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At least 19 recordsLinked to original sources

PubMed1989

Comparison of tracheal intubating conditions and neuromuscular blocking profiles after intubating doses of mivacurium chloride or succinylcholine in surgical outpatients.

Thirty ASA physical status I or II outpatients scheduled to undergo short procedures (less than 1 hr in duration) requiring tracheal intubation received either 1.0 mg/kg succinylcholine or 0.20 mg/kg (2.5 x ED95) or 0.25 mg/kg (3 x ED95) mivacurium. A N2O/O2/narcotic anesthetic technique was utilized and the ulnar nerve was stimulated with subcutaneous electrodes placed at the wrist. Tracheal intubation was attempted in all patients either 2 min after mivacurium or 1 min after succinylcholine. Intubation conditions were not different between the succinylcholine and mivacurium groups or between the two mivacurium groups. The onset and duration of neuromuscular blockade were shorter with succinylcholine than with mivacurium. Suppression of the T1 response to 90% of baseline occurred in 0.9 min with 1.0 mg/kg succinylcholine and at 2.2 and 1.5 min respectively, with 0.20 mg/kg and 0.25 mg/kg mivacurium. Initial recovery of the T1 response occurred at 6.4 min after 1.0 mg/kg succinylcholine and 12.7 and 13.6 min respectively after 0.20 mg/kg and 0.25 mg/kg mivacurium. Subsequent to initial recovery from the intubating dose of relaxant, infusions of mivacurium or succinylcholine were administered to maintain approximately 95% block. The mean infusion rates were 6.6 micrograms.kg-1.min-1 mivacurium and 41.2 micrograms.kg-1.min-1 for succinylcholine. Spontaneous recovery from neuromuscular blockade occurred more quickly after succinylcholine than after mivacurium: the time from cessation of infusion to recovery of T1 to 95% of baseline was 6.5 min in patients given succinylcholine and 16.7 min in patients given mivacurium. When reversal was in order, residual mivacurium-induced blockade was readily antagonized by 0.045 mg/kg neostigmine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1986

Increases in intracranial pressure from succinylcholine: prevention by prior nondepolarizing blockade.

Whether succinylcholine causes an increase in intracranial pressure (ICP) in patients with brain lesions is uncertain and, if increased ICP does occur, its pathophysiology remains unknown. The authors investigated both the effect of succinylcholine on ICP and its modification with prior neuromuscular blockade by measuring ICP (subarachnoid bolt) in 13 consecutive patients with brain tumors who received succinylcholine both before and after complete neuromuscular blockade with vecuronium. Anesthesia was induced with thiopental, 6 mg X kg-1 iv, and nitrous oxide, 70% in oxygen, while ventilation was controlled (PaCO2 = 37.2 mmHg +/- 1.7 SE). Succinylcholine, 1 mg X kg-1 iv, was administered and ICP, heart rate (HR), and blood pressure (BP) were recorded until normal twitch tension was restored. Complete neuromuscular blockade was then established with vecuronium, 0.14 mg X kg-1 iv; 3 min later, succinylcholine, 1 mg X kg-1 iv, was repeated. The resulting changes in ICP, HR, and BP were recorded for 3 min. Following the first dose of succinylcholine, mean ICP increased from 15.2 mmHg +/- 1.3 SE to 20.1 mmHg +/- 2.0 SE (P less than 0.05), with five of the patients sustaining increases in ICP of 9 mmHg or greater. In contrast, when succinylcholine was given after vecuronium-induced paralysis, no patient developed an increase in ICP greater than 3 mmHg (P less than 0.05 compared with the incidence of ICP greater than or equal to 9 mmHg observed after the first dose of succinylcholine). A second group of six patients received two doses of succinylcholine according to the same protocol but without an intervening dose of vecuronium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Prolongation of succinylcholine block by metoclopramide.

