Background and objective Midazolam may occasionally precipitate hostility and violence instead of tranquillity. We characterized these episodes, their rate of occurrence, the potential paradoxical responders and possible predisposing circumstances among patients undergoing lower body surgery under spinal or epidural anaesthesia and midazolam sedation.

Patients and methods Fifty-eight patients who fulfilled the study entry criteria and who underwent surgery within a 3-month period in a large metropolitan, university-affiliated hospital were enrolled. Sedation and restlessness in all patients were controlled by midazolam administered intravenously by the attending anaesthesiologist; these parameters were later objectively confirmed by recorded actigrams. If ‘paradoxical’ events occurred, flumazenil 0.1 mg 10 s−1 was injected until the aberrant behaviour ceased. Patients with paradoxical reactions were later compared with matched control patients selected from the study group to identify epidemiological characteristics.

Results The incidence of paradoxical events was 10.2% (six out of 58 patients, confidence limits 2.3–18.3%) and they occurred 45–210 min after sedation started; the only independent predictor was an age older than that of the entire study group. The mean cumulative and per weight doses of midazolam were similar for both the experimental and the study groups of patients: 7.3 ± 2.8 to 10.1 ± 3.6 mg, and 0.1 ± 0.04 to 0.12 ± 0.05 mg kg−1. Flumazenil 0.2–0.3 mg (range 0.1–0.5 mg) effectively stopped the midazolam-induced paradoxical activity within 30 s and surgery continued uneventfully.

Conclusions Flumazenil completely reverses midazolam-induced paradoxical reactions and they are more frequent in older patients.

Background and objective Serum hyaluronate is thought to be an indicator of derangement in hepatocellular integrity, and the change in serum hyaluronate is a useful indicator in various liver disorders. We assessed the changes in serum hyaluronate in patients undergoing coronary artery bypass graft surgery.

Methods Eleven patients scheduled for elective coronary artery bypass graft surgery were studied. An oximetry oxygen saturation catheter was inserted into the right hepatic vein to permit monitoring of hepatic venous oxygen saturation. Perioperative measurements included: haemodynamic variables; systemic oxygen delivery and uptake; arterial, mixed venous and hepatic venous oxygen saturation; arterial and hepatic venous plasma concentrations of lactate, arterial ketone body ratio (ratio of acetoacetate to 3-hydroxybutyrate); and arterial and hepatic venous hyaluronate were measured.

Results Arterial and hepatic venous hyaluronate increased during cardiopulmonary bypass compared with the prebypass period. These increases returned to prebypass values after the cessation of bypass (hepatic venous hyaluronate value at the prebypass period: 26 ± 13 ng mL−1, during bypass: 77 ± 40 ng mL−1; 1 h after bypass: 57 ± 42 ng mL−1; 6 h after bypass: 32 ± 15 ng L−1, 24 h after bypass; 62 ± 21 ng mL−1; mean ± SD, P < 0.05). The arterial and hepatic venous hyaluronate during cardiopulmonary bypass was correlated with total bilirubin and hepatic venous lactate concentrations 6 h after bypass (arterial hyaluronate at cardiopulmonary bypass period vs. total bilirubin at 6 h after bypass; r = 0.793, P = 0.0036, hepatic venous hyaluronate during bypass vs. that at 6 h after bypass; r = 0.795, P = 0.0035).

Conclusions Hepatocellular integrity might be disturbed during cardiopulmonary bypass when propofol anaesthesia is used.

Background and objective Despite the fact that both general anaesthetics and hypotensive drugs influence autonomic nervous activity, no study has yet examined the heart rate variability during deliberate hypotension and general anaesthesia. The aim of this was to clarify the heart rate variability changes during deliberate hypotension under sevoflurane–nitrous oxide anaesthesia.

Methods Autonomic nervous system activity in patients (n = 45) subjected to deliberate hypotension during sevoflurane in nitrous oxide and oxygen anaesthesia was investigated by a heart rate variability measurement. Three different types of hypotensive drugs, a calcium channel antagonist (nicardipine), a nitric oxide donor (nitroglycerin) and a vasodilatory prostaglandin (alprostadil), were used to induce hypotension.

Results In all groups, low frequency power (sympathetic and parasympathetic indicator) and the ratio of low frequency to high frequency power (the LF/HF ratio, sympathetic indicator) were suppressed by induction of anaesthesia. In the control group, preanaesthesia low frequency power was 195 ± 139 ms2, the LF/HF ratio 10.3 ± 5.7, during anaesthesia 5 ± 9 ms2, 0.6 ± 0.8, respectively, P = 0.0093, 0.0034, whereas high frequency power (parasympathetic indicator) was not significantly changed. In those patients receiving nicardipine or nitroglycerin during anaesthesia, these variables did not differ significantly from those in the control group. During prostaglandin E1 infusion, high frequency power was higher compared with the values in the other groups (17 ± 12 ms2 in the prostaglandin group, 7 ± 6 ms2 in the nicardipine group, 6 ± 5 ms2 in the nitroglycerin group and 6 ± 4 ms2 in the control group, respectively, P = 0.0326, 0.0251, 0.0197).

