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PubMed1987

Dose-response curves for edrophonium, neostigmine, and pyridostigmine after pancuronium and d-tubocurarine.

To determine the potencies of neostigmine, pyridostigmine, and edrophonium in reversing pancuronium and d-tubocurarine blockade, dose-response curves were established for first twitch height recovery and train-of-four ratio. One hundred and twenty ASA physical status I or II patients scheduled for elective surgery received either 0.06 mg/kg pancuronium or 0.36 mg/kg d-tubocurarine during a thiopental-nitrous oxide-enflurane anesthetic. Train-of-four stimulation was applied every 12 s, and the force of contraction of the adductor pollicis muscle was recorded. When first twitch height had recovered spontaneously to 10% of its initial value, neostigmine (0.005, 0.01, 0.02 or 0.05 mg/kg), pyridostigmine (0.02, 0.04, 0.1, or 0.2 mg/kg), or edrophonium (0.1, 0.2, 0.4 or 1 mg/kg) was injected by random allocation. Recovery was measured 10 min after the injection of the antagonist. First twitch ED50's were 0.013, 0.085, and 0.17 mg/kg after pancuronium, and 0.017, 0.11, and 0.27 mg/kg after d-tubocurarine, for neostigmine, pyridostigmine, and edrophonium, respectively. The ED50 for pyridostigmine and edrophonium obtained after d-tubocurarine was significantly larger (P less than 0.05) than that after pancuronium. The train-of-four dose-response curves were significantly flatter for edrophonium than for the other two agents, indicating a greater ability of edrophonium to antagonize fade at low doses. It is concluded that the potency of reversal agents may be different for different relaxants, and that potency ratios might depend upon the end-point chosen as full neuromuscular recovery.

Adult↗
PubMed1988

Cardiovascular effects of and interaction between calcium blocking drugs and anesthetics in chronically instrumented dogs. VI. Verapamil and fentanyl-pancuronium.

To assess the interaction between verapamil and fentanyl-pancuronium, dogs were chronically instrumented to measure heart rate; PR interval; aortic, left ventricular, and left atrial pressures; and coronary, carotid, and renal blood flows. The effect of fentanyl citrate infusion on single-dose verapamil pharmacokinetics was examined in six animals. The effects of verapamil infusion (3 micrograms.kg-1.min-1 and 6 micrograms.kg-1.min-1) were examined in the conscious state and during fentanyl infusion plus pancuronium on two separate occasions in nine dogs. In addition, the effects of fentanyl citrate (500 micrograms.kg-1 followed by 1.5 micrograms.kg-1.min-1) were examined over 1 h of infusion. Fentanyl infusion did not affect single-dose verapamil pharmacokinetics. In the conscious animals, verapamil increased heart rate and PR interval, and slightly decreased LV dP/dt. Fentanyl combined with pancuronium increased mean arterial pressure and LV dP/dt. During fentanyl infusion, verapamil decreased mean arterial pressure and LV dP/dt, increased PR interval, and did not change heart rate. The hemodynamic effects of fentanyl infusion were steady over 1 h. In contrast to the inhalational anesthetics, which alter verapamil pharmacokinetics and have mainly additive effects with verapamil on left ventricular contractility, cardiac conduction, and regional blood flows, fentanyl-pancuronium had no effect on verapamil pharmacokinetics and minimal effect on verapamil pharmacodynamics in healthy dogs.

Animals↗
PubMed1988

Uptake and excretion of vecuronium bromide and pancuronium bromide in the isolated perfused rat liver.

Using the isolated perfused rat liver preparation, the disappearance from the perfusate and the excretion in the bile of vecuronium bromide and pancuronium bromide and their metabolites were followed for 2 h after the addition of 1 mg of either drug to the perfusate. In addition, the rate of change of the hepatic content of these two compounds was calculated by serially subtracting the amount of the compound and the metabolites in the bile and in the perfusate from the dose of drug added to the perfusate. It was found that, whereas the concentration of pancuronium in the perfusate declined slowly and monoexponentially, vercuronium concentration in the perfusate declined rapidly in a biexponential manner. No metabolites of either drug were detected in the perfusate. Approximately 40% of the injected dose of vecuronium was excreted in the bile as unchanged vecuronium and another 30% as the 3-hydroxy metabolite. No other metabolites of vecuronium were found in the bile. In total only about 7% of pancuronium (unchanged) was collected in the bile by the end of the experiment. It is concluded that, in comparison to pancuronium, the rat liver takes up large amounts of vecuronium rapidly, half of which is eliminated as unchanged vecuronium and half as the 3-hydroxy derivative. A small amount of vecuronium or its 3-hydroxy metabolite is returned to the perfusate from the liver. Some possible mechanisms underlying these differences are discussed.