Laboratory and clinical evidence of the inhibition of plasma cholinesterase by metoclopramide was demonstrated. When succinylcholine is used as the substrate and the product choline assayed by choline oxidase-peroxidase-quinone dye colorimetry, the rate of the choline production as optical density change was reduced to 50% by 19.5 X 10(-6) M metoclopramide at 20 degrees C. Prolongation of neuromuscular blockade produced by concurrent administration of succinylcholine and metoclopramide was studied in 22 patients aged between 18 and 40 years undergoing elective gynecological surgery. EMG activity in the adductor pollicis muscle was recorded in response to a train-of-four (TOF) stimulus delivered every 10 s. Patients were randomly divided into two groups: A and B. In both groups, anesthesia was induced with thiopental and maintained with sufentanil and nitrous oxide. Tracheal intubation followed intravenous succinylcholine. Intraoperatively, after returning of neuromuscular function, patients in both groups received 20 mg succinylcholine for the determination of duration of neuromuscular blockade. Time from 95% suppression of baseline twitch following a 20 mg increment of succinylcholine until recovery to 25% of control activity was determined. Thereafter, in group A, patients receive metoclopramide (10 mg iv) followed by succinylcholine 20 mg iv, and patients in group B received succinylcholine 20 mg iv alone. Recovery times were again measured and found to be prolonged in patients receiving metoclopramide compared with those not receiving metoclopramide (P less than 0.05). Metoclopramide has no intrinsic neuromuscular blocking activity, but its ability to inhibit plasma cholinesterase probably is the mechanism by which it prolongs succinylcholine block. Reducing the dose of succinylcholine may be appropriate when metoclopramide is given concurrently.

Adult↗

PubMed1992

Evaluation of the endotracheal intubating conditions of rocuronium (ORG 9426) and succinylcholine in outpatient surgery.

The time-course of action and tracheal intubating conditions of rocuronium and succinylcholine under intravenous anesthesia with propofol, alfentanil, and nitrous oxide were studied in 30 patients undergoing outpatient surgery. The neuromuscular effects of both drugs were quantified by recording the indirectly evoked twitch response of the adductor pollicis muscle after ulnar nerve stimulation (0.1 Hz, 0.2 ms supramaximal stimuli). Patients were given either 0.6 mg/kg rocuronium (n = 20) or 1 mg/kg succinylcholine (n = 10) intravenously. Sixty seconds after the administration of the muscle relaxant, the trachea was intubated and the intubating conditions were scored by a "blinded" assessor. Intubating conditions were not different (P = 0.34) between the rocuronium and succinylcholine groups. The onset and duration of neuromuscular blockade were shorter with succinylcholine than with rocuronium. The depression of the twitch response to 5% of control value occurred in 0.8 +/- 0.1 min with 1 mg/kg succinylcholine and 1.2 +/- 0.5 min with 0.6 mg/kg rocuronium (P less than 0.01). The recovery of the twitch response to 25%, 75%, and 90% of its control value was shorter after succinylcholine (P less than 0.001) and occurred at 8.1 +/- 2.6, 10.3 +/- 3.9, 11.3 +/- 4.6 and 25.3 +/- 5.0, 33.1 +/- 5.9, 36.1 +/- 6.3 min after succinylcholine and rocuronium, respectively. Also the time required for spontaneous recovery from 25% to 75% of the control twitch response was significantly shorter (P less than 0.001) after succinylcholine (2.2 +/- 1.4 min) than after rocuronium (7.8 +/- 2.1 min). It is concluded that in spite of the pharmacodynamic differences between succinylcholine and rocuronium, the intubating conditions after administration of both compounds are similar and develop at the same rate.

Adult↗

PubMed1992

Rapid-sequence intubation of head trauma patients: prevention of fasciculations with pancuronium versus minidose succinylcholine.

