containing pancuronium but no 14C-NA for 1 h. Pancuronium infusion did not significantly alter the release of 14C-NA from the heart after 1 h of perfusion. The infusion of pancuronium caused a reduction in both the rate and strength of myocardial contraction of the isolated heart which was reversed by perfusion with perfusate free of pancuronium. Following perfusion with pancurnium the rate and strength of contraction of the heart was seen to "rebound" above pre-pancuronium values for a short period. The rebound of myocardial rate and contraction may have been due to the presence of myocardial noradrenaline previously blocked from reuptake by pancuronium since hearts removed from reserpinized animals did not demonstrate "rebound."

Animals↗
PubMed1978

Sympathomimetic effects of pancuronium bromide on the cardiovascular system of the pithed rat: a comparison with the effects of drugs blocking the neuronal uptake of noradrenaline.

1. The effects of pancuronium bromide on the cardiovascular system of the pithed rat were examined. Pancuronium had two effects, a short-lasting cardiovascular stimulation following injection and a longer-lasting potentiation of responses to sympathetic nerve stimulation. 2 The initial effect of pancuronium was compared with that of tyramine. The cardioaccelerator but not the pressor responses to both pancuronium and tyramine were significantly reduced following sympathectomy with 6-hydroxydopamine (6-OHDA). 3 The action of pancuronium in potentiating sympathetic nerve responses was compared with that of known blockers of the neuronal uptake of noradrenaline (NA). Pancuronium (1 mg/kg) and cocaine (0.5 mg/kg) potentiated cardioaccelerator and pressor responses to sympathetic stimulation. These effects of pancuronium could be obtained following adrenalectomy and during neuromuscular blockade with gallamine. Pancuronium and uptake blockers potentiated the cardioaccelerator response to NA, reduced the response to tyramine, but did not affect the response to isoprenaline. Pancuronium and uptake blockers potentiated the pressor response to NA, but did not affect the response to tyramine or clonidine. 4 Following sympathectomy with 6-OHDA, pancuronium failed to potentiate cardioaccelerator and pressor responses to NA. 5 These results are discussed in relation to two main cardiovascular effects of pancuronium; an indirect sympathomimetic action and blockade of the neuronal uptake of NA.

Adrenalectomy↗
PubMed1977

Kinetic analysis of pancuronium interaction with sodium channels in squid axon membranes.

The interaction of pancuronium with sodium channels was investigated in squid axons. Sodium current turns on normally but turns off more quickly than the control with pancuronium 0.1-1mM present internally; The sodium tail current associated with repolarization exhibits an initial hook and then decays more slowly than the control. Pancuronium induces inactivation after the sodium inactivation has been removed by internal perfusion of pronase. Such pancuronium-induced sodium inactivation follows a single exponential time course, suggesting first order kinetics which represents the interaction of the pancuronium molecule with the open sodium channel. The rate constant of association k with the binding site is independent of the membrane potential ranging from 0 to 80 mV, but increases with increasing internal concentration of pancuronium. However, the rate constant of dissociation l is independent of internal concentration of pancuronium but decreases with increasing the membrane potential. The voltage dependence of l is not affected by changine external sodium concentration, suggesting a current-independent conductance block, The steady-state block depends on the membrane potential, being more pronounced with increasing depolarization, and is accounted for in terms of the voltage dependence of l. A kinetic model, based on the experimental observations and the assumption on binding kinetics of pancuronium with the open sodium channel, successfully simulates many features of sodium current in the presence of pancuronium.

Action Potentials↗
PubMed1985

Precurarization with vecuronium and pancuronium in awake, healthy volunteers: the influence on neuromuscular transmission and pulmonary function.