Animals↗
PubMed1988

Actions of enflurane, isoflurane, vecuronium, atracurium, and pancuronium on pulmonary resistance in dogs.

The effects of enflurane, isoflurane, vecuronium, atracurium, and pancuronium on pulmonary resistance and heart rate were studied in 30 vagotomized dogs lying supine and anesthetized with chloralose-urethane. None of the five drugs affected pulmonary resistance when the airway was unstimulated. Enflurane and isoflurane significantly attenuated the increase in pulmonary resistance induced by electrical stimulation of the vagus nerves. This effect was dose-dependent and similar for both anesthetics at equivalent multiples of their minimum alveolar concentration. Atracurium significantly (P less than 0.05) enhanced the increase in pulmonary resistance induced by vagus nerve stimulation; vecuronium had no significant effect. Pancuronium, up to a cumulative dose of 0.14 mg/kg, also significantly (P less than 0.05) enhanced the increase in pulmonary resistance induced by vagus nerve stimulation; but this effect was reversed by further increasing the dose. Pancuronium also attenuated the cardiodecelerator response to vagus nerve stimulation in a dose-dependent fashion. The underlying mechanisms for the attenuation of responses to vagus nerve stimulation by enflurane or isoflurane or for the increase in response with atracurium are unknown. Pancuronium at lower doses increases the response most likely by blocking prejunctional muscarinic receptors (M2) that physiologically inhibit vagally mediated increases in pulmonary resistance.

Airway Resistance↗
PubMed1992

Enhanced cerebral blood flow autoregulation in the newborn piglet by d-tubocurarine and pancuronium but not by vecuronium.

Neuromuscular blockers may affect cerebral blood flow (CBF) regulation in the newborn. We studied the effects of d-tubocurarine (0.1 mg.kg-1, n = 8), pancuronium (0.1 and 0.4 mg.kg-1, n = 6 and 7), and vecuronium (0.1 and 0.4 mg.kg-1, n = 6 and 7) on CBF measured over the same range of mean systemic blood pressure ([BP] 15-122 mmHg) in each group of newborn pigs; controls received normal saline (n = 7). The levels of BP during hypotension and hypertension were scaled at intervals of 5 +/- 1.6 mmHg and adjusted by inflating balloon-tipped catheters placed in the aorta. After saline, the low dose of pancuronium (0.1 mg.kg-1), and the two doses of vecuronium, CBF was constant over the BP range of 50-90 mmHg (r = -0.07-0.35, P greater than 0.20) but varied directly with BP beyond this range (tau = 0.38 - 0.60, P less than 0.05). In contrast, in pigs treated with d-tubocurarine and high-dose pancuronium, CBF remained constant from 35 to 122 mmHg of BP (r = 0.14 - 0.37, P greater than 0.10) and changed minimally (4-12%) with BP greater than 105 mmHg compared to the other groups (41-59%, P less than 0.01). When BP was reduced below 30 mmHg, CBF also decreased less (20-38%) in animals treated with d-tubocurarine and high dose-pancuronium than after the other treatments (58-67%, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Residual postoperative paralysis. Pancuronium versus mivacurium, does it matter?