Conclusions Sevoflurane in nitrous oxide and oxygen anaesthesia reduces sympathetic autonomic activity considerably, and the expected increases caused by hypotensive agents that occur in awake volunteers were not seen.

Background and objective We investigated whether glibenclamide (glyburide) affects myocardial metabolism and hydroxyl radical formation in the rat heart–lung preparation with or without inhalation anaesthetics.

Methods Thirty-seven male Wistar rats were allocated to four groups: (a) control group (C), received vehicle only; (b) group G, received glibenclamide 10 μM L−1; (c) group I, received glibenclamide 10 μM L−1 and 1.4% isoflurane during perfusion; (d) group S, received glibenclamide 10 μM L−1 and 2.7% sevoflurane during perfusion. Glibenclamide was administered 7 min after the start of perfusion. Ten minutes later, the heart was rendered globally ischaemic for 10 min by reducing the preload and afterload to zero, and then the heart was reperfused for 10 min. The formation of hydroxyl radicals in perfusate blood and heart was measured with high performance liquid chromatography using salicylic acid. Hydroxyl radicals react with salicylic acid, yielding dihydroxybenzoic acids.

Results The recovery time from ischaemia in group G was significantly longer than the other groups. However, there were no differences in myocardial metabolites and dihydroxybenzoic acids concentrations in the perfusate and heart among the four groups.

Conclusions Glibenclamide prolonged recovery time from ischaemia, but did not affect hydroxyl radical formation in the postischaemic reperfused heart. In addition, isoflurane and sevoflurane shortened this time. These facts suggest that mechanisms other than effects of volatile anaesthetics on hydroxyl radical formation are responsible for their protective effects in this model.

Background and objective To investigate the ability of lidocaine to inhibit reactive oxygen and/or nitrogen species generation by either human leukocytes or cell-free systems via luminol- and lucigenin-enhanced chemiluminescence.

Methods Venous blood was obtained from healthy volunteers and leukocytes were isolated, from which chemiluminescence was generated. Also, chemiluminescence, induced by H2O2, HOCl, peroxynitrite or ferrous iron, was generated in cell-free systems.

Results Lidocaine produced a concentration-dependent inhibition in chemiluminescence generated by leukocytes (92 ± 1%, 1 mM). In cell-free experiments, lidocaine (1 mM) markedly inhibited chemiluminescence of xanthine-xanthine oxidase (24 ± 3%), while it slightly suppressed hypochlorous acid-induced chemiluminescence (9 ± 2%). Peroxynitrite-induced luminol- and lucigenin-enhanced chemiluminescence were also inhibited by lidocaine at 1 mM (19 ± 3% and 48 ± 8%, respectively). Lidocaine did not affect chemiluminescence generated by FeSO4. However, lidocaine produced a biphasic effect on H2O2-induced chemiluminescence (37 ± 5% inhibition at 0.01 mM and 61 ± 17% activation at 1 mM).

Conclusions Lidocaine can elicit direct scavenging activity at high concentrations that might be important at or near the site of injection in local anaesthetic use.

Background and objective The efficiency of intraoperative autotransfusion in scoliosis surgery is poorly known but needs to be evaluated, not least because of the large blood losses in these patients. This is a retrospective analysis of transfusion requirements of 43 such patients.

Methods Records from 43 patients were studied. During surgery, the shed blood was salvaged and washed in an autotransfusion device (AT1000 Autotransfusion Unit®) and a suspension of red cells was reinfused.

Results Fifty-eight per cent of the intraoperative blood loss was salvaged. The total blood loss during the patients' hospital stay was calculated from the haemoglobin balance; 24% of this loss was salvaged by the device. Moreover, 36 of the patients needed allogeneic blood transfusion.

Conclusion The efficiency of the autotransfusion device was relatively low in relation to the total extravasation, mainly because the postoperative blood loss is substantial.

Occipital nerve block is usually considered to be a very simple and safe regional anaesthetic technique. We describe a case of sudden unconsciousness during a lesser occipital nerve block in a patient with an occipital bone defect. A 63-year-old man complained of headache, which was localized to the right occipital region. A right lesser occipital nerve block with a local anaesthetic was performed for treatment. During the lesser occipital nerve block, the patient suddenly became disturbed and lost consciousness. Two hours after the incident, the patient was fully awake without neurological sequelae. He had previously undergone a microvascular decompression for right trigeminal neuralgia. The patient had a bone defect following craniotomy. We believed that the loss of consciousness during lesser nerve block may be due to a subarachnoid injection. Occipital nerve block is relatively contraindicated in the presence of a bone defect.