INTRODUCTION: Fasciculations during rapid-sequence intubation may lead to increased intracranial pressure and emesis with aspiration. Standard rapid-sequence intubation requires a nondepolarizing blocking agent before succinylcholine administration. HYPOTHESIS: Prevention of fasciculations during rapid-sequence intubation of head trauma patients can be accomplished as safely and effectively with minidose succinylcholine as with a defasciculating dose of pancuronium. DESIGN: A prospective, randomized, double-blind study. SETTING: An inner-city county trauma center with 70,000 patient visits per year. PARTICIPANTS: Sequential adult head trauma patients requiring rapid-sequence intubation who had no contraindications to succinylcholine or pancuronium. INTERVENTIONS: Each head trauma patient requiring rapid-sequence intubation who met the inclusion criteria received standard rapid-sequence intubation maneuvers and lidocaine (1 mg/kg) IV. Patients were randomized to receive either minidose succinylcholine (0.1 mg/kg) or pancuronium (0.03 mg/kg) IV one minute prior to the full paralytic dose of succinylcholine (1.5 mg/kg) IV. Fasciculations were recorded using a graded visual scale. RESULTS: Of 46 patients, eight of 19 (42%) in the pancuronium group and six of 27 (22%) in the succinylcholine group experienced fasciculations. No statistically significant difference in fasciculations was detected between the two groups using chi 2 analysis. Complete relaxation of the cords was present in all but two patients, one in each group. No patient in either group experienced emesis or significant dysrhythmias. CONCLUSION: Pretreatment with minidose succinylcholine causes no greater incidence of fasciculations than pancuronium in rapid-sequence intubation of head trauma patients in an ED setting. Thus succinylcholine may be used as the sole paralytic agent in rapid-sequence intubation of head trauma patients.

Adult↗

PubMed1992

Tyraminelike action of succinylcholine in the isolated, blood-perfused canine atrium.

The mechanisms of succinylcholine-induced cardiac effects have not been fully elucidated. Accordingly, we studied the effects of succinylcholine on atrial rate and contractile force in the isolated canine atrium perfused with donor blood. The sinus node artery was perfused with heparinized blood from the common carotid artery of the donor dog at a constant pressure of 100 mm Hg. When succinylcholine in a dose range of 30-1000 micrograms was injected directly into the sinus node artery of the isolated atrium, increases in atrial rate and contractile force were observed in a dose-related manner. The atrial rate and contractile force were increased to 10.5% +/- 1.8% (mean +/- SEM) and 56.8% +/- 8.5% above the control values after the administration of 1000 micrograms of succinylcholine, respectively. After treatment with propranolol, the positive chronotropic and inotropic effects of succinylcholine and norepinephrine were significantly suppressed. Hexamethonium or tetrodotoxin pretreatment inhibited the cardiac effects of nicotine but did not modify the succinylcholine-induced cardiac effects. The succinylcholine-induced effects were significantly inhibited by treatment with imipramine, which also suppressed the tyramine-induced effects. We conclude that succinylcholine has cardioexcitatory properties mediated by release of catecholamine due to a tyraminelike action.

Animals↗

PubMed1989

Ketamine enhances phase I and phase II neuromuscular block of succinylcholine.

The effect of intravenous injection of ketamine 2, 5 and 10 mg.kg-1 on the neuromuscular blocking action of succinylcholine was studied on the indirectly stimulated adductor pollicis muscle twitch of monkeys anaesthetized with 0.5-1.0 per cent halothane in oxygen. Neuromuscular block was quantified by single twitches evoked at 0.1 Hz. The changing nature of neuromuscular block from Phase I to Phase II was monitored periodically by train-of-four fade. In the absence of succinylcholine, ketamine had no consistent neuromuscular effect of its own. In the presence of succinylcholine, ketamine in a dose-dependent manner potentiated both the Phase I and the Phase II neuromuscular blocking effect of succinylcholine. In Phase I, 2 mg.kg-1 of ketamine reduced the ED50 of succinylcholine from 0.46 +/- 0.07 mg.kg-1 to 0.33 +/- 0.06 mg.kg-1 (P less than 0.01), and increased its 25-75 per cent recovery index from 4.0 +/- 0.4 min to 5.3 +/- 0.1 min (P less than 0.01). In Phase II, ketamine in the same dose deepened a steady neuromuscular block maintained by succinylcholine infusion from 48 +/- 3 per cent block to 71 +/- 2 per cent block (P less than 0.01). We concluded that ketamine potentiates the Phase I and the Phase II neuromuscular blocks of succinylcholine.