The influence of pretreatment with pancuronium and vecuronium on the neuromuscular transmission was compared in 24 healthy, awake, non-premedicated volunteers using train-of-four (TOF) nerve stimulation and measurement of respiratory frequency, vital capacity, inspiratory force and peak expiratory flow (PEF). The subjects were randomly allocated to one of three groups. Each subject received one dose of pancuronium and one dose of vecuronium: Group I pancuronium 0.01 mg/kg and vecuronium 0.005 mg/kg; Group II pancuronium 0.01 mg/kg and vecuronium 0.01 mg/kg and Group III pancuronium 0.01 mg/kg and vecuronium 0.015 mg/kg intravenously. The median TOF ratio decreased significantly in Groups I and II following both pancuronium and vecuronium. The TOF ratio following vecuronium in Group II was significantly lower compared to the TOF ratio following vecuronium in Group I. Only PEF decreased significantly in Group I following pancuronium and in Group II following both pancuronium and vecuronium. There was no significant difference between Group I and Group II regarding the number of subjects with signs or symptoms of partial neuromuscular blockade. Following vecuronium 0.005 mg/kg, one subject was unable to swallow and the twitch height decreased to 0.25. In Group II one subject was unable to lift her head and had difficulty in swallowing following pancuronium 0.01 mg/kg. Only four subjects entered Group III because of an unacceptably high frequency of signs and symptoms of partial neuromuscular blockade and a decrease in median TOF ratio to 0.64 following vecuronium. The subjects felt it difficult to swallow, and one subject could just sustain head lift for 10 s following vecuronium 0.015 mg/kg.(ABSTRACT TRUNCATED AT 250 WORDS)

Consciousness↗
PubMed1990

The influence of pancuronium and vecuronium combined with balanced anaesthesia on haemodynamics and myocardial oxygen balance.

The effects of the non-depolarizing muscle relaxants pancuronium (Pancuronium) and vecuronium (Norcuron) (0.1 mg/kg) on myocardial blood flow, myocardial oxygen consumption, myocardial lactate balance, cardiovascular dynamics and electrocardiogram were studied in two groups of eight patients undergoing coronary artery bypass surgery. After induction of anaesthesia with 0.015-0.02 mg/kg flunitrazepam, isoflurane (0.5 vol%) and N2O/O2 (l/l), neuromuscular blockade was induced with pancuronium or vecuronium (0.1 mg/kg) combined with a single dose of 0.005 mg/kg fentanyl. Haemodynamic measurements were performed and the electrocardiogram was recorded before anaesthesia, in steady-state anaesthesia, after relaxation with pancuronium or vecuronium combined with fentanyl, and after intubation. The haemodynamic data consisted of heart rate, cardiac index, stroke volume index, mean arterial pressure, total peripheral resistance, pulmonary arterial pressure, pulmonary capillary wedge pressure, right atrial pressure, myocardial blood flow, coronary vascular resistance, myocardial oxygen consumption, coronary aterio-mixed venous content difference, myocardial lactate extraction and rate pressure product. In the vecuronium group, heart rate decreased significantly more (21%) than in the pancuronium group (9%). Therefore myocardial oxygen consumption (48% resp. 35%) and coronary blood flow (31% resp. 18%) decreased more in the vecuronium than in the pancuronium group. The higher metabolic demand in the pancuronium group induced a significantly lower coronary vascular resistance, because the decrease in coronary perfusion pressure was similar in both groups. None of the other haemodynamic parameters differed significantly in either patient group. We did not observe ST-segment depressions or elevations in the ECG, increases in PCWP or myocardial lactate production. Therefore extended myocardial ischaemia can be excluded in our patients who received pancuronium or vecuronium for neuromuscular blockade.

Aged↗
PubMed1975

[The metabolism of pancuronium in man].

The metabolic disposition of pancuronium was investigated in man under clinical condition. Pancuronium and its desacetylated derivatives were determined in body fluids using the previously described bromophenol blue method (3). The metabolites were isolated by thin layer chromatography. One minute after the intravenous injection of a mg of pancuronium the drug reaches a serum concentration of 2,2 plus or minus 0,2mug/ml. As an exponential function the concentration curve then falls to half of the initial value during the first 30 to 60 min. The end of the neuromuscular block conincides with a concentration of 0,1 to 0,3 mug/ml serum which is reached about 2 hours after the injection. After 3 to 4 hours no more pancuronium can be detected in the serum. The renal elimination of pancuronium can be folowed up for 12 hours. On average half of the injected dose is recovered in the urine. 80% of this proportion is unchanged pancuronium and 20% desacetylated metabolites. The monodesacetylated derivatives of pancuronium are still pharmacologically active. The biliary excretion 24 hours after the administration of pancuronium accounts for 5 to 10% of the injected dose...

Bile↗
PubMedDate not supplied

[Evaluation of the degree of muscle blockade: a comparative study using electromyography of the muscular relaxation induced by pancuronium, atracurium and vecuronium].

