There is a high incidence of pain following intravenous injection of propofol, and many studies have been conducted to find a way of reducing this. The administration of lidocaine and, recently, remifentanil has also been used for this purpose, but it is only partially effective. Thus, the purpose of this study was to investigate the analgesic effect of a combination of pretreatment with remifentanil and premixture of lidocaine with propofol and to compare either treatment alone during propofol injection in dorsal hand-veins.

In a prospective, randomized, double-blinded trial, we studied 141 adult patients scheduled for elective surgery. The combination of pretreatment of remifentanil (0.35 μg kg−1 min−1) and a premixture of lidocaine with propofol (mixture of propofol 1% and lidocaine 1% in a 10 : 1 ratio) was compared with either treatment alone in the prevention of pain on propofol injection. Pain was assessed on a four-point scale (0 = none, 1 = mild, 2 = moderate, 3 = severe) during propofol injection. Patients in Group B received remifentanil (0.35 μg kg−1 min−1) 30 s before the injection of propofol.

The reduction of pain on propofol injection was similar in both the remifentanil pretreatment and lidocaine premixture groups (62.2% vs. 62.2%). Combination therapy was associated with a higher incidence of patients without pain (91.3%) than either treatment alone (P < 0.001). On analysing the injection pain scores, we found a significant reduction of the score in the remifentanil and lidocaine Group C compared with the lidocaine Group A (P < 0.001) and the remifentanil Group B (P < 0.001).

The combination of pretreatment of remifentanil and premixture of lidocaine with propofol was more effective in reducing the incidence of pain on injection of propofol than either treatment alone.

This study was conducted to compare bispectral index, state entropy and response entropy in patients undergoing coronary artery bypass grafting.

In 66 patients, anaesthesia was maintained at two different levels using bispectral index. Doses of sufentanil and midazolam were adjusted to achieve a bispectral index in the range of 45–55 in 33 patients (BIS 50 group) and 35–44 in another 33 patients (BIS 40 group). Simultaneously, state entropy and response entropy were recorded.

The targeted values of bispectral index were achieved in both groups and the bispectral index values differed significantly during whole anaesthesia. Median response entropy and state entropy fell to 19–26 during anaesthesia in both groups. Response entropy and state entropy values in the two groups differed significantly only after induction of anaesthesia and did not differ during further anaesthesia. There was no explicit intraoperative recall in both groups. Patients in Group BIS 40 received significantly (P < 0.05) more sufentanil than the BIS 50 group (704 ± 181 μg vs. 490 ± 107 μg, respectively) and midazolam (18.5 ± 6.1 mg vs. 15.6 ± 3.8 mg, respectively). After cardiopulmonary bypass, significantly (P < 0.05) more patients in Group BIS40 needed inotropic support with dobutamine (79%) than in the BIS50 group (52%). Time to extubation did not differ between the two groups.

In patients undergoing coronary artery bypass grafting, no relationship was found between bispectral index levels and state entropy and response entropy at two different stages of a sufentanil–midazolam anaesthesia. A bispectral index level of 45–55 reduced anaesthetic medications used and the need for inotropic support.

The importance of monitoring the breathing pattern during sedation of children undergoing magnetic resonance scans is indicated in guidelines, but no appropriate magnetic resonance-compatible devices are available. We report preliminary findings from a technique referred to as remote pressure sensor respiratory plethysmography.

A data acquisition system was developed, enabling measurement of respiratory rate, plethysmogram amplitude, proportion of inspiratory time over cycle time, thoraco–abdominal phase shift and sigh rate. Correlation between plethysmogram amplitude and tidal volume was investigated on adult volunteers. Twenty-seven children undergoing sedation were monitored with remote pressure sensor respiratory plethysmography, in addition to SPO2 and PetCO2. Differences in monitoring parameters were searched for among three groups: patients who received chloral hydrate only (chloral succeeded, CS group), those who received a supplementation of sodium thiopental (chloral failed, CF group), and those who were sedated with sodium thiopental directly (no chloral, NC group). Correlations were searched for among monitoring parameters, and with total dose of thiopental. The long-term behaviour of respiratory rate, proportion of inspiratory time over cycle time and phase shift was studied.

