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    Effect of epidural levobupivacaine on recovery from vecuronium-induced neuromuscular block in patients undergoing lower abdominal surgery
    (Australian Soc Anaesthetists, 2011) Sahin, S. H.; Colak, A.; Sezer, A.; Arar, C.; Sevdi, S.; Gunday, I.; Sut, N.
    The aim of this study was to evaluate the effect of epidural levobupivacaine on recovery from vecuronium-induced neuromuscular block. Ninety patients undergoing lower abdominal surge, were randomised into two groups after an epidural test dose: the epidural group (n=45) received a bolus of 15 nil of 0.5% levobupivacaine whereas the control group (n=45) did not. Anaesthesia was induced and maintained with propofol, fentanyl, vecuronium and nitrous oxide. Neuromuscular block was induced with vecuronium 0.1 mg/kg and monitored with acceleromyographic train-of-four at the adductor pollicis. Patients in each group received neostigmine at 25% recovery of the first twitch of train-of-four during recovery from anaesthesia. The effect of epidural levobupivacaine on the speed of recovery of neuromuscular function was evaluated. The lag time, onset time and time from vecuronium administration until 25% T1 recovery did not differ between the groups. The times of the recovery index (the time from 25% to 75% recovery of T1) and of the DUR 25-train-of-four 90 (time from 25% T1 to train-of-four ratio of 0.9) in the epidural group were significantly longer than those for the control group (5.2 [2.1] vs 3.04 [1.02] minutes and 10.8 [3.3] vs 8.2 [2.3] minutes, P < 0.001). This study shows that epidural levobupivacaine significantly delays the train-of-four recovery from vecuronium-induced block. Although the interaction is small in the clinical setting, anaesthetists should take this interaction into consideration when combining general and epidural anaesthesia during surgery.
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    Effects of halothane, isoflurane, and sevoflurane on lipid peroxidation following experimental closed head trauma in rats
    (Wiley, 2008) Yurdakoc, A.; Gunday, I.; Memis, D.
    Background: In a rat closed head trauma model we examined both the time course of lipid peroxidation and the effects of halothane, isoflurane, and sevoflurane on it by analysis of malondialdehyde (MDA) formation. Methods: Animals were divided randomly into five groups: sham-operated (SO), n=18; control-closed head trauma to left frontal pole, n=18; closed head trauma model+halothane, n=18; closed head trauma model+isoflurane, n=18; and closed head trauma model+sevoflurane, n=18. Halothane, isoflurane, or sevoflurane were applied 15 min after trauma for 30 min. Rats were euthanized 1,3, and 5 h after the inhalation agents. Brain tissue samples were taken 5 mm from the left and right frontal poles. MDA was considered to reflect the degree of lipid peroxidation. Results: MDA concentrations were greater in the control, halothane, sevoflurane, and isoflurane groups than in SO animals (P < 0.001). No statistical difference between the hemispheres was found between the halothane, isoflurane, or sevoflurane groups, but MDA levels were lower with isoflurane than in the halothane, sevoflurane, and control groups at 1, 3, and 5 h (P < 0.001). MDA levels were higher as compared with the halothane and sevoflurane groups at 1 h but not at 3 or 5 h (P < 0.001). Conclusion: MDA levels with the isoflurane group were lower than in the other trauma groups, which suggest that isoflurane, given after closed head trauma, might be protective against lipid peroxidation of cerebral injury.