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Background: We examined the effects of etomidate on recovery of contractile function after hypoxia reoxygenation and hypoxic preconditioning in vitro using isolated human myocardium., Methods: Human right atrial myocardium were obtained at the time of cardiac surgery from 38 adults patients. We recorded isometric force of contraction (FoC) of atrial trabeculae suspended in an oxygenated Tyrode's solution (34 degrees C, stimulation frequency 1 Hz). In all groups, a 30-min hypoxic period was followed by 60 min of reoxygenation (HR). In separate groups, muscles were exposed to etomidate (10(-7), 10(-6), 10(-5) M) 10 min before and throughout the HR periods. Hypoxic preconditioning was induced by 4-min hypoxia followed by 7-min reoxygenation applied before HR periods. Etomidate 10(-5) M was administered before, throughout, and after the hypoxic preconditioning stimulus. Recovery of FoC (expressed as % of baseline value) at the end of HR was compared among groups., Results: Compared with the control group (FoC: 52%+/-10%), etomidate 10(-7) M (FoC: 57%+/-9%; P=0.24), 10(-6) M (FoC: 61%+/-11%; P=0.10), and 10(-5) M (FoC: 54%+/-9%; P=0.29) did not modify the recovery of FoC after HR. Hypoxic preconditioning-induced increase in the recovery of FoC (87%+/-5%; P<0.001 vs control group) was not modified in the presence of etomidate 10(-5) M (FoC: 86%+/-7%; P=0.74 vs hypoxic preconditioning group)., Conclusions: Etomidate did not modify the in vitro FoC of human myocardium exposed to HR. Furthermore, etomidate did not modify the protective effect of hypoxic preconditioning.

Background: Etomidate and ketamine are used during induction of anesthesia in high-risk patients. However, their effects on action potential (AP) variables and ischemia/reperfusion-induced arrhythmias and conduction blocks are unknown., Methods: Guinea pig right ventricular muscle strips were mounted in a 5-mL double chamber bath with the strips separated into two zones by an impermeable latex membrane. One-half (normal zone) was exposed to normal perfusate while the other half (altered zone) was exposed to hypoxia, hyperkalemia, acidosis, and lack of glucose. AP variables were recorded continuously in the normal and altered zones. Spontaneous arrhythmias and conduction blocks were noted. Etomidate (10(-7), 10(-6), and 10(-5) M) and ketamine (10(-6), 10(-5), and 10(-4) M) were superfused into the bath throughout the experiment and the electrophysiologic effects compared with the control group., Results: We found that under control conditions, etomidate and ketamine did not modify resting membrane potential, maximal upstroke velocity, AP amplitude, or AP duration at 90% of repolarization (APD90). Ketamine (10(-4) M), but not weaker concentrations and none of the concentration of etomidate, reversed the ischemia-induced shortening of APD90 and APD dispersion. Etomidate and ketamine did not modify the occurrence of conduction block during simulated ischemia. In contrast, ketamine (25% at 10(-6) M, 13% at 10(-5) M, and 13% at 10(-4) M vs 90% in the control group, P < 0.05) but not etomidate (38% at 10(-7) M, 63% at 10(-6) M, and 63% at 10(-5) M vs 90% in the control group, NS) decreased the incidence of reperfusion-induced spontaneous arrhythmias., Conclusions: In guinea pig myocardium, our data suggest that ketamine, in clinically relevant concentrations, decreases ischemia-induced AP shortening and spontaneous reperfusion-induced ventricular arrhythmias. Further study is required to precisely determine the effect of etomidate on reperfusion-induced arrhythmias.

