Summary

Background and objective: Extremity surgery with tourniquet to provide a bloodless field may be a good human model for ischaemia reperfusion (IR) injury. The aim of this study was to investigate the effects of three different modes of propofol use on tourniquet induced IR injury in lower extremity operations. Methods: Thirty-three consecutive ASA Grade I and II patients were randomized into three groups of 11 patients each. In the spinal group (Group S), after intrathecal anaesthesia, sedation was given with a propofol infusion at 2 mg kg−1 h−1 after a 0.2 mg kg−1 bolus dose and fentanyl 100 μg. In the general (Group G) and TIVA (Group T) groups, general anaesthesia was induced with propofol 2 mg kg−1 with fentanyl 100 μg and maintained with inhalation of halothane or infusion of propofol respectively. Venous blood samples were obtained at different time points for measurements of plasma malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) levels. Results: Plasma MDA levels were increased significantly in the Group G at 1 min before tourniquet release and 5 and 20 min after tourniquet release compared with before induction of general anaesthesia (baseline). Before intrathecal anaesthesia and before induction of general anaesthesia significantly decreased levels of MDA were observed both before and after tourniquet release compared to baseline. Plasma SOD and CAT concentrations were decreased significantly only at tourniquet release in the Group G compared with baseline. In the Groups S and T these enzymes were not changed significantly. Plasma GPx levels were not altered in any groups. Conclusion: Propofol administration may inhibit lipid peroxidation and restore antioxidant enzyme levels in extremity surgery requiring tourniquet application.

Summary

Introduction: The influence of the twitch height of the adductor pollicis muscle during baseline measurements on the pharmacodynamic parameters of mivacurium was prospectively evaluated. Patients and methods: Fifty adult patients were anaesthetized with propofol and alfentanil. Neuromuscular function was monitored mechanomyographically by measuring the force of the adductor pollicis muscle following stimulation of the ulnar nerve. Following a stabilization period of 20 min, the individual twitch height of the adductor pollicis muscle was determined before a single bolus of mivacurium (75 μg kg−1) was administered. Patients were divided into two groups. The data of patients whose thumb adduction force was below the median value of all patients were the ‘low force’ group (9.1 ± 1.4 N) and the data of all other patients were the ‘high force’ group (13.7 ± 1.8 N). Results: In the ‘high force’ group, maximum neuromuscular blockade of mivacurium was deeper (0.97 ± 0.05 vs. 0.93 ± 0.06; P < 0.05) and onset faster (2.9 ± 1.1 min vs. 4.0 ± 1.2 min; P < 0.05). Neuromuscular recovery did not differ between the groups. Conclusion: The different onset speeds reflect either different sensitivity to neuromuscular blocking agents with respect to patients' muscle power or a problem of the mechanomyographic measuring technique.

Summary

Background and objective: To compare the inotropic and lusitropic effect of lidocaine and mepivacaine on rat papillary muscle. Methods: Effects of lidocaine and mepivacaine (10−8−10−3 M) were studied in rat left ventricular papillary muscles in vitro at a calcium concentration of 1 mmol, under low (isotony) and high (isometric) loads. Results: Lidocaine induced a significant negative inotropic effect in isotonic and isometric conditions whereas mepivacaine did not. Mepivacaine only induced a negative inotropic effect when added as a bolus for the highest concentration and this effect was significantly more pronounced with lidocaine than with mepivacaine (active force at 10−3 M: 63 ± 10 vs. 84 ± 10% of baseline, P < 0.05). Increasing calcium concentration resulted in a greater positive inotropic effect in the control (199 ± 11% of baseline) and mepivacaine groups (197 ± 22% of baseline) when compared to the lidocaine group (163 ± 19% of baseline, P < 0.05 vs. lidocaine and control groups), suggesting an impairment on intracellular Ca2+ handling by lidocaine. A negative lusitropic effect under low load was observed only for mepivacaine and suggested an impairment of sarcoplasmic reticulum function. Lidocaine and mepivacaine did not modify postrest potentiation but significantly depressed the force–frequency relationship. Conclusions: The negative inotropic and lusitropic effects induced by lidocaine were more important than that of mepivacaine and may involve an impairment of intracellular Ca2+ handling.