To compare the muscle relaxing effect of pancuronium, atracurium and vecuronium, 99 patients operated on under neuroleptanesthesia were divided in three groups depending on whether they had received, during induction, pancuronium 0.1 mg/kg, atracurium 0.5 mg/kg, or vecuronium 0.1 mg/kg. One-fourth of the initial dose was repeated if necessary. The electromyographic study of the muscle relaxing effect was carried out with stimulation of the cubital nerve with courses of supramaximal square wave electric stimuli in 'trains of four'. The time to maximal blockade (TMB), the time of clinical effectiveness (TCE), the total duration time (TDT), the time of duration of the maintenance dose (DM 25) and the recovery index (RI) were measured. TMB was 4.3 +/- 1 min for pancuronium, 3.5 +/- 0.8 min for atracurium, and 3.3 +/- 0.98 min for vecuronium. The differences between pancuronium and the other drugs were statistically significant, but they were not so between the latter two. TCE was 67.9 +/- 13.5 min for pancuronium, significantly longer than with vecuronium and atracurium (28.2 +/- 5.7 and 31.5 +/- 4.7, respectively). TDT was 126.2 +/- 19.9 min for pancuronium, 61.2 +/- 11.5 min for atracurium and 55.5 +/- 16.7 for vecuronium. The mean duration of the repeated dose was 52.7 +/- 8.4 min for pancuronium, 19.9 +/- 5 min for vecuronium and 10.9 +/- 5 min for atracurium. RI, which was similar for atracurium and vecuronium (12.7 +/- 1.7 min and 12.8 +/- 3.3 min), was longer for pancuronium (27.7 +/- 4.3 min).

Adolescent↗
PubMed1989

[Suppression by pancuronium and tubocurarine of the afferent discharge of the muscle spindle induced by succinylcholine].

Effect of pancuronium on the increased afferent discharge of the muscle spindle induced by succinylcholine (SCC) (Succinylcholine induced discharge, SID) was studied in the decerebrate cat by recording the discharge of the muscle nerve going to the gastrocnemius muscle. This action of pancuronium was compared with that of tubocurarine and the antagonistic action if any by neostigmine of this action of pancuronium and tubocurarine was also studied. Pancuronium 0.025 or 0.05mg.kg-1 reduced the peak values of SID to 25.2% and 6.8% of the control value respectively. Tubocurarine 0.125mg.kg-1 reduced this to 38.2%. Inhibition of the SID by pancuronium or tubocurarine was not reversed by the administration of neostigmine. Thus pancuronium reduced SID depending on its dose. The ability of pancuronium and tubocurarine to suppress SID is related to their neuromuscular blocking effects, but the failure by neostigmine to reverse this action of pancuronium or tubocurarine might suggest a different type of reaction at the acetylcholine receptor of the intrafusal fiber compared with the one at the acetylcholine receptor of the skeletal muscle.

Animals↗
PubMed1986

Pharmacokinetics and pharmacodynamics of vecuronium and pancuronium in anesthetized children.

The pharmacokinetics and pharmacodynamics of vecuronium and pancuronium were determined in 12 children (3-6 yr) undergoing minor surgery under 60% nitrous oxide, 1 MAC halothane anesthesia. When the level of anesthesia and the electromyograph (EMG) recording of the adductor pollicis were stable, an intravenous bolus of vecuronium (100 micrograms/kg) or pancuronium (100 micrograms/kg) was administered. Plasma concentrations of the two muscle relaxants were determined for 6 hr after the administration by means of a fluorimetric assay followed by a thin layer chromatography. Plasma concentrations of vecuronium and pancuronium declined biexponentially in children and no metabolites could be detected in plasma. The elimination half-lives of vecuronium and pancuronium did not differ significantly. The volume of distribution at steady state (Vdss) was greater (P less than 0.05) after vecuronium (320 +/- 181 ml/kg; mean +/- SD) than after pancuronium (203 +/- 36 ml/kg). Plasma clearance of vecuronium (2.8 +/- 0.9 ml X min-1 X kg-1) was greater than that of pancuronium (1.7 +/- 0.2 ml X min-1 X kg-1; P less than 0.05). Plasma concentrations measured at 10%, 50%, or 90% recovery of the EMG response did not differ significantly for vecuronium and pancuronium. Thus the shorter duration of action of vecuronium is probably due to its greater apparent volume of distribution, as well as to its higher plasma clearance. Thus although the elimination half-lives are comparable, the plasma disappearance of vecuronium is more rapid than that of pancuronium.