Background: We examined the role of reactive oxygen species (ROS) in sevoflurane- and desflurane-induced preconditioning on isolated human right atrial myocardium., Methods: We recorded isometric contraction of human right atrial trabeculae suspended in an oxygenated Tyrode's solution (34 degrees C, stimulation frequency 1 Hz). In all groups, a 30-min hypoxic period was followed by 60 min of reoxygenation. Ten minutes before hypoxia reoxygenation, muscles were exposed to 5 min of sevoflurane 2% or desflurane 6%. In separate groups, the sevoflurane 2% (Sevo + N-(2-mercaptopropionyl)-glycine [MPG]) or desflurane 6% (Des + MPG) was administered in the presence of 0.1 mM MPG, a ROS scavenger. The effect of 0.1 mM MPG alone was tested. Recovery of force after a 60-min reoxygenation period was compared between groups (mean +/- sd)., Results: Preconditioning with sevoflurane 2% (85% +/- 4% of baseline) or desflurane 6% (86% +/- 7% of baseline) enhanced the recovery of the force of myocardial contraction after 60 min reoxygenation compared with the control group (53% +/- 11% of baseline, P < 0.001). This effect was abolished in the presence of MPG (56% +/- 12% of baseline for Sevo + MPG, 48% +/- 13% of baseline for Des + MPG). The effect of MPG alone on the recovery of force was not different from the control group (57% +/- 7% of baseline versus 53% +/- 11%; P = NS)., Conclusions: In vitro, sevoflurane and desflurane preconditioned human myocardium against hypoxia through a ROS-dependent mechanism.

Unlabelled: Hypotension is common after mivacurium injection in healthy patients. This hemodynamic event had not been investigated in hypertensive patients characterized by more intense hemodynamic instability. In this open-label, multicenter, randomized, and controlled study, we sought to determine whether mean arterial blood pressure (MAP) and heart rate variations were larger in hypertensive versus normotensive patients after a bolus dose of mivacurium injected over 10 or 30 s. After the induction of anesthesia with fentanyl and etomidate, normotensive (n = 149) and hypertensive (n = 57) patients received a single dose of mivacurium 0.2 mg/kg injected over 10 or 30 s by random allocation. Heart rate and MAP were recorded electronically. The incidence of hypotension (defined as a 20% MAP decrease from the control value before mivacurium injection) was 21% and 36% (10-s injection) or 11% and 10% (30-s injection) in the Normotensive and Hypertensive groups, respectively. In Hypertensive patients, the maximum decrease in MAP was significantly greater when mivacurium was injected over 10 s compared with 30 s: 20% vs 11%, respectively (P = 0.002). This difference was not observed in Normotensive patients. Hypotension after rapid (e.g., 10 s) mivacurium injection was more frequent and more pronounced in Hypertensive than in Normotensive patients., Implications: When mivacurium (0.2 mg/kg) is injected rapidly (e.g., 10 s) the incidence and the intensity of hypotension are greater in hypertensive patients than in healthy patients.

Unlabelled: Early reversal of rapacuronium may accelerate return of neuromuscular function. This study was designed to compare early (2 min after rapacuronium) or late (at 25% recovery of the first twitch [T1] of train-of-four) reversal of rapacuronium with neostigmine. We studied 119 subjects between the ages of 18 and 75 yr. Anesthesia was induced with fentanyl and thiopental and maintained with nitrous oxide, propofol, and fentanyl. Mechanomyographic neuromuscular monitoring was performed by using train-of-four stimulation of the ulnar nerve. Two groups received 1.5 mg/kg rapacuronium followed by neostigmine (50 microg/kg) and glycopyrrolate (10 microg/kg) either at 2 min after rapacuronium bolus or at 25% T1 recovery. The other two groups received 2.0 mg/kg rapacuronium, after which neostigmine was similarly given. For each rapacuronium dose, the time from the administration of rapacuronium to the start of T1 recovery or 25% T1 recovery was significantly shorter in subjects who received the reversal 2 min after rapacuronium. However, late recovery, defined by times from administration of rapacuronium to 70%, or 80% T4/T1 recovery, was not influenced by early reversal administration. We conclude that initial recovery is accelerated by early administration of neostigmine. Time to full recovery after rapacuronium administration is, however, dose-dependent and not significantly altered by early administration of neostigmine., Implications: "Rescue reversal," which includes the administration of neostigmine shortly after the administration of rapacuronium, may accelerate the return of spontaneous breathing (early recovery), but does not shorten the time to complete recovery of upper airway function.

