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PubMed1997

Residual neuromuscular block is a risk factor for postoperative pulmonary complications. A prospective, randomised, and blinded study of postoperative pulmonary complications after atracurium, vecuronium and pancuronium.

BACKGROUND: After anaesthesia involving pancuronium a high incidence of both residual neuromuscular block and postoperative pulmonary complications (POPC) has been reported. The aim of this study was to compare the incidence of POPC following the use of pancuronium, atracurium, and vecuronium, and to examine the effect of residual neuromuscular block on the incidence of POPC. METHODS: A total of 691 adult patients undergoing abdominal, gynaecological, or orthopaedic surgery under general anaesthesia were randomised to receive either pancuronium, atracurium, or vecuronium. Perioperatively, the response to train-of-four (TOF) nerve stimulation was evaluated manually. Postoperatively, the TOF ratios were measured mechanomyographically, and through a 6-day follow-up the patients were examined for pulmonary complications. RESULTS: The incidence of residual block, defined as a TOF ratio < 0.7, was significantly higher in the pancuronium group (59/226: 26%) than in the atracurium/vecuronium groups (24/450: 5.3%). In the pancuronium group, significantly more patients with residual block developed POPC (10/59: 16.9%) as compared to patients without residual block (8/167: 4.8%). In the atracurium/vecuronium groups, the incidence of POPC was not significantly different in patients with (1/24: 4.2%) or without (23/426: 5.4%) residual block. Multiple regression analysis indicated that abdominal surgery, age, long-lasting surgery, and a TOF ratio < 0.7 following the use of pancuronium were potential risk factors for the development of POPC. CONCLUSION: Postoperative residual block caused by pancuronium is a significant risk factor for development of POPC.

Adult↗
PubMed1979

On the mechanism of pancuronium-induced supersensitivity to noradrenaline in rat smooth muscle.

1. Pancuronium bromide (5 x 10(-5) M) caused supersensitivity to noradrenaline in the rat isolated vas deferens and hepatic portal vein. This supersensitivity was manifest as a parallel leftward shift of the dose-response curve for noradrenaline with no alteration of the maximum response to the agonist. 2. Pancuronium did not potentiate the response of the vas and portal vein to St 91, an alpha-adrenoceptor agonist which is not a substrate for Uptake1. 3. Pancuronium did not potentiate the response of the vas to CaCl2. 4. In vasa deferentia made supersensitive to noradrenaline by treatment with cocaine (1 x 10(-5) M) pancuronium induced no further potentiation of the response to noradrenaline. However, the supersensitivity to noradrenaline induced by pancuronium alone was augmented by the addition of cocaine. 5. Histofluorescence studies showed that pancuronium inhibited neuronal uptake of alpha-methyl noradrenaline in various noradrenergically-innervated tissues from reserpine-treated rats. 6. This study, with support from the literature, suggests that pancuronium induces noradrenaline supersensitivity by blockade of Uptake1.

Animals↗
PubMed1992

Effects of pancuronium bromide on cerebral blood flow changes during seizures in newborn pigs.