Anesthesia, Inhalation↗

PubMed1990

Paraben preservatives but not succinylcholine are cerebral vasodilators in vitro.

Since the increase in intracranial pressure produced by succinylcholine is temporally associated with intravenous administration, we investigated in vitro a possible direct cerebrovascular effect of this nicotinic drug. Isometric responses were recorded from dog and guinea pig basilar artery rings suspended in modified Krebs' solution at 37 degrees C. After precontracting with a voltage (KCl)- or a receptor (5-hydroxytryptamine)-mediated agonist, cumulative concentration-relaxation curves were established for: pure succinylcholine; Quelicin from multidose vials containing 20 mg/ml succinylcholine, 1.8 mg/ml methylparaben, and 0.2 mg/ml propylparaben; Anectine from single-dose vials containing 20 mg/ml succinylcholine; multidose Anectine containing 20 mg/ml succinylcholine and 1.0 mg/ml methylparaben; and methylparaben and propylparaben alone. When required, the endothelium of dog artery was removed by gentle mechanical rubbing and the response to the drugs reevaluated. Both Quelicin and multidose Anectine produced statistically significant (P less than 0.05) relaxation; Quelicin was the more potent of the two. Methylparaben and propylparaben produced relaxation in an additive manner and completely accounted for the relaxation produced by Quelicin and multidose Anectine. The vascular relaxation was found to be independent of the presence of a functional endothelium. Consistent with a nicotinic induced contraction, pure succinylcholine maintained vessel tone. It is concluded that the pharmaceutically ubiquitous preservatives methylparaben and propylparaben but not pure succinylcholine have vasoactive properties in vitro.

Animals↗

PubMed1991

Pretreatment with d-tubocurarine, vecuronium, and pancuronium attenuates succinylcholine-induced increases in plasma norepinephrine concentrations in humans.

We studied in patients the effect of d-tubocurarine, which has sympathetic ganglion blocking action, on succinylcholine-induced increases in plasma levels of catecholamines, and compared it with the effects of vecuronium and pancuronium, which have little sympathetic ganglion blocking action. Thirty-two patients were divided into five groups: seven were given 3 mL saline; seven received 1 mg/kg succinylcholine; and six, seven, and five patients were given 0.08 mg/kg d-tubocurarine, 0.01 mg/kg vecuronium, and 0.01 mg/kg pancuronium, respectively, all of which were injected 5 min before 1 mg/kg succinylcholine. Succinylcholine alone significantly increased plasma norepinephrine concentrations, systolic blood pressure, and heart rate from 187 +/- 39 pg/mL (mean +/- SEM), 93 +/- 2 mm Hg, and 77 +/- 4 beats/min to 429 +/- 61 pg/mL, 120 +/- 7 mm Hg, and 102 +/- 6 beats/min, respectively, with onset of fasciculations. Pretreatment with d-tubocurarine, vecuronium, and pancuronium significantly and equally attenuated both the fasciculations and the cardiovascular responses to succinylcholine. These results suggest that the sympathetic ganglion blocking action of neuromuscular relaxants when given before succinylcholine is not an important factor in attenuation of succinylcholine-induced increases in plasma levels of catecholamines.

Adult↗

PubMed1991

Effects of succinylcholine on the pharmacodynamics of pipecuronium and pancuronium.