BACKGROUND: Based on a train-of-four (TOF) ratio greater than 0.70 as the standard of acceptable clinical recovery, undetected postoperative residual paralysis occurs frequently in postanesthesia care units. In most published studies, detailed information regarding anesthetic management is not provided. The authors reexamined the incidence of postoperative weakness after the administration of long- and short-acting neuromuscular blockers because few, if any, such comparative studies are available. METHODS: Ninety-one adult patients were studied. In group 1 (mivacurium, n = 35), anesthesia was induced with propofol/ fentanyl and maintained with nitrous oxide, desflurane, and opioid supplementation. The response of the adductor pollicis to ulnar nerve stimulation was estimated by palpating the thumb. Mivacurium (0.20 mg/kg) was administered for tracheal intubation, and an infusion was adjusted to maintain the TOF count at 1. When surgery was completed, the infusion was discontinued. When a second twitch could be detected, 7.0 micrograms/kg atropine and then 0.5 mg/kg edrophonium were administered. At 5 and 10 min, the mechanical TOF response was measured. Additional measurements were recorded if possible. Patients were tracheally extubated and discharged from the operating room when they could respond to verbal commands and no TOF fade was palpable. In group 2 (pancuronium-desflurane anesthesia, n = 29), the protocol was identical to that of group 1, except that 0.07 mg/kg pancuronium was administered for tracheal intubation. Additional increments (0.5 to 1 mg) were given as needed. Antagonism was accomplished with 0.05 mg/kg neostigmine and 0.01 mg/kg glycopyrrolate. In group 3 (pancuronium propofol-opioid, n = 27), the protocol was identical to that of group 2, except that anesthesia was maintained with nitrous oxide and a propofol-alfentanil infusion. In all groups, patients were assessed until a TOF ratio of 0.90 or more was achieved. RESULTS: All of the patients in group 1 had TOF ratios greater than 0.80 on arrival in the postanesthesia care unit. Twenty of 35 patients had TOF ratios 0.90 or more while they were still in the operating room. Thirty-three of 35 patients had TOF ratios 0.90 or more within 30 min of reversal, and this value was reached in all patients by 45 min. Recovery parameters in groups 2 and 3 did not differ from each other. Hence data from these groups were pooled. Fifty-four of 56 patients who received pancuronium had TOF values of 0.70 or more, the remaining two patients had values of 0.6 to 0.7. In contrast to the mivacurium group, however, only four patients achieved a TOF ratio of 0.90 or greater while still in the operating room. Finally, eight of these patients did not achieve this degree of recovery within 90 min of reversal. CONCLUSIONS: These results suggest that if nondepolarizing neuromuscular blockers are administered using tactile evaluation of the TOF count as a guide, critical episodes of postoperative weakness in the postanesthesia care unit should occur infrequently even with long-acting relaxants. Nevertheless, if full recovery is defined as return to a TOF ratio of 0.90 or more, then short-acting agents would appear to offer a wider margin of safety.

Adult↗
PubMed1979

Adverse effects of pancuronium in patients with hemorrhagic shock.

Thirty-five patients with hemorrhagic shock had surgical repair of trauma to the great vessels using a ketamine-pancuronium-nitrous oxide sequence for anesthesia. The data of the cardiovascular and respiratory changes occurring during anesthesia and the operation were tabulated and subjected to multifactorial computer analysis. Fifteen patients died during or after operation because the injury was beyond repair. Twenty survived the oepration. Profound hypotension associated with mild tachycardia occurred with surprising regularity each time incremental doses of pancuronium were administered in nearly all patients. This hypotension was not associated with the administration of any other drug or with any other parameter and strongly implicates pancuronium as the causative factor. Pancuronium should be used cautiously and administered in small increments to this type of patient if it is used as a muscle relaxant.

Anesthesia, Endotracheal↗
PubMed1984

Comparison of intubating conditions with atracurium, vecuronium and pancuronium.

A blind trial, comparing time of onset of satisfactory conditions for tracheal intubation with atracurium 0.6 mg/kg, vecuronium 0.1 mg/kg and pancuronium 0.1 mg/kg is described. Intubation was attempted at 30-second intervals in 60 patients, randomly allocated to receive one of the above muscle relaxants. Patients receiving atracurium 0.6 mg/kg could be intubated from 30 to 120 seconds. Patients receiving either vecuronium 0.1 mg/kg or pancuronium 0.1 mg/kg were able to be intubated between 60 and 240 seconds. The results showed a statistically significant earlier onset of satisfactory intubating conditions with atracurium than with vecuronium or pancuronium in these doses but no difference between vecuronium and pancuronium.

Adolescent↗
PubMed1993

Suxamethonium myalgia: an ethnic comparison with and without pancuronium pretreatment.

