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    The effects of magnesium sulphate on sevoflurane minimum alveolar concentrations and haemodynamic responses
    (Cambridge Univ Press, 2006) Durmus, M; But, AK; Erdem, TB; Ozpolat, Z; Ersoy, MO
    Background and objective: Magnesium administered before anaesthesia induction results in a significant reduction in intravenous anaesthetic consumption. The purpose of this study was to evaluate whether the dose of intravenous magnesium sulphate reduces the minimum alveolar anaesthetic concentration of sevoflurane for endotracheal intubation (MACE,) and skin incision (MAC), and attenuates haemodynamic responses. Methods: We studied 60 patients who were scheduled for elective surgery. Patients were not premedicated before induction of anaesthesia and were randomly assigned to receive intravenous saline 0.9% (Group I, n = 20) or magnesium sulphate 30 mg kg(-1) bolus + 10mg kg(-1) h(-1) continuous infusion (Group II, n = 20) or 50 mg kg(-1) bolus + 10 mg kg(-1) h(-1) continuous infusion (Group III, n = 20). Results: Median and 95% confidence limits for sevoflurane MAC(EI) were 2.68 (2.48-2.85), 2.88 (2.70-3.06) and 2.96 (2.70-3.16), and for sevoflurane MAC were 2.08 (1.76-2.40), 2.26 (2.08-2.47) and 2.40 (2.19-2.68) in Groups 1, 11 and 111, respectively. The differences in MACEI and MAC among groups were not statistically significant, except Group III in MAC study (P < 0.05). Mean arterial pressures and heart rate did not increase in Groups II and III after endotracheal intubation and skin incision. Conclusions: Magnesium sulphate administered before induction of anaesthesia increases MAC of sevoflurane and reduces cardiovascular responses to intubation.
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    Hyperbaric bupivacaine affects the doses of midazolam required for sedation after spinal anaesthesia
    (Lippincott Williams & Wilkins, 2005) Toprak, HI; Ozpolat, Z; Ozturk, E; Ulger, MH; Sagir, O; Ersoy, MO
    Background and objective: Patients having spinal anaesthesia with hyperbaric bupivacaine may become sensitive to sedative drugs but no data exists about any dose-related effect of the local anaesthetic on the sedative requirement. We aimed to investigate whether hyperbaric bupivacaine dose in spinal anaesthesia has any effect on midazolam requirements. Methods: Sixty unpremedicated patients were allocated to three equal groups. Patients in Groups I and II received hyperbaric bupivacaine 0.5% 10 and 17.5 mg respectively for spinal anaesthesia and Group III was a control group without spinal anaesthesia. In Groups I and II, after the evaluation of sensory block, patients received intravenous midazolam I mg per 30 s until the Ramsay sedation score reached 3 (drowsy but responsive to command). In Group III, general anaesthesia was induced after sedation score had reached 3 using midazolam. The total dose of midazolam (mg kg(-1)) given to each patient, the level of sensory block and complications were recorded. Results: The level of sensory block was higher in Group II (T7) than Group I (T9) (P < 0.01). The doses of midazolam were 0.063 mg kg(-1) in Group I, 0.065 mg kg(-1) in Group II and 0.101 mg kg(-1) in Group III (P < 0.001). There was no correlation between level of sensory block and dose of midazolam in Group I (r = -0.293, P = 0.21) and Group II (r = 0.204, P = 0.39). Conclusions: Different doses of hyperbaric bupivacaine for spinal anaesthesia do not affect the midazolam requirements for sedation. However, spinal anaesthesia with hyperbaric bupivacaine with a maximum spread in the middle thoracic dermatomes may be associated with sedative effects and thus a reduced need for further sedation with midazolam.