To study the effects of succinylcholine on subsequent pharmacodynamics of nondepolarizing muscle relaxants, a comparative pharmacodynamic study was carried out in patients having balanced anesthesia (thiopental, fentanyl, nitrous oxide/oxygen) in whom equipotent doses of pipecuronium (80 micrograms/kg) and pancuronium (100 micrograms/kg) were given with or without prior administration of succinylcholine (1 mg/kg). Fifty-two patients were randomly assigned to one of the following four groups: 1, pancuronium (100 micrograms/kg); 2, pipecuronium (80 micrograms/kg); 3, succinylcholine (1 mg/kg) plus pancuronium (100 micrograms/kg); and 4, succinylcholine (1 mg/kg) plus pipecuronium (80 micrograms/kg). In groups 3 and 4, the nondepolarizing relaxant was given after succinylcholine when the twitch height recovered to 75% of its control value. For maintenance of neuromuscular blockade, additional increments of pancuronium (20 micrograms/kg) or pipecuronium (15 micrograms/kg) were given. Neuromuscular function was monitored throughout induction, maintenance, spontaneous recovery, and pharmacologic reversal of the neuromuscular block. Mean onset times for pancuronium (group 1) and pipecuronium (group 2) given without succinylcholine were (mean +/- SEM) 2.5 +/- 0.3 and 2.8 +/- 0.2 min, respectively. Mean onset times (times to maximum twitch depression) of the two drugs given after succinylcholine (groups 3 and 4) were significantly shorter (1.4 +/- 0.4 and 1.6 +/- 0.1 min, respectively). Clinical durations (i.e., until 25% twitch recovery of pancuronium and pipecuronium) were not significantly different among the four groups, varying from 81.1 +/- 5.4 (group 4) to 107.0 +/- 17.0 (group 2) min.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1979

Effect of pancuronium on intraocular pressure changes induced by succinylcholine.

The study was undertaken to evaluate the influence of pretreatment with a small dose of pancuronium on intraocular pressure changes associated with administration of succinylcholine and tracheal intubation. Thirty patients divided into control and study groups were anaesthetized with sodium thiopentone (3-5 mg mg.kg-1) and intubation with the aid of succinylcholine (1 mg.kg-1). The control group received saline pretreatment while the study group received pancuronium 1 mg three minutes before succinylcholine. Anaesthesia was maintained with nitrous oxide and oxygen (70:30). A Schiotz tonometer was used to measure intraocular pressure before induction of anaesthesia, one minute after succinylcholine and immediately after intubation. Patients in the control group demonstrated significant elevation of intraocular pressure at one minute after succinylcholine and immediately after intubation, while the study group showed no significant change at the same observation periods. These findings indicate that pretreatment with pancuronium 1 mg three minutes before succinylcholine may be beneficial in patients with high intraocular pressure and penetrating injuries of the eye.

Adolescent↗

PubMed1977

Dual action of pancuronium on succinylcholine block.

The effects of pretreatment with both sub-paralyzing and paralyzing doses of pancuronium and d-tubocurarine, on the onset and duration of succinylcholine-induced neuromuscular blockade were evaluated and compared in 225 patients. D-tubocurarine antagonized both onset and duration of succinylcholine block, while pancuronium produced a dual effect, antagonizing the onset and potentiating the duration of succinylcholine block. Pretreatment with d-tubocurarine (0.07 mg/kg, 0.3 mg/kg and 0.6 mg/kg) increased the time to onset of succinylcholine paralysis from 28 to 118%, and decreased the duration from 16 to 37%. Pancuronium (0.02 mg/kg, 0.04 mg/kg and 0.08 mg/kg) also antagonized the onset of succinylcholine paralysis with increases of 32 to 114%, but potentiated its duration from 30 to 103% compared with succinylcholine alone in the same patients. Although pancuronium markedly inhibited serum cholinesterase in vitro (I50=5 X 10(-7) mol) there was only a 10% inhibition of cholinesterase in vivo after pancuronium 0.08 mg/kg.

Adult↗

PubMed1987

The effects of succinylcholine on mouth opening.