We investigated the effects of pancuronium bromide pretreatment on cerebral blood flow (CBF) during bicuculline-induced seizures in anesthetized piglets. Arterial blood pressure, gases, pH, cerebral electrocortical activity, and CBF (radioactive microsphere) were monitored at baseline, 10 min after administration of pancuronium (0.3 mg/kg i.v.; n = 9) or vehicle (normal saline; n = 8), and again at 5, 15, and 60 min after bicuculline (3 mg/kg i.v.). No change in CBF from baseline was observed at 10 min after either saline or pancuronium treatment, before induction of seizures. In the saline group, CBF was 36 +/- 3 mL.min-1.100 g-1 before bicuculline and increased to 166 +/- 24 and 205 +/- 35 mL.min-1.100 g-1 at 5 and 15 min, respectively, after bicuculline, returning toward baseline by 60 min. In the pancuronium group at 5 min after bicuculline, CBF increased from 45 +/- 7 to 169 +/- 26 mL.min-1.100 g-1, but fell to 88 +/- 17 mL.min-1.100 g-1 at 15 min in contrast to saline-treated piglets. Also, at 15 min of seizures, differences between groups were observed in arterial blood pressure, gases, and pH. Although these variables were in the normal range with pancuronium treatment, the saline-treated animals had increased arterial blood pressure (81 +/- 6 mm Hg) and PCO2 (6 +/- 0.4 kPa) and decreased PO2 (7 +/- 0.5 kPa) and pH (6.91 +/- 0.06). Electrocortical activity was abnormal during seizures in both groups. At 60 min, reversal to normal activity was observed in six of nine pancuronium-treated animals versus two of eight saline-treated animals. These data suggest that pancuronium limits cerebral hyperemia during prolonged seizures by attenuating increases in blood pressure as a result of elimination of skeletal muscle activity. This leads to minimal alteration of arterial PCO2, PO2, and pH during seizures.

Animals↗
PubMed1994

Pancuronium or vecuronium for treatment of shivering after cardiac surgery.

This randomized double-blind study compared the hemodynamic and metabolic effects of pancuronium and vecuronium during treatment of shivering after cardiac surgery with hypothermic cardiopulmonary bypass. Thirty sedated and pain-free patients who shivered after cardiac surgery were treated with pancuronium (n = 15) or vecuronium (n = 15) 0.08 mg/kg. Baseline values of heart rate (HR), mean arterial pressure, arterial and venous blood gases, total body oxygen consumption indexed to body surface area (VO2-I), and pressure work index (PWI, an estimate of myocardial oxygen consumption) were measured on arrival in the intensive care unit, at onset of shivering, and repeatedly for 2 h after treatment. Continuous ST segment analysis of leads II and V5 were used for detection of myocardial ischemia. Treatment of shivering with pancuronium decreased VO2-I by 32% (P = 0.0001). This was accompanied by a 14% increase in HR (P = 0.001) and a 10% increase in PWI (P = 0.03). Vecuronium decreased VO2-I by 36% (P = 0.003) with a 4% decrease in HR (P = 0.04) and a 6% decrease in PWI (P = 0.06). Myocardial ischemia (n = 3) and ventricular arrhythmias (n = 3) occurred in five patients treated with pancuronium. Only one patient treated with vecuronium had ventricular arrhythmia (P = 0.08). Seven patients treated with pancuronium and eight treated with vecuronium were taking beta-adrenergic blockers preoperatively which was associated with lower HR (96 +/- 16 vs 109 +/- 15 bpm; P = 0.025) and lower PWI (8.8 +/- 1.2 vs 10.7 +/- 1.92 mL.min-1 x 100 g-1; P = 0.003) at onset of shivering. However, beta-adrenergic blockers did not attenuate the relative HR increase induced by pancuronium. No relationship was found between hypercapnia and tachycardia or hypertension. These results suggest that, when compared to pancuronium for treatment of postoperative shivering, vecuronium may be advantageous because it does not increase myocardial work. The disproportionate relationship between VO2-I and PWI after treatment with muscle relaxants indicates that increased VO2-I does not contribute significantly to the hemodynamic disturbances associated with shivering. These disturbances are more likely the results of increased adrenergic activity related to pain and recovery from anesthesia. Shivering and its associated hemodynamic disturbances appear to be concomitant but independent signs of awakening.

Acid-Base Equilibrium↗
PubMed2004

Postanesthesia care unit recovery times and neuromuscular blocking drugs: a prospective study of orthopedic surgical patients randomized to receive pancuronium or rocuronium.