The incidence of myalgia after suxamethonium was determined in 200 fit military male dental patients of European, Chinese and Nepalese descent. Half received pancuronium 1 mg and the other half received saline pretreatment on a randomised double-blind basis. The percentage incidence of postsuxamethonium myalgia after saline or pancuronium was found to be: Europeans 26%, 13%; Chinese 13%, 7%; Nepalese 20%, 14%. Although pancuronium reduced the incidence of myalgia by about 50% overall, these values were not significantly different from each other. The recovery of spontaneous ventilation following suxamethonium was quicker in the Europeans than in the Asians (p < 0.05). Pancuronium pretreatment also delayed the recovery of spontaneous ventilation and recovery from neuromuscular block (p < 0.05) but this was independent of ethnicity. The Europeans recovered from anaesthesia more quickly than the Asians. It was concluded that ethnicity affected recovery from suxamethonium and from anaesthesia but was not of clinical relevance to the incidence of myalgia in male Asians and Europeans.

Adolescent↗
PubMed1975

Ketamine-pancuronium induction in patients with aortic stenosis.

In 15 patients with severe aortic stenosis who were to undergo aortic valve replacement, the induction sequence ketamine followed by pancuronium caused a 25% rise in systolic blood pressure. In a similar series, the induction sequence diazepam + morphine followed by pancuronium caused a 22% fall in systolic blood pressure. This shows that the blood pressure rise caused by ketamine is not blocked by pancuronium, although pancuronium may possibly modify the cardiovascular responses to this drug.

Aged↗
PubMed1985

Circulatory effects of pancuronium and alcuronium in patients with coronary artery stenosis.

Heart rate and systemic arterial blood pressure were recorded during induction of anaesthesia up to 9 min after endotracheal intubation in 92 patients scheduled for coronary artery bypass surgery, in order to study to what degree the circulatory response to induction of anaesthesia and intubation was modified by different relaxants. Pancuronium (pancuronium bromide) 0.1 mg X kg b.w.-1 and alcuronium (diallyl-nortoxiferine) 0.25 mg X kg b.w.-1 were randomly studied in 36 patients during induction with high-dose fentanyl and in 36 patients induced with thiopentone, diazepam, fentanyl and nitrous oxide. In patients given high-dose fentanyl anaesthesia, systolic blood pressure before, during and after intubation was significantly lower with alcuronium (P less than 0.01). The same difference between alcuronium and pancuronium was observed in balanced anaesthesia before endotracheal intubation. Induction of anaesthesia and intubation were followed by a moderate increase in heart rate, irrespective of the type of anaesthesia and relaxant. Subsequently, 20 patients (10 with high-dose fentanyl and 10 with balanced anaesthesia) were studied. They received pancuronium 0.05 mg X kg b.w.-1 + alcuronium 0.125 mg X kg b.w.-1. This mixture of relaxants produced an intermediate blood pressure response.

Adjuvants, Anesthesia↗
PubMed1988

Neostigmine and edrophonium as antagonists of atracurium and pancuronium.

Edrophonium 0.5 mg/kg or neostigmine 0.04 mg/kg were administered to two groups of 30 patients each for antagonism of atracurium- or pancuronium-induced neuromuscular block at 25% single twitch recovery. Neuromuscular block was studied using both single twitch and train-of-four (TOF) nerve stimulation. The times to 100% single twitch recovery were significantly more rapid for patients receiving edrophonium (P less than 0.01) in both groups (atracurium and pancuronium); the TOF ratios were similar for atracurium, but for pancuronium they were greater after neostigmine than after edrophonium, and only at 25 min were these ratios similar. It is concluded that edrophonium in a dose of 0.5 mg/kg antagonizes neuromuscular blockade induced by atracurium, as does neostigmine in a dose of 0.04 mg/kg, but the former does not consistently antagonize neuromuscular blockade induced by pancuronium even at 25% of single twitch recovery.

Adult↗
PubMed1991

Pretreatment with pancuronium before suxamethonium administration in patients heterozygous for the usual and the atypical plasma cholinesterase gene.

