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At least 19 recordsLinked to original sources
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↗
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↗
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↗
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↗
PubMed1992

Intraocular pressure changes in response to endotracheal intubation facilitated by atracurium or succinylcholine with or without lidocaine.

Changes in intraocular pressure (IOP) and hemodynamics (SP, DP and HR) were measured in 105 patients ASA I and II randomly assigned into seven equal and comparable groups (A to G) during induction of anesthesia and endotracheal intubation facilitated either by succinylcholine or atracurium with or without lidocaine. IOP decreased significantly (p less than 0.01) after induction of anesthesia with thiopentone in all the groups. While atracurium with or without lidocaine did not affect IOP following complete suppression of train-of-four (groups A, B, and C), succinylcholine per se or in combination with lidocaine (groups F and G) significantly (p less than 0.01) increased IOP after induction with thiopentone but not exceeding the baseline IOP level. IOP was significantly elevated (p less than 0.01) immediately after endotracheal intubation in all the groups when compared to IOP following thiopentone administration. In those patients given atracurium (groups A to E), IOP increased (p less than 0.05) in response to endotracheal intubation above the baseline level only in group B where atracurium was divided into a priming and intubating doses. However, the priming dose did not have any significant effect on the onset time of complete twitch suppression of train-of-four and did not affect the intubation conditions compared with the uniformly excellent conditions found with atracurium over an equivalent bolus dose of the relaxant. In patients who received succinylcholine only (group F), IOP immediately after endotracheal intubation was significantly greater (p less than 0.01) as compared to the baseline and did not return to the baseline level until 3 minutes after endotracheal intubation. The use of lidocaine in combination with atracurium (group D) or succinylcholine (group G) for a rapid sequence intubation did not affect IOP following endotracheal intubation. However, atracurium when used in a rapid sequence intubation could not produce similar intubation conditions when compared with succinylcholine. Consequently, we cannot endorse atracurium as an alternative to succinylcholine for patients with penetrated eye injuries and full stomach requiring rapid sequence intubations. In this context, the role of IV lidocaine in mitigating or preventing the systemic and ocular reactions and especially the acute increase in IOP associated with endotracheal intubation should be emphasized.

Anesthesia, Endotracheal↗
PubMed1991

Enhancing effect by nicotinic acetylcholine receptor channel blockers, including beta-eudesmol, on succinylcholine-induced inhibition of twitch tension and intracellular Ca++ in mouse diaphragm muscle.

To elucidate the mechanism of neuromuscular block by succinylcholine, nerve-evoked changes in intracellular Ca(++)-aequorin luminescence and twitch tension were measured simultaneously in the presence of several different types of blockers for the nicotinic acetylcholine receptor channel. Mouse diaphragm muscles were pretreated for 30 to 60 min with 3 to 40 microM bupivacaine, chlorpromazine, phencyclidine and beta-eudesmol. The effects of these noncompetitive blockers on the succinylcholine-induced response were also compared with those for pancuronium. These channel blockers potentiated (2- to 10-fold) both the blocking effects on intracellular Ca++ and twitch tension of succinylcholine (13-100 microM), but not the pancuronium (0.3-1.1 microM)-induced block. These channel blockers also suppressed succinylcholine (1.3-5 microM)-induced enhancement of evoked Ca++ transients. On the other hand, the channel blockers inhibited the succinylcholine (2.5-100 microM)-induced increase in basal Ca++ transients. These results suggest that neuromuscular block induced by succinylcholine is mainly due to desensitization of the nicotinic acetylcholine receptor.

Aequorin↗
PubMed1977

Effects of trimethaphan and sodium nitroprusside on hydrolysis of succinylcholine in vitro.

The use of hypotensive agents in combination with succinylcholine may be necessary. Since trimethaphan has been reported to prolong the action of succinylcholine, the authors studied the abilities of trimethaphan and sodium nitroprusside to inhibit hydrolysis of succinylcholine by pseudocholinesterase in vitro. Trimethaphan was found to be a potent noncompetitive inhibitor of pseudocholinesterase (KI = 0.24 micronM). It could be calculated that a typical dose of trimethaphan would approximately double the duration of paralysis produced by the usual dose of succinylcholine. Nitroprusside had no inhibitory effect in vitro. It is concluded that nitroprusside is preferable when a hypotensive agent must be used in conjunction with succinylcholine.