Mouth opening and the resistance to opening developed by the muscles of mastication were measured in 63 children anesthetized with halothane and relaxed with succinylcholine, pancuronium, or vecuronium. Measurement of mouth opening, induced by a constant test force, was made when each patient was deeply anesthetized, as judged by clinical parameters. Succinylcholine, vecuronium, or pancuronium was then administered. The mouth opening measurement was repeated immediately after the loss of limb muscle twitch response and 45 s following the loss of twitch response. For the 24 patients receiving succinylcholine, there was a significant reduction in mean mouth opening (P less than 0.0001) and a significant increase in jaw stiffness (P less than 0.0001) immediately after limb relaxation. Forty-five seconds after full limb relaxation was attained, the mean mouth opening was still reduced (P less than 0.0001) and the mean jaw stiffness was still increased (P less than 0.0003) in the succinylcholine group. Patients receiving either vecuronium or pancuronium did not show a significant change of mouth opening or jaw stiffness following limb relaxation. Three patients, who received succinylcholine, required several attempts at tracheal intubation due to increased resistance to mouth opening. Anesthesia and surgery proceeded in all patients. None of the patients developed malignant hyperthermia. In view of the fact that a reduction in mouth opening was a constant finding when succinylcholine was administered during halothane anesthesia, the assumption that isolated "masseter spasm" or jaw stiffness heralds malignant hyperthermia should be reconsidered.

Anesthesia, Inhalation↗

PubMed1990

Quantitation of the interaction between atracurium and succinylcholine using closed-loop feedback control of infusion of atracurium.

The authors used closed-loop feedback control of infusion of atracurium to study the effect of prior administration of succinylcholine on neuromuscular blockade induced by atracurium in patients undergoing otolaryngologic surgery. Anesthesia was maintained with nitrous oxide in oxygen, flunitrazepam, and fentanyl. Of 14 patients given atracurium, seven were given prior administration of succinylcholine and seven were not. Interaction between the two drugs was quantified by determining the asymptotic steady-state rate of infusion necessary to produce a constant 90% neuromuscular blockade. This was accomplished by applying nonlinear curve-fitting to data on the cumulative dose requirement during anesthesia. The neuromuscular blocking effect of atracurium was found to be greater after prior administration of succinylcholine. The asymptotic steady-state rate of infusion (+/- SD) for atracurium was 0.27 +/- 0.06 mg.kg-1.h-1 for patients given succinylcholine and 0.38 +/- 0.10 mg.kg-1.h-1 for those not given succinylcholine. The clinical implication of this study is that the clinician should be aware of the fact that an induction dose of 1 mg/kg of succinylcholine does reduce atracurium requirement for 90% neuromuscular blockade by approximately 30%.

Adult↗

PubMedDate not supplied

Thiopental and succinylcholine: Action on intraocular pressure.

Intraocular pressure (IOP) measurements were made in a series of 92 male surgical patients, to assess the effects of timing and dosage of succinylcholine given after a standardized sleep dose of thiopental (3 mg./kg.). The major findings of this study were as follows: (1) thiopental alone lowered IOP; (2) a small (0.5 mg./kg.) dose of succinylcholine, given immediately after thiopental, returned IOP to normal; (3) a large (1 mg./kg.) dose of succinylcholine immediately after thiopental maintained the IOP at a low value; (4) if 2 minutes elapsed between thiopental and 1 mg./kg. of succinylcholine, the relaxant raised the IOP to slightly above preanesthetic control values; (5) tracheal intubation caused a significant rise in IOP, more than any effect from succinylcholine itself; (6) succinylcholine drip (0.1 percent), begun after establishment of satisfactory endotracheal halothane-nitrous oxide anesthesia, caused significant IOP elevation in 4 of 11 patients.

Adult↗

PubMed1990

Succinylcholine does not increase serum potassium levels in patients with acutely ruptured cerebral aneurysms.