Unlabelled: The onset time of neuromuscular blockade at the adductor pollicis (AP) is different among neuromuscular blocking drugs, but these discrepancies had never been studied at the orbicularis oculi (OO). The purpose of this study was to verify if the differences in onset time observed at the AP still existed at the OO and to score the intubating conditions using monitoring at the OO after five muscle relaxants. The study included 172 adults aged 18-75 yr. Anesthesia was induced with fentanyl and propofol. Atracurium (0.5 mg/kg), mivacurium (0.20 mg/kg), rocuronium (0.6 mg/kg), succinylcholine (1.0 mg/kg), or vecuronium (0.08 mg/kg) was injected by random allocation. Time to complete disappearance of the response at the OO was assessed visually after train-of-four stimulation of the facial nerve. Laryngoscopy was then performed, and intubating conditions were determined on a scale of 1-4. Results were based on 150 patients. Onset time at the OO was (mean +/- SD): succinylcholine (57 +/- 17 s) < mivacurium (99 +/-19 s) = rocuronium (99 +/- 47 s) < atracurium (129 +/-33 s) = vecuronium (135 +/- 38 s) (P < 0.05). Overall intubating conditions were excellent (84%), good (14%), poor (1.3%), impossible (0.7%), and were similar among the five groups. We conclude that differences in onset time of muscle relaxants observed at the AP were also found at the OO. Visual estimation of the response at the OO correctly predicted good-to-excellent intubating conditions in more than 90% of cases for all the currently available muscle relaxants., Implications: Onset time of neuromuscular blockade, as estimated visually at the orbicularis oculi, depends on the muscle relaxants given. Regardless of the relaxant used, intubating conditions at loss of orbicularis oculi are acceptable.

In pediatric practice, complications due to the laryngeal mask airway (LMA) have been studied with size 2 LMA, but not with size 1 LMA. We, therefore, compared prospectively the complications induced by LMA size 1 and 2 in 141 children aged 21 days to 11 yr. Intraoperative and lowest SpO2 values after removal of LMA were recorded. The following complications were recorded: cough, laryngospasm, bronchospasm, apnea, and airway obstruction. In 14 patients in the size 1 LMA group and 26 patients in the size 2 LMA group, pharyngolaryngeal structures were checked with fiberoptic examination. The number of attempts, complications, intraoperative SpO2, and lowest SpO2 values were similar when using size 1 and size 2 LMA. Fiberoptic examination of size 1 LMA showed a high incidence of impinging of the epiglottis in the LMA bars without airway obstruction. In conclusion, there was no difference in the complication rate between the two pediatric sizes of LMA when used in pediatric patients.

To quantify the effects of succinylcholine at the laryngeal adductor muscles and the adductor pollicis, 17 adult patients were studied during propofol-fentanyl anesthesia. Train-of-four stimulation was applied to the ulnar nerve at the wrist and the recurrent laryngeal nerve at the notch of the thyroid cartilage. Laryngeal response was measured as pressure changes in the cuff of the tracheal tube positioned between the vocal cords. The force of contraction of the laryngeal adductor muscles and of the adductor pollicis were compared after administration of 0.25 or 0.5 mg/kg of succinylcholine. With 0.25 mg/kg, maximum blockade of first twitch (T1) was 66% +/- 10% (mean +/- SEM) and 45% +/- 13% at the vocal cords and the adductor pollicis, respectively (P less than 0.01). After 0.5 mg/kg, maximum blockade at the vocal cords (93% +/- 2%) and the adductor pollicis (84% +/- 6%) did not differ significantly. For both doses, time to maximal blockade was shorter for the vocal cords (0.9 +/- 0.1 min) than for the adductor pollicis (1.7 +/- 0.2 min; P less than 0.01). Time to 90% recovery of T1 after a bolus of 0.5 mg/kg was similar at the vocal cords (4.3 +/- 0.5 min) and the adductor pollicis (5.2 +/- 0.8 min) (NS). The ED50 was less at the laryngeal adductors (0.170 mg/kg) than at the adductor pollicis (0.278 mg/kg). It is concluded that, in adults, succinylcholine-induced blockade is more rapid and more intense at the laryngeal muscles than at the adductor pollicis.