Plethysmogram amplitude was found to correlate linearly with tidal volume (r > 0.92), with a slope varying up to 22%. While 11% of patients did not tolerate the capnometric probe and readings were discontinuous in 26%, all of them tolerated remote pressure sensor respiratory plethysmography belts. Sighs and non-respiratory movements of the torso could be distinguished on remote pressure sensor respiratory plethysmography waveforms. No significant inter-group differences were found in PetCO2, SPO2, respiratory rate and phase shift. Proportion of inspiratory time over cycle time was higher in the NC group when compared to the CS group (0.497 ± 0.03 vs. 0.463 ± 0.008; P = 0.02), the CF group being characterized by intermediate values (0.480 ± 0.008); when compared to the CS group, sigh rate was lower in the CF group (0.04 ± 0.04 vs. 0.14 ± 0.08; P = 0.04) and in the NC group (0.06 ± 0.05 vs. 0.14 ± 0.08, P = 0.03). A positive correlation was found between total dose of thiopental and proportion of inspiratory time over cycle time, with r = 0.4 and P = 0.04. A large baseline variability in phase shift was found. No long-term trends predictive of patient movement could be identified.

Breathing pattern monitoring is feasible through pneumatic devices, which are well tolerated. The resulting correlation with changes in tidal volume can be better when compared to visual inspection. Proportion of inspiratory time over cycle time and sigh rate convey information related to the state of the sedated patient. These results are not specific to the technology employed, and large-scale studies on the clinical usefulness of breathing pattern monitoring are motivated.

In most studies of cardiac output changes after spinal anaesthesia, the time-resolution is limited. The aim of this study was to demonstrate cardiac output changes with high time-resolution during onset of spinal anaesthesia in elderly patients.

We investigated 32 patients aged ⩾60 yr scheduled for elective lower limb surgery. Fourteen received concurrent cardiovascular medication. Cardiac output was measured every 10 s using a pulse wave algorithm derived from the radial artery pressure curve, after calibration with lithium chloride (LiDCO™plus). Data collection ended when the patients were ready for surgery, or if ephedrine was given to raise the mean arterial pressure.

Cardiac output increased initially reaching a maximum after a mean of 7 min. The average increase was 1.1 L min−1 (P < 0.0001). This occurred when mean arterial pressure was reduced 14 mmHg on average. At the end of data collection, cardiac output decreased 0.5 L min−1 from baseline (P = 0.02). Mean arterial pressure decreased progressively in all patients, and only minimal changes in heart rate were found.

Using this high time-resolution method, we detected biphasic changes in cardiac output during onset of spinal anaesthesia. Initially, cardiac output increased. Subsequently, it was significantly reduced from baseline, although this decrease was of minor clinical importance.

An increased risk of awareness during general anaesthesia in patients receiving tramadol has been reported. We studied whether tramadol affects the amount of propofol required for induction of anaesthesia.

In this prospective controlled study, we evaluated 46 patients, half of whom used tramadol regularly. Entropy indices, state entropy and response entropy, were used to assess the level of hypnosis. Patients were anaesthetized with a propofol infusion (1 mg kg−1 min−1) until they first became unconscious, and further until they developed a burst suppression pattern in the electroencephalogram. The doses of propofol needed to reach these end-points were recorded.

The amount (median, (range)) of propofol required for loss of consciousness was 2.0 (1.0–5.5) mg kg−1 and 2.4 (0.9–8.3) mg kg−1 (P = 0.95) in the tramadol users and controls, respectively. The amount of propofol required for burst suppression was 5.8 (3.9–12.7) mg kg−1 and 6.4 (2.9–15.1) mg kg−1 (P = 0.89) in the tramadol users and controls. There was no difference between the groups in state entropy and response entropy during different stages of induction of anaesthesia.

Tramadol did not affect the dose of propofol required to achieve loss of consciousness or burst suppression pattern in electroencephalogram during induction of general anaesthesia. However, there was a ninefold inter-individual variation in propofol dose requirement for loss of consciousness and a fivefold variation for reaching burst suppression. Due to extensive inter-individual variability, monitoring the level of hypnosis during general anaesthesia using propofol may enhance the correct dosage.

To examine a possible mechanism for the antinociceptive action of the N-methyl-d-aspartate receptor antagonist ifenprodil, we compared its effects with those of ketamine on tetrodotoxin-resistant Na+ channels in rat dorsal root ganglion neurons, which play an important role in the nociceptive pain pathway.

Experiments were performed on dorsal root ganglion neurons from Sprague–Dawley rats, recordings of whole-cell membrane currents being made using patch-clamp technique.