Succinylcholine-induced hyperkalemia has been reported to occur in many neurological disorders including subarachnoid hemorrhage. The purpose of this study was to compare the effect of succinylcholine on serum potassium levels in patients with ruptured cerebral aneurysms undergoing either early (less than or equal to 4 days; n = 14) or delayed (5-16 days; n = 20) surgery. Thirty-four patients were classified according to the number of days from subarachnoid hemorrhage to surgery. Arterial serum potassium levels were measured after induction of anesthesia but before succinylcholine, and 1, 5, and 10 min after the administration of succinylcholine. The electrocardiogram was continuously monitored. The mean ( +/- SD) increase in serum potassium level of 0.4 +/- 0.2 mmol/L occurred at 10 min but was not statistically significant, nor was there any statistically significant difference in serum potassium levels related to time between subarachnoid hemorrhage and administration of succinylcholine. We found no evidence of succinylcholine-induced hyperkalemia in patients undergoing either early or delayed cerebral aneurysm surgery.

Adult↗

PubMed1990

Effect of d-tubocurarine pretreatment on succinylcholine twitch augmentation and neuromuscular blockade.

Subparalyzing doses of d-tubocurarine (dTC) given before succinylcholine decrease the duration of neuromuscular blockade. In animal preparations, they also abolish succinylcholine-induced twitch augmentation, defined as a greater-than-maximal contraction in response to a single stimulus. To determine quantitatively the effect of dTC on succinylcholine potency and on twitch augmentation in humans, 60 adult patients, ASA physical status I or II, were assigned randomly to receive either 0.05 mg/kg of dTC or saline 2 min before induction of anesthesia with fentanyl and thiopental. Train-of-four stimulation was applied every 12 s to the ulnar nerve and the force of contraction of the adductor pollicis muscle was measured. One minute after induction of anesthesia, 0.15, 0.20, 0.25, 0.35, or 0.50 mg/kg of succinylcholine was given. The height of the first twitch (T1) reached 121% +/- 6% (mean +/- SEM) of control without dTC, and was virtually abolished by dTC pretreatment (105% +/- 1%, P less than 0.01). Twitch augmentation was more noticeable with lower doses of succinylcholine, and was not observed in the response to the fourth stimulus of the train of four (T4). The potency of succinylcholine was decreased by approximately one-half in the dTC-pretreated groups. The ED50 was 0.27 +/- 0.04 mg/kg without dTC and 0.50 +/- 0.06 mg/kg with dTC (P less than 0.002). The corresponding values for ED90 were 0.51 +/- 0.07 and 1.02 +/- 0.12 mg/kg, respectively (P less than 0.02). The ED95 values were 0.63 +/- 0.09 and 1.28 +/- 0.15 mg/kg, respectively (P less than 0.02). The slopes of the regression lines did not deviate significantly from parallelism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1991

Nitrous oxide potentiates succinylcholine neuromuscular blockade in humans.

Sixty ASA physical status I and II adults received 0.3 mg/kg succinylcholine to determine the effect of prolonged administration of thiopental and that of nitrous oxide on succinylcholine neuromuscular blockade. Succinylcholine was administered either 1 min (group 1) or 6 min (groups 2 and 3) after induction of anesthesia with thiopental. In group 2, anesthesia was maintained with thiopental and the patients' lungs were ventilated with oxygen. In group 3, anesthesia was maintained with only 70% nitrous oxide in oxygen. Train-of-four stimulation of the ulnar nerve was started 30 s before the administration of succinylcholine and repeated every 12 s. The force of contraction of the adductor pollicis muscle was measured. Maximum blockade (mean +/- SEM) did not vary significantly between group 1, where thiopental had been administered for 1 min, and group 2, where it had been administered for 6 min (group 1: 61% +/- 6%; group 2: 54% +/- 8%). However, the addition of nitrous oxide increased neuromuscular blockade (group 3: 80% +/- 6%; P less than 0.05 compared with group 2). The degree of twitch augmentation, i.e., greater than maximal response, and times to twitch augmentation and to maximum blockade did not vary significantly among the groups. It is concluded that nitrous oxide increases succinylcholine neuromuscular blockade and that this is manifest within 6 min. This effect is not due to the duration of the anesthetic because thiopental, administered over a similar time period, did not potentiate succinylcholine.

Drug Synergism↗