UNLABELLED: In this study, we examined the effect of choice of neuromuscular blocking drug (NMBD) (pancuronium versus rocuronium) on postoperative recovery times and associated adverse outcomes in patients undergoing orthopedic surgical procedures. Seventy patients were randomly allocated to a pancuronium or rocuronium group. On arrival to the postanesthesia care unit (PACU) and again 30 min later, train-of-four ratios were quantified by using acceleromyography. Immediately after acceleromyographic measurements, patients were assessed for signs and symptoms of residual paresis. During the PACU admission, episodes of hypoxemia, nausea, and vomiting were recorded. The time required for patients to meet discharge criteria and the time of actual PACU discharge were noted. Forty percent of patients in the pancuronium group had train-of-four ratios <0.7 on arrival to the PACU, compared with only 5.9% of subjects in the rocuronium group (P < 0.001). Patients in the pancuronium group were more likely to experience symptoms of muscle weakness (blurry vision and generalized weakness; P < 0.001) and hypoxemia (10 patients in the rocuronium group versus 21 patients in the pancuronium group; P = 0.015) during the PACU admission. Significant delays in meeting PACU discharge criteria (50 min [45-60 min] versus 30 min [25-40 min]) and achieving actual discharge (70 min [60-90 min] versus 57.5 min [45-61 min]) were observed when the pancuronium group was compared with the rocuronium group (P < 0.001). In conclusion, our study indicates that PACU recovery times may be prolonged when long-acting NMBDs are used in surgical patients. IMPLICATIONS: Clinical recovery may be delayed in surgical patients administered long-acting neuromuscular blocking drugs. During the postanesthesia care unit admission, patients randomized to receive pancuronium (versus rocuronium) were more likely to exhibit symptoms of muscle weakness, develop hypoxemia, and require more time to meet discharge criteria.

Adult↗
PubMed1991

[Nitroglycerin reduces requirement of pancuronium in surgical patients].

We performed a study on 34 adult surgical patients between 15 and 56 years of age, to evaluate whether synergism between nitroglycerin and pancuronium exists or not. Neuromuscular (NM) transmission was measured by electromyography of the thenar muscle using transcutaneous electrodes. Anesthesia was induced by droperidol 0.2 mg.kg-1, fentanyl 50 micrograms, thiamylal 150-250 mg, and succinylcholine 1 mg.kg-1, and maintained with nitrous oxide and O2 (67:33) supplemented with repeated i.v. doses of fentanyl (within 15 micrograms.kg-1). Pancuronium 4 mg was given at the 20% recovery from succinylcholine induced NM block. Sequential i.v. doses of pancuronium 1 mg were injected repeatedly at the every 20% recovery until the end of operation. To control blood pressure, nitroglycerin, ranging from 0 to 5 micrograms.kg-1.min-1, was given intravenously. The linear multiple regression analysis was performed between the dose of pancuronium (micrograms.kg-1.hr-1) and the dose of nitroglycerin (micrograms.kg-1.min-1), the age, sex, or body weight of the patients. The results show that the dose of pancuronium decreases with increasing dose of nitroglycerin. No relationship was found between the dose of pancuronium and the age, sex, or body weight of the patients. In conclusion, nitroglycerin reduces requirement of pancuronium in surgical patients.

Adolescent↗
PubMed1989

[The effect of pancuronium and norcuron on hemodynamics, coronary circulation and myocardial oxygen consumption in coronary surgery patients].

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 an introduction of anaesthesia with 0.015-0.02 mg/kg rohypnol, isoflurane (0.5 Vol%) and N2O/O2 neuromuscular blockade was induced with pancuronium or vecuronium combined with a single dose of 0.005 mg/kg fentanyl. Measurements and electrocardiogram were performed before anaesthesia, in steady state of anaesthesia and after relaxation with pancuronium or vecuronium, combined with fentanyl. The measurements consisted of heart rate (HR), cardiac index (CI), stroke volume index (SVI), mean arterial pressure (AP), total peripheral resistance (TPR), pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), right atrium pressure (RAP), myocardial blood flow (MBF), coronary vascular resistance (CVR), myocardial oxygen consumption (MVO2), coronary ateriomixed venous oxygen content difference (AVDO2cor), myocardial lactate extraction (LE) and rate pressure product (RPP). In the vecuronium group heart rate (HR) decreased significantly greater (21%) than in the pancuronium group (9%). Therefore myocardial oxygen consumption (MVO2) and coronary blood flow (CBF) diminished more in the vecuronium (48% resp. 35%) than in the pancuronium group (31% resp. 18%). The higher metabolic demand in the pancuronium group induced a significantly lower coronary vascular resistance (CVR). All the other hemodynamic parameters did not differ significantly in both patients groups. In all the patients we could not observe ST-segment depressions or elevations in the ECG, increases of PCWP or myocardial lactate productions.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1984