The object of this study was to investigate whether pretreatment with pancuronium before i.v. injection of suxamethonium could cause prolonged neuromuscular blockade in patients heterozygous for the usual and the atypical plasma cholinesterase gene (E1uE1a). Forty-three patients, 23 with genotype E1uE1a and 20 with normal genotype (E1uE1u), were pretreated with pancuronium 0.01 mg.kg-1 followed by suxamethonium 1.5 mg.kg-1, and received either neurolept anaesthesia or halothane anaesthesia. Seven patients (E1uE1a) were given suxamethonium 1.5 mg.kg-1 without pretreatment. The duration and type of neuromuscular block were evaluated using train-of-four (TOF) nerve stimulation. Type of anaesthesia did not significantly influence the results. The duration of block following pretreatment was significantly longer in heterozygous patients than in normal patients. Time to 90% twitch height recovery was 10.7 +/- 1.2 min (mean +/- s.d.) in genotypically normal patients, and 18.0 +/- 4.2 min in patients with genotype E1uE1a. Pretreatment with pancuronium caused a significantly slower recovery of the TOF ratio (phase II block). Thus, a TOF ratio of 0.7 was always reached within 13 min in genotypically normal patients. In genotypically abnormal patients, the same TOF ratio was reached within 20 min in all but three patients. In these three patients time to 90% twitch height recovery was prolonged (18-31 min), and TOF ratio did not return to normal, but stabilized at about 0.35, 0.50, and 0.65, respectively. Injection of edrophonium restored normal neuromuscular function in 10 min. It is concluded that in patients heterozygous for the usual and the atypical gene, pretreatment with pancuronium in combination with an increased dose of suxamethonium may cause a phase II block and thus a prolonged neuromuscular block.

Adult↗
PubMed1995

Train-of-four recovery after pharmacologic antagonism of pancuronium-, pipecuronium-, and doxacurium-induced neuromuscular block in anaesthetized humans.

Previous studies have suggested that the increased duration of action of long-acting neuromuscular relaxants may make their pharmacologic antagonism more difficult and, thus, increase the likelihood of residual block. This hypothesis was tested in healthy, adult humans who received a background of isoflurane/N2O/fentanyl anaesthesia. Study subjects were paralyzed with either pancuronium (N = 8), pipecuronium (N = 8), or the longer-acting relaxant, doxacurium (N = 8). Neuromuscular function was monitored, and, using a blinded, randomized study design, the relaxants were titrated to identify the ED95 dose in each patient. Thereafter, spontaneous recovery was observed until there was 25% of baseline response to the first supramaximal twitch (T1) in a train-of-four (TOF). At this time, the block was antagonized with neostigmine 0.07 mg/kg and glycopyrrolate 0.014 mg/kg i.v., and recovery of TOF was recorded. Spontaneous recovery to 25% of the baseline T1 response occurred at 52 +/- 14 min (mean +/- SD) following administration of either pancuronium and pipecuronium, and 85 +/- 33 min following doxacurium (P < 0.05 for doxacurium versus pancuronium and pipecuronium). In doxacurium-treated patients, reversal of block with neostigmine was less predictable and less complete than with the other two relaxants. For example, the ratio of the fourth to first twitch (T4/T1) of the TOF at 10 and 15 min after reversal was significantly less with doxacurium (59 +/- 14% and 61 +/- 16%, respectively) than with either pancuronium (75 +/- 6% and 75 +/- 10%) or pipecuronium (76 +/- 9% for both).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1989

In vitro time course studies on train-of-four fade induced by hexamethonium, pancuronium and decamethonium in the rat hemidiaphragm.

1. In vitro time course studies on the effects of hexamethonium (7 mmol/L), pancuronium (5 mumol/L) and decamethonium (220 mumol/L) on nerve-evoked (2 Hz for 2 s every 20 s) maximal twitches (T1, T2, T3, T4) of the rat hemidiaphragm were conducted. All three drugs progressively depressed all four twitches in a given train but at different rates (T4 greater than T3 greater than T2 much greater than T1). 2. The response-time profiles for T1 and T4 varied widely for the three drugs such that, for the same degree of T1-block, each drug produced a different magnitude of T4-block during the onset of and recovery from neuromuscular blockade. 3. Analysis of the T1 versus T4/T1 plot showed that, at 50% T1-block, the corresponding T4/T1 (i.e. train-of-four ratios) during the onset (and recovery) phase were 0.16 (0.29), 0.46 (0.40) and 0.66 (0.53) for hexamethonium, pancuronium and decamethonium, respectively. Thus, for the same degree (i.e. 50%) of twitch (T1) tension depression, the three drugs differed widely in their ability (hexamethonium much greater than pancuronium greater than decamethonium) to produce fade as reflected in the respective train-of-four ratio. 4. Our results therefore show that the train-of-four ratio (T4/T1) at 50% T1-block obtained from such in vitro time course studies is a useful quantitative index of the potential of various drugs to cause train-of-four fade. Based on this index a classification of various compounds already studied is proposed as follows: hexamethonium much greater than pancuronium approximately (+)-tubocurarine greater than decamethonium approximately succinylcholine much greater than alpha-bungarotoxin.