Butyrylthiocholine↗
PubMed1991

Effects of caffeine, halothane, succinylcholine, phenylephrine and isoproterenol on myocardial force of contraction of malignant hyperthermia susceptible swine.

The effects of caffeine, halothane, succinylcholine, phenylephrine and isoproterenol on force of contraction were studied in electrically driven (0.2 Hz) trabeculae isolated from the right ventricles of the hearts of malignant hyperthermia susceptible (MHS) and healthy control (nMHS) swine. Caffeine (0.1-10 mmol/l) had positive inotropic effects, amounting to 275 +/- 35% of control in nMHS and 268 +/- 34% in MHS (n = 16). Halothane (0.25-4 vol%) decreased the force of contraction maximally to 52 +/- 4% in nMHS and 51 +/- 5% of control in MHS (n = 16). Propranolol did not change these effects. Succinylcholine (0.1-10000 mumol/l) had a small positive inotropic effect in both groups, which was blocked by propranolol. Phenylephrine (0.1-300 mumol/l) increased the force of contraction maximally to 188 +/- 24% of control in nMHS and to 193 +/- 23% in MHS (n = 16). The inotropic effect was blocked by prazosin but not by succinylcholine (1 mmol/l). Isoproterenol (0.01-10 mumol/l) had a positive inotropic effect of maximally 275 +/- 21% of control in nMHS and 396 +/- 31% in MHS (n = 17) (P less than 0.05). Succinylcholine potentiated this effect, and propranolol shifted the concentration-response curves to the right. We conclude that caffeine, halothane, succinylcholine and phenylephrine have similar inotropic effects in the hearts of nMHS and MHS, whereas isoproterenol has a significantly greater effect in MHS than in nMHS.

Animals↗
PubMed1991

[Effect of succinylcholine on recovery of atracurium-induced neuromuscular blockade].

If muscle relaxation is inadequate at the end of surgery, a transient increase in neuromuscular (NM) blockade should be needed to facilitate closure. Succinylcholine is the only agent of short duration available currently and could be used in the just mentioned circumstance. Therefore, the study was designed to investigate the effects of succinylcholine on the recovery of atracurium-induced NM blockade. Sixty-four female patients who underwent elective surgery under general anesthesia were allocated into 6 groups. Before anesthesia, no patient had received drugs which affect NM transmission. In all patients anesthesia was induced with thiopental, diazepam and fentanyl and maintained with 50% nitrous oxide in oxygen and 0.5-1.5% isoflurane. During anesthesia, blood pressure and electrocardiogram were monitored and end-tidal CO2 was maintained at 30-40 mmHg. Control records of the integrated electromyography responded to train-of-four supramaximal stimulation using a Datex Relaxograph were obtained after induction of anesthesia before a block was produced with an initial dose of succinylcholine 1.0 mg in group I (n = 8) or atracurium 0.4 mg/kg in groups II-VI. On first twitch (T1) recovering to 50% of control, 0.4 mg/kg, 0.6 mg/kg, 0.8 mg/kg, 1.0 mg/kg and 1.2 mg/kg of succinylcholine were given in groups II (n = 11), III (n = 14), IV (n = 11), V (n = 10), VI (n = 10) respectively. It was seen that succinylcholine 0.4 mg/kg antagonized NM blockade by atracurium but at 0.6 mg/kg, 0.8 mg/kg, 1.0 mg/kg, 1.2 mg/kg it enhanced that.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Stability of succinylcholine chloride injection.