Time course of muscle relaxation with a combination of pancuronium and tubocurarine.

A combination of pancuronium and d-tubocurarine is associated with potentiation of the neuromuscular blocking effects of each drug used singly. The time to onset of maximum block and the time to 25% recovery after administration of equipotent (ED95) doses of pancuronium (0.07 mg/kg) alone, d-tubocurarine (0.51 mg/kg) alone, and pancuronium (0.024 mg/kg) in combination with d-tubocurarine (0.144 mg/kg) were studied in three groups of 10 patients each. The time to onset of maximum block was slightly but not significantly shorter with the combination (3.5 min) than with pancuronium (4.78 min) or d-tubocurarine (4.88 min). The time to 25% recovery with the pancuronium-d-tubocurarine combination (39.7 min) was significantly shorter than it was after d-tubocurarine (57.6 min) but not significantly different from pancuronium (54.4 min). The combination of pancuronium and d-tubocurarine also was associated with greater cardiovascular stability.

Adult↗
PubMed1980

Nitroglycerin and the neuromuscular blockade produced by gallamine, succinylcholine, d-tubocurarine, and pancuronium.

The finding in cats of prolonged pancuronium neuromuscular blockade in conjunction with intravenous infusion of nitroglycerin was previously reported by this laboratory. To expand on this finding the present study compared the effects of nitroglycerin on neuromuscular blockade produced by gallamine, d-tubocurarine, succinylcholine, and pancuronium, and further characterized the nitroglycerin-pancuronium interaction. The results indicate that of the relaxants studied only pancuronium neuromuscular blockade is prolonged, and that the prolongation is not due to altered plasma elimination of pancuronium. In vitro pancuronium blockade was not affected by nitroglycerin, suggesting the involvement of a metabolite in the block prolongation response. Reversibility of the prolonged pancuronium block by neostigmine is not influenced by nitroglycerin.

Animals↗
PubMed1978

Hypothermia and the pharmacokinetics and pharmacodynamics of pancuronium in the cat.

We tested the effect of hypothermia on the pharmacokinetics and pharmacodynamics of pancuronium in the cat. In 14 cats given pancuronium, 120 microgram/kg i.v., we found that neuromuscular block lasted between 2.5 and 3.0 times longer at 29 degrees C (N = 5) than at 34 degrees C (N = 5) or 39 degrees C (N = 4). The apparent plasma elimination half-life was 46 +/- 7 min (S.E.) at 29 degrees C as compared to 21 +/- 2 and 25 +/- 6 min at 34 and 39 degrees C, respectively. The volume of distribution of the central compartment and total volume of distribution at steady state were less at 29 and 34 dgrees C than at 39 degrees C. Total plasma clearance was 4.3 +/- 0.4 ml/kg/min at 29 degrees C and 10.7 +/- 0.9 and 10.9 +/- 1.5 ml/kg/min at 34 and 39 degrees C, respectively. The reduced plasma clearance resulted at least in part from a markedly reduced biliary and urinary excretion of pancuronium at 29 degrees C as compared to 34 and 39 degrees C. In four other cats, the plasma concentration of pancuronium was correlated with depression of twitch tension under steady-state conditions. The ED50 of pancuronium (plasma concentration required for a 50% depression of twitch tension) was 0.035 and 0.073 microgram/ml at 29 and 38 degrees C, respectively. We conclude that a pancuronium neuromuscular block is prolonged at 29 degrees C because of an increased sensitivity of the neuromuscular junction to pancuronium and delayed biliary and urinary excretion.

