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Study Objective: To investigate the effect of intravenous (IV) landiolol, a novel β(1)-adrenergic blocker, on the minimum alveolar concentration (MAC) of sevoflurane in adult women., Design: Prospective, randomized study., Setting: University hospital., Patients: 42 ASA physical status 1 and 2 women, aged 24-57 years, who were scheduled to undergo elective abdominal surgery., Interventions: Anesthesia was induced in all patients by vital capacity rapid inhalation induction of sevoflurane. In the landiolol group, administration of landiolol began when patients took a vital-capacity breath: 0.125 mg/kg/min for one minute and then 0.04 mg/kg/min. Normal saline was administered in the control group., Measurements: MAC was determined by a technique adapted from the conventional up-down method., Main Results: The MAC of sevoflurane was 2.2% ± 0.2% in the control group and 1.7% ± 0.2% in the landiolol group, a statistically significant difference (P = 0.0005)., Conclusions: IV landiolol reduces the MAC of sevoflurane in women by approximately 20%., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Study Objectives: To examine whether prophylactic, atomized lidocaine blunts hyperdynamic responses and catecholamine release after an abrupt increase in volatile anesthetic administration., Design: Prospective, randomized, double-blind, placebo-controlled study., Setting: University-affiliated hospital., Patients: 22 ASA physical status I adult patients scheduled for elective surgery., Interventions: Patients were randomly assigned to the saline or lidocaine group, and abruptly inhaled 5% isoflurane (4.3 MAC) after inhalation of ultrasonically nebulized lidocaine or saline via endoscopy mask. An esophageal Doppler probe was inserted via the mask to assess global hemodynamic performance., Measurements and Main Results: Immediately after abrupt inhalation of isoflurane, heart rate (HR) in the saline group increased significantly and mean arterial pressure (MAP) remained unchanged, whereas HR in the lidocaine group remained unchanged, and MAP decreased significantly. No significant differences were noted between the saline and lidocaine groups in aortic blood flow, stroke volume in the aorta, total systemic vascular resistance in the aortic circuit, or aortic diameter. The plasma norepinephrine concentration increased in both groups after isoflurane inhalation, significantly so in the saline group but not in the lidocaine group., Conclusion: Prophylactic ultrasonically nebulized lidocaine (2 mg/kg) obtunds the hyperdynamic responses to abrupt inhalation of 5% isoflurane but does not completely block catecholamine release.

Purpose: Nitrous oxide (N(2)O) is a frequently used adjunct to propofol anesthesia. Although N(2)O reduces the requirement of propofol for induction and maintenance, the effects of both drugs on overall hemodynamics remain controversial. We tested the hypothesis that the addition of N(2)O to therapeutic doses of propofol alters hemodynamics and Doppler-derived variables evaluated with the esophageal Doppler monitor in a randomized, double-blinded, placebo-controlled design., Methods: Thirty ASA I-II patients (aged 30-66 yr) were randomly assigned to receive propofol with oxygen-enriched air (FIO(2) = 0.3; air group) or propofol with 70% N(2)O (N(2)O group). Following intubation, a computerized target-controlled infusion technique was used to administer propofol from 0 micro g x mL(-1) (baseline) to 5 micro g x mL(-1) in 1 micro g x mL(-1) increments., Results: Mean arterial pressure (MAP) decreased more in the N(2)O group than in the air group only at 5 micro g x mL(-1). Aortic blood flow (ABF) showed a similar dose-dependent decrease in both groups. Peak aortic flow acceleration, as a myocardial contractility index, decreased significantly and similarly in both groups in a dose-dependent manner whereas peak velocity of ABF, as another measure of myocardial contractility, remained unchanged. Heart rate-corrected left ventricular ejection time, as a measure of preload, remained constant in both groups at any target plasma concentration., Conclusion: Propofol causes dose-dependent decreases in ABF and MAP; however, 70% N(2)O produces minimal hemodynamic and Doppler-derived variable changes under target-controlled propofol infusion at therapeutic concentrations.

Electroconvulsive therapy is an effective treatment for severe and medication-resistant depression. There have been no reports describing how a volatile anaesthetic affects haemodynamic responses, seizure duration, and recovery characteristics during electroconvulsive therapy. We carried out a repeated-measure crossover study to compare the effects on haemodynamic responses, seizure duration, and recovery characteristics of the following types of anaesthesia in electroconvulsive therapy: propofol alone, sevoflurane alone, and propofol combined with sevoflurane. We recruited 50 patients requiring electroconvulsive therapy for depression. For anaesthesia induction, 1.5 mg/kg propofol (condition P), 5% sevoflurane in oxygen following a vital capacity rapid inhalation induction (condition S), or 1.5 mg/kg propofol followed by 5% sevoflurane in oxygen (condition PS) was administered. Succinylcholine 1.5 mg/kg was then given. Electrical stimulation was administered after fasciculation. Measurements were obtained before anaesthesia induction (baseline), prior to succinylcholine administration, prior to electroconvulsive therapy, and at the peak after electroconvulsive therapy. After electroconvulsive therapy, peak heart rate and peak mean arterial pressure were highest in condition S. Whereas recovery time was longest in condition PS, motor seizure duration was significantly shorter than in either condition P or S. Electroencephalographic seizure duration was significantly shorter in condition PS than in condition P and significantly shorter in condition S than in condition P. Sevoflurane anaesthesia alone is most disadvantageous in terms of haemodynamics. Propofol-sevoflurane anaesthesia is advantageous in terms of haemodynamics, but disadvantageous in terms of seizure duration and recovery time. Propofol alone is most advantageous in terms of seizure duration.

Unlabelled: Tizanidine, an alpha2-adrenoceptor agonist, has an antinociceptive effect in animals. In humans premedicated with oral tizanidine, the increase in blood pressure associated with laryngoscopy and intubation was attenuated, and the amount of midazolam required for loss of consciousness was significantly reduced. We speculated that the oral administration of tizanidine might reduce the minimum alveolar anesthetic concentration (MAC) of sevoflurane. Fifty-two ASA physical status I-II patients, aged 24-56 yr, were randomly allocated into two groups: a Control group (n = 26) and a Tizanidine group (n = 26). As premedication, the Control group received a placebo, and the Tizanidine group received 4 mg of oral tizanidine 90 min before surgical skin incision. Anesthesia was induced in all patients by using vital capacity rapid inhaled induction with sevoflurane (5%). Loss of consciousness was defined as both the loss of the eyelid reflex and the lack of a response to a verbal command. MAC was determined by a technique adapted from the conventional up-down method for quantal responses. The MAC of sevoflurane was 2.2% +/- 0.2% in the Control group and 1.8% +/- 0.2% in the Tizanidine group (P = 0.0004). The time to loss of consciousness in the Tizanidine group (60.2 +/- 22.5 s) was significantly shorter than that in the Control group (73.7 +/- 26.3 s) (P = 0.03). The oral administration of tizanidine 4 mg successfully reduced the MAC of sevoflurane by 18% in human adults., Implications: Oral tizanidine (4 mg), an alpha2-adrenoceptor agonist, reduces the minimum alveolar concentration of sevoflurane by 18%.