Animals↗
PubMed1980

A comparison of the effects of pancuronium bromide and its monoquaternary analogue, ORG NC 45, on autonomic and somatic neurotransmission in the rat.

1 Potentiation by pancuronium of the effects of adrenergic nerve stimulation, previously shown in cardiovascular tissues, was also found in rat anococcygeus and vas deferens, in vitro or in vivo. 2 In the pithed rat, in the presence of pancuronium, pre-junctional alpha-adrenoceptor-mediated feedback inhibition of cardiac sympathetic transmission was uncovered at relatively low stimulation frequencies by phentolamine or yohimbine. 3 The effects of pancuronium and its mono-quaternary analogue Org NC 45 on autonomic and somatic neuromuscular transmission were compared, in the pithed rat. Org NC 45 was less potent than pancuronium at blocking somatic neuromuscular transmission by a factor of 2.1, at blocking cardiac, parasympathetic transmission by a factor of 538 and at potentiating sympathetic transmission by a factor of 33.

Animals↗
PubMed1985

Failure of gallamine and pancuronium to inhibit selectively (-)-[3H]quinuclidinyl benzilate binding in guinea-pig atria.

Binding of (-)-[3H]quinuclidinyl benzilate (QNB) to muscarinic sites in guinea-pig atrial and ileal longitudinal muscle homogenates showed the presence of a single population of binding sites in atria (KD = 41 (32-53) (95% confidence limits) pM; Bmax = 0.225 +/- 0.02 pmol/mg protein (3)) and two binding sites in the ileum (KD = 20.9 (8.8-49) pM and 11.3 nM; Bmax = 0.436 +/- 0.09 and 11.85 +/- 2.63 pmol/mg protein (4), respectively). Atropine, gallamine, and pancuronium displaced (-)-[3H]QNB binding from the high affinity binding sites in the two tissues in a dose-dependent manner with -log Ki values of 8.6, 6.4, and 6.9, respectively, in atria and 8.7, 6.8, and 6.9, respectively, in ileal longitudinal muscle. The lack of selectivity of gallamine and pancuronium in binding experiments differed from results obtained in isolated tissue experiments where these antagonists showed a marked difference in their ability to antagonize cholinomimetics in the two tissues. In addition, the Ki values for gallamine and pancuronium in ileal homogenates were ca. 130- and 16-fold lower, respectively, than their KB values determined from isolated tissue experiments. Attempts to correlate data from binding experiments and isolated tissue experiments using combinations of antagonists led to variable results attributed to differences in the rates of dissociation of the antagonists from muscarinic receptors. It is concluded that the interaction of gallamine or pancuronium with agonists or antagonists at muscarinic receptors is not a simple bimolecular interaction.

Animals↗
PubMed1994

Pre- and postsynaptic mechanisms involved in tetanic fade induced by pancuronium in the isolated rat muscle.

The mechanisms underlying the fade of the tetanic contraction induced by pancuronium were studied in vitro by means of myographical and electrophysiological techniques in the extensor digitorum longus muscle of the rat. Pancuronium (0.5 mumol/l) induced a complete fade of the tetanic contraction while leaving the twitch unaffected. At the same concentration it decreased the amplitude and increased the tetanic rundown of trains of endplate potentials (e.p.ps) evoked in the frequency of 50 Hz. The electrophysiological changes induced by pancuronium were due to decreases in both quantal sizes and quantal contents of the e.p.ps. The former effect was the result of a postsynaptic competitive action and the latter of a presynaptic inhibitory action of that compound. The decrease in quantal content affected the e.p.ps starting from the first in the train and became larger during the generation of the sequence of e.p.ps. This intensified their tetanic rundown. It is concluded that the fade of the tetanic contraction induced by pancuronium is due to a summation of pre- and postsynaptic actions and, therefore, not only to an increase in the tetanic rundown of e.p.ps. Possible explanations for the distinct abilities of neuromuscular blockers in affecting tetani and twitches in a differential manner are also discussed.

Animals↗