Animals↗
PubMed1995

Contribution of brain injury to hypertension following intravenously-administered pancuronium in rats.

Abnormal hypertension sometimes occurs following intravenous administration (i.v.) of pancuronium in patients with brain injury. The present experiment was designed to determine whether brain injury contributes to the hypertensive response of i.v. pancuronium. Forty-six Wister strain rats were studied, of which 39 had induced brain injury at (a) upper pons (b) midbrain (c) thalamus region (excluding hypothalamus) and (d) cerebellum or a combination of these sites. The injury was made by single insertion of a 22 Gauge needle through the skull surface. The quantity of pancuronium solution administered i.v. in each case was 1.0 ml containing either 0.8 mg/kg or 8 mg/kg of pancuronium. Group A (n = 7) had no brain injury and the mean arterial pressure (MAP) did not change following i.v. administration of pancuronium. In Group B (n = 9) (a+b+c, 8.0 mg/kg) MAP rose from 90.9 +/- 15.4 to 102 +/- 22.0 mmHg and in Group C (n = 7) (a+b+c, 0.8 mg/kg) MAP rose from 148.4 +/- 13.3 to 160 +/- 14.4 mmHg. In Group D (n = 5) (b+c, 8.0 mg/kg) MAP remained unchanged. In Group E (n = 5) (a, 8.0 mg/kg) MAP rose from 130.3 +/- 18.7 to 146 +/- 27.6 mmHg and in Group F (n = 6) (a, 0.8 mg/kg) MAP rose from 129.7 +/- 15.6 to 135.8 +/- 13.8 mmHg. In Group G (n = 7) (d, 8.0 mg/kg) MAP remained unchanged. Since the MAP was elevated in only those groups that received injury in the upper pons, we concluded that injury in the upper pons can lead to hypertension following i.v. administration of pancuronium.

Animals↗
PubMed2003

Prospective randomised double-blind comparative study of rocuronium and pancuronium in adult patients scheduled for elective 'fast-track' cardiac surgery involving hypothermic cardiopulmonary bypass.

The majority of cardiac anaesthetists in the UK use pancuronium for fast-track cardiac surgery. We compared the duration of action of pancuronium and rocuronium in patients undergoing fast-track hypothermic cardiopulmonary bypass and cardiac surgery. We determined whether patients would have had residual neuromuscular blockade at extubation. Twenty patients were randomly allocated to receive either pancuronium 0.1 mg x kg(-1) or rocuronium 1 mg x kg(-1). Neuromuscular function was assessed by acceleromyography; spontaneous recovery was evaluated by the train-of-four ratio measured at the adductor pollicis longus muscle. Median times to recover train-of-four ratio of 0.9 were 3 h 38 min for rocuronium and 7 h 52 min for pancuronium. The median difference in recovery times was 4 h 15 min (95% CI 2 h 30 min to 6 h 20 min; p = 0.0003 by Mann-Whitney test). None of the patients in the rocuronium group and seven of 10 patients in the pancuronium group had their extubations delayed because of residual neuromuscular blockade. Unless fast-track patients have neuromuscular function assessed before extubation, pancuronium should not be used.

Aged↗
PubMed1975

The inhibition of cholinesterases by pancuronium.