Anesthesia, General↗
PubMed1977

Bradycardia during antagonism of pancuronium-induced neuromuscular block.

Heart rate was compared in matched patients during antagonism of neuromuscular block induced by tubocurarine, pancuronium or alcuronium with neostigmine 0.03 mg kg-1 preceded by atropine 0.015 mg kg-1. The frequency of bradycardia was greater during antagonism of pancuronium compared with alcuronium. Although there was a difference between the group receiving pancuronium and that receiving tubocurarine, it was not statistically significant. The decrease in heart rate was more rapid and profound in the pancuronium group; seven of the 15 patients who received pancuronium required an additional dose of atropine as compared with only one patient who received tubocurarine. However, the difference in heart rate between those who received pancuronium and those receiving tubocurarine was short-lasting, whereas the heart rate of those who received alcuronium was higher than that in the other groups during the entire 60-min period of observation. The findings with pancuronium may be a result of its inhibitory effect on serum cholinesterase.

Adult↗
PubMed1978

Pancuronium pharmacokinetics in patients with liver cirrhosis.

The serum and urinary concentrations of pancuronium were measured in 14 surgical patients with cirrhosis and 12 patients free from liver disease undergoing abdominal surgery. A two-compartment open model was used in the pharmacokinetic analysis of the data. A two-fold increase in both the distribution half-life (T 1/2 alpha) from 11 min to 24 min and in the elimination half-life (T 1/2 beta) from 114 min to 208 min was observed in patients with cirrhosis. In these individuals, the total apparent volume of distribution of pancuronium was increased by 50%. Plasma clearance of pancuronium was decreased by 22%. No significant difference was found in the urinary excretion and biotransformation pattern of pancuronium. These results suggest that there is a risk of prolonged duration of action of pancuronium in patients with cirrhosis. In these patients, the initial dose to achieve adequate muscle relaxation is high and simultaneously there is slow disappearance of pancuronium from plasma. These alterations are mainly a consequence of the increase in the distribution volume of pancuronium in patients with cirrhosis.

Abdomen↗
PubMed1979

Pre- and postsynaptic effects of pancuronium at the neuromuscular junction of the mouse.

The dose-effectiveness of pancuronium as it relates to membrane potentials, action potentials, electrical membrane constants, miniature endplate potentials, endplate potentials, and quantal release was studied in murine phrenic nerve-diaphragm preparations in vitro. Emphasis was placed on comparison of presynaptic with postsynaptic effects of pancuronium under similar experimental conditions. At low concentrations of pancuronium (5 X 10(-8) g/ml or less), no presynaptic effect was found. At high concentration (5 X 10(-7) g/ml), pancuronium depressed quantal release to 26 per cent of control in cut-fiber preparations and 40 per cent of control in high-magnesium preparations. Postsynaptic effects as measured by the amplitude of miniature endplate potentials and relative depolarization induced by 20 microns carbachol, revealed depression to 16 and 22 per cent of control, respectively, at a pancuronium concentration of 5 X 10(-7) g/ml. Pancuronium had no effect on directly elicited action potentials and electrical membrane constants. The authors conclude that presynaptic as well as postsynaptic effects of pancuronium in paralytic doses are essential in contributing to the total efficacy of neuromuscular depression.

Action Potentials↗
PubMed1987

The interaction of pancuronium and vecuronium with cardiac muscarinic receptors.

The interaction of vecuronium, a monoquaternary analogue of pancuronium, with the cardiac muscarinic receptors in canine hearts was investigated in vitro by [3H] QNB binding assay and compared with that of pancuronium. Both pancuronium and vecuronium, which are nicotinic antagonists of competitive types, inhibited the binding of [3H] QNB to cardiac muscarinic receptors with values of IC50 of 5.41 X 10(-7) mol/l and 3.97 X 10(-6) mol/l respectively. According to the Kd and Bmax values on the Scatchard plot, pancuronium, while not influencing the number of receptors, had a 3-fold greater inhibitory effect than vecuronium on the affinity of the muscarinic receptors. The KI values of vecuronium and pancuronium showed that pancuronium had a 7.3-fold greater affinity with the receptors than vecuronium. We concluded that vecuronium had a direct inhibitory action on the binding of [3H] QNB to the canine heart muscarinic receptors, but this action was much weaker than pancuronium.

Animals↗