The stability of succinylcholine chloride injection prepared by a hospital pharmacy was studied under a wide variety of conditions. Batches of succinylcholine chloride injection 10 mg/mL containing sodium chloride, methyl-4-hydroxybenzoate, hydrochloric acid, and water were prepared. Samples were tested for the effect of initial pH (3.0 and 4.2) and sterilization (steam treatment at 100 degrees C for 30 minutes and 121 degrees C for 20 minutes) on stability after three weeks; long-term stability under refrigeration (12, 17, and 23 months of storage at 4 degrees C); and the effect of storage temperature (4-6 degrees C, 20-26 degrees C, 35 degrees C, and 70 degrees C) and light exposure at various intervals up to 12 months. Samples were analyzed by thin-layer chromatography (TLC) and high-performance liquid chromatography (HPLC). Unlike heating at 121 degrees C, heating at 100 degrees C produced no significant loss of succinylcholine chloride, independent of the initial pH. Succinylcholine chloride was hydrolyzed only minimally over 23 months if the solution was stored at 4-6 degrees C. A 10% loss of drug content occurred if solutions were kept at 20-26 degrees C for five months, at 35 degrees C for one month, or at 70 degrees C for one day. Initial degradation was slowed if the solution was protected from light. The assessments by TLC proved to be more sensitive than the HPLC measurements. Succinylcholine chloride injection sterilized at 100 degrees C for 30 minutes can be stored for up to five months at room temperature if protected from light. The preparation is stable for at least two years under refrigeration.

Chromatography, High Pressure Liquid↗
PubMedDate not supplied

Comparative trial of succinylcholine vs low dose atracurium-lidocaine combination for intubation in short outpatient procedures.

Despite its many disadvantages, succinylcholine is the most commonly used drug for intubation of patients for short out-patient procedure. This double blind trial compared a low dose atracurium/lidocaine combination to succinylcholine for intubation in 40 ASA1 adult patients. Low dose atracurium/lidocaine provided clinical intubating conditions at two minutes and cardiovascular stability equivalent to succinylcholine with significantly less myalgia. Spontaneous respiration was slower after low dose atracurium/lidocaine relative to succinylcholine. Low dose atracurium/lidocaine may provide an acceptable alternative to succinylcholine for intubation in short outpatient procedures.

Adult↗
PubMed1979

Succinylcholine drug interactions during electroconvulsive therapy.

Electroconvulsive therapy (ECT) is frequently described as being almost free of absolute contraindications. However, drug interactions with succinylcholine pose potential hazards to which this paper calls attention. In addition to its neuromuscular-blocking action, succinylcholine has other acetylcholine-like effects. Drugs which inhibit cholinesterase activity or which inhibit acetylcholine release or synthesis may produce prolonged respiratory paralysis when combined with succinylcholine. The increasing longevity of the population receiving chemotherapy for physical ailments implies that greater numbers of these patients may also become candidates for ECT and therefore be at risk for adverse drug interactions with succinylcholine. Of particular importance to the psychiatrist are the various psychotropic drugs that have been reported to interact with succinylcholine. Precautions in using drug combinations and treatment of complications are described.

Animals↗
PubMedDate not supplied

Comparative effects of (+)- and (-)-isomers of propranolol and INPEA on (+)-tubocurarine- and succinylcholine-induced neuromuscular blockade.

The effects of the (+)- and (-)-isomers of propranolol and INPEA on the neuromuscular blocking action of (+)-tubocurarine and succinylcholine were studied in the tibialis anterior-peroneal nerve preparation of the rabbit and the isolated phrenic nerve-diaphragm preparation of the rat. (+)-Tubocurarine-induced neuromuscular blockade was intensified by (+)- and (-)-isomers of INPEA whereas it was unaffected by isomers of propranolol in both preparations. In the rabbit tibialis anterior-peroneal nerve preparation, only the (-)-isomers of propranolol and INPEA increased the duration of succinylcholine-induced neuromuscular blockade without affecting its magnitude. Higher doses of both (+)- and (-)-isomers of propranolol and INPEA potentiated succinylcholine-induced blockade in the rat phrenic nerve-diaphragm preparation. The results obtained indicate that only the increase in duration of succinylcholine-induced blockade with beta-adrenoceptor blockers can be related to beta-blocking property of these compounds.

Animals↗