Pancuronium causes a powerful and highly selective inhibition of human serum cholinesterase in vitro. The inhibition was studied in serum from 14 individuals of both sexes (5-60 years of age) with normal reactions to suxamethonium. Pancuronium, in a concentration of 2.3 x 10(-7) M, caused a 50% inhibition of the enzymatic hydrolysis of acetylcholine, when this substrate was present in a concentration of 10 x 10(-3) M. The same I50 value was also found for a commercial preparation of human serum cholinesterase. The inhibition was reversible and competitive in type. Pancuronium inhibition of the acetylcholinesterase in human red blood cells and from the electric eel was more than one thousand times weaker. Thus pancuronium is one of the most selective inhibitors of serum cholinesterase described so far. The in vivo activity of the serum cholinesterase in four patients receiving pancuronium 0.1 mg/kg decreased, during the first 3 min, by 60-80%, from the pre-induction value. After this a slow recovery occurred with 40% depression remaining at 45 min after the injection. The tachycardia produced by pancuronium may be related to this selective inhibition of serum cholinesterase. It is suggested that relaxants which selectively inhibit serum cholinesterase also selectively block the cardiac muscarinic receptors.

Acetylcholine↗
PubMed1981

Hepatic and renal disposition of pancuronium and gallamine in patients with extrahepatic cholestasis.

The plasma clearance of pancuronium in patients with extrahepatic cholestasis was 16% lower than in a control group (1.47 +/- 0.11 ml min-1 kg-1 v. 1.76 +/- 0.21 ml min-1 kg-1), but the difference was not significant. A significant increase in the elimination half-life T 1/2 beta of pancuronium (from 141 to 224 min) and a significant increase in the volume of the peripheral compartment (V2) was found in patients with extrahepatic cholestasis when compared with control patients. There was a significantly lower cumulative biliary excretion of pancuronium (0.3 +/- 0.3% v. 10.9 +/- 3.2% in the controls) during the 48-h period of observation. The biotransformation and cumulative urinary excretion patterns of pancuronium revealed no significant differences between the two groups of patients. The increase of T 1/2 beta pancuronium in patients with extrahepatic cholestasis was mainly a consequence of the increase in the volume of distribution. No significant differences in the plasma clearance, T 1/2 beta or in the volume of distribution were observed with gallamine in the patients with extrahepatic cholestasis when compared with the control group. The cumulative urinary excretion of gallamine during 48 h in both groups of patients was approximately 100%. We concluded that in patients with cholestasis and normal glomerular filtration, gallamine is probably more reliable than pancuronium for neuromuscular blockade.

Adult↗
PubMed1984

Potentiation of neuromuscular blockade using a combination of pancuronium and dimethyltubocurarine. Studies in children following acute burn injury or during reconstructive surgery.

The neuromuscular effects of the combined administration of pancuronium and dimethyltubocurarine were evaluated in children undergoing reconstructive surgery (n = 6), or the skin grafting of acute burn wounds: body surface area (BSA) burns less than 40% (n = 5); and BSA burns greater than 40% (n = 6). A dose of pancuronium 0.005 mg kg-1 was considered to be equipotent with dimethyltubocurarine 0.02 mg kg-1, and each dose was defined as being equal to 1 relaxant equivalent (RE). Incremental doses of the combination of pancuronium and dimethyltubocurarine were administered until a 95% depression of twitch height was achieved (ED95). These results were compared with previously published data for pancuronium and dimethyltubocurarine alone. The mean ED95 of the combination in the control population (reconstructive surgery) was 5.1 RE, compared with 10.8 RE and 10.0 RE for pancuronium and dimethyltubocurarine , respectively, administered alone. In the acutely burned population, the mean ED95 for the combination was 9.9 and 15.9 RE, respectively, compared with 26 RE for pancuronium alone in burned patients. In all groups of patients, significantly less total drug was required when the combined therapy was used.

Burns↗
PubMed1979

Prolongation of pancuronium-induced neuromuscular blockade by intravenous infusion of nitroglycerin.