Both drugs blocked tetrodotoxin-resistant Na+ currents dose dependently, their half-maximal inhibitory concentrations being 145 ± 12.1 μmol (ketamine) and 2.6 ± 0.95 μmol (ifenprodil). Ifenprodil shifted the inactivation curve for tetrodotoxin-resistant Na+ channels in the hyperpolarizing direction and shifted the activation curve in the depolarizing direction. Use-dependent blockade of tetrodotoxin-resistant Na+ channels was more marked with ifenprodil than with ketamine. When paired with lidocaine, these drugs produced similar additive inhibitions of tetrodotoxin-resistant Na+ channel activity.

The observed suppressive effects on tetrodotoxin-resistant Na+ channel activity may, at least in part, underlie the antinociceptive effects of these N-methyl-d-aspartate receptor antagonists.

Neuromuscular blocking effects according to the severity of liver dysfunction have not been evaluated. We assessed the neuromuscular effects of mivacurium in carbon tetrachloride (CCl4)-treated rabbits with toxic hepatitis in vivo.

We compared the dose–response relationships and the neuromuscular blocking effects of mivacurium in 66 rabbits randomly treated with 0.3 mL kg−1 of corn oil, 0.3 mL kg−1 of CCl4 or 0.6 mL kg−1 of CCl4 for 11 weeks, respectively. Train-of-four stimuli were applied every 10 s to the common peroneal nerve and the force of contraction of the tibialis anterior muscle was measured.

Severe hepatitis was associated with a rightward shift of the mivacurium dose–response curves, but mild hepatitis had no effect. The calculated ED50 values for the control, mild and severe hepatitis were 17.1 ± 2.6, 18.2 ± 2.7 and 31.8 ± 3.2 μg kg−1, respectively. Rabbits with severe hepatitis had a significantly prolonged recovery time from neuromuscular blockade compared with other rabbits. Cholinesterase activity had a negative correlation with recovery indices of mivacurium even in severe hepatic injury. Severe hepatitis induced a prolongation of action duration of repeated doses, but maintained the constant intervals.

The dose–response and the time course of neuromuscular blockade of mivacurium differ in mild hepatitis compared with severe hepatitis, but required no adjustments of different doses for repeated injection after the desired depth of neuromuscular block, and had a negative correlation with the activity of plasma cholinesterase in both hepatic injuries.

Because the incidence of asthma appears to be increasing, the importance of proper perioperative management of individuals with asthma will also continue to increase. Although its mechanism of smooth muscle relaxation is unknown, propofol has been associated with less bronchoconstriction during anaesthetic induction. The aim of this study was to investigate the possible mechanism of these effects and the effects of propofol on the isolated trachea preparations from control and ovalbumin-sensitized guinea pigs.

Adult male guinea pigs, weighing 280–330 g, were randomly allocated to two experimental groups, each consisting of 10 animals. Ten guinea pigs were sensitized by intramuscular injections of 0.30 mL of a 5% (w/v) ovalbumin/saline solution into each thigh (0.6 mL total) on days 1 and 4, whereas the remaining 10 served as controls receiving a total of 0.6 mL distilled water on days 1 and 4 as placebo. The isolated trachea preparations were mounted in tissue baths with modified Krebs–Henseleit solution and aerated with 95% oxygen and 5% carbon dioxide. We tested the effects of propofol (10−7–10−3 M) on resting tension and after precontraction with carbachol and histamine on isolated trachea preparations from control and ovalbumin-sensitized guinea pigs. We also tested the effect of propofol on isolated trachea preparations precontracted with carbachol and histamine in the absence and presence of different inhibitors or antagonists. We investigated propofol responses in tracheal smooth muscle precontracted with CaCl2.

Propofol (10−7–10−3 M) produced a concentration-dependent relaxation of isolated tracheal preparations precontracted by carbachol (10−6 M) and histamine (10−6 M) in both groups. Preincubation with N(w)-nitro l-arginine methyl ester (3 × 10−5 M), indomethacin (10−5 M) or propranolol (10−4 M) did not produce a significant alteration on propofol-induced relaxation responses (P > 0.05), while preincubation with tetraethylammonium (3 × 10−4 M) significantly decreased the propofol-induced relaxation responses in both groups (P < 0.05). Propofol (10−7–10−3 M) induced concentration-dependently relaxations in isolated trachea rings precontracted with CaCl2 in both the control and ovalbumin-sensitized groups.

Propofol induced concentration-dependent relaxations in precontracted, isolated trachea smooth muscle of guinea pigs in both the control and ovalbumin-sensitized groups. These relaxations were independent of epithelial function and stimulation of β adrenergic receptors. Opened Ca2+-sensitive K+ channels and inhibited L-type Ca2+ channels can contribute to these relaxations.