Based upon clinical observation of undue prolongation of pancuronium-induced blockade in the presence of intravenous infusion of nitroglycerin, neuromuscular blockades produced by pancuronium, succinylcholine and d-tubocurarine were studied in 51 cats using the sciatic-gastrocnemius nerve-muscle preparation. Pancuronium-induced blockade was found to be significantly prolonged (P less than 0.1) in the presence of a nitroglycerin infusion of 1 microgram/kg/min (65 vs. 127 min). Less, but still significant, prolongation occurred when nitroglycerin, 0.5 microgram/kg/min, was infused. The intravenous infusion of nitroglycerin must be started prior to the pancuronium injection for the block to be prolonged. Neuromuscular blocks produced by succinylcholine and d-tubocurarine were not altered by nitroglycerin. In experiments using the isolated rat diaphragm preparation, the depth of pancuronium-induced block was found not to be changed by nitroglycerin, suggesting an effect of nitroglycerin on the process of recovery from blockade. These findings indicate a selective pancuronium-nitroglycerin interaction.

Animals↗
PubMed1979

Dose-response and plasma concentration-response relationships of pancuronium in man.

The dose-response and plasma concentration-response relationships for pancuronium in man were studied during its intravenous administration to eight patients at a rate of 1.62 microgram/kg/min. The (log) dose-response relationships resulted in a sigmoid curve that was linear in its central range. At 20, 50 and 80 per cent paralysis the cumulative dosages (mean +/- SEM) were 0.04 (+/- 0.01), 0.06 (+/- 0.01), and 0.08 (+/- 0.02) mg/kg, respectively. Administration of pancuronium, 56 microgram/kg, to another 12 patients at a more rapid rate resulted in a maximum intensity of blockade of more than 50 per cent. The (log) plasma concentration-response curve was not parallel to the dose-response curve, with mean (+/- SEM) concentrations at 20, 50 and 80 per cent paralysis of 0.21 (+/- 0.04), 0.25 (+/- 0.04), and 0.30 (+/- 0.04) microgram/ml, respectively during the onset of paralysis. Following cessation of the infusion, plasma concentrations of pancuronium were usually lower for the same intensity of paralysis. Using data for the entire response range during recovery from paralysis, the mean effective plasma concentration of pancuronium for a 50 per cent response was 0.20 microgram/ml. Recovery from blockade to 95 per cent paralysis (5 per cent of control twitch height) was associated with a plasma concentration of 0.25 microgram/ml, a value in agreement with plasma concentrations obtained following a single bolus administration of pancuronium, 6 mg, to 30 patients. For 27 patients the rate of decline of paralysis from 80 to 20 per cent showed a highly statistically significant relationship to the apparent rate of decline in the plasma concentrations of pancuronium.

Adult↗
PubMed1979

Plasma concentrations of pancuronium and neuromuscular blockade after injection into the isolated arm, bolus injection, and continuous infusion.

To establish whether the plasma concentration of pancuronium reflects magnitude of neuromuscular blockade, the authors determined times of recovery from neuromuscular blockade and associated plasma concentrations following equipotent doses of pancuronium using three methods of pancuronium administration: the isolated-arm technique in conscious volunteers (n = 4), and the bolus intravenous injection (n = 7) and continuous-infusion methods (n = 3) in anesthetized patients. Although maximum depressions of twitch tension were similar (85 +/- 11,91 +/- 6, and 92 +/- 4 per cent, respectively) with the three techniques, times to recovery from neuromuscular blockade differed significantly, being 10 +/- 2 min with the isolated-arm technique, 23 +/- 7 min with the bolus-injection technique, and 46 +/- 5 min with the continuous-infusion method. The plasma concentration of pancuronium necessary for neuromuscular blockade was least with the isolated-arm technique and greatest with continuous infusion. At 25 and 75 per cent recovery, mean plasma concentrations were 0.07 +/- 0.01 and 0.04 +/- 0.01 microgram/ml in the isolated arm; 0.13 +/- 0.04 and 0.09 +/- 0.02 microgram/ml after bolus injection, and 0.20 +/- 0.04 and 0.11 microgram/ml during continuous infusion, respectively. It is concluded that the relationship between plasma concentration of pancuronium and magnitude of neuromuscular blockade depends on the method of pancuronium administration.

Humans↗