The Effects of Lidocaine on the Onset Time of Rocuronium-induced Neuromuscular Blockade and Intubation Condition in Children / 대한마취과학회지

BACKGROUND: Many studies have demonstrated that lidocaine directly relaxes airway smooth muscle by decreasing Ca2+. Lidocaine is well known as an agent to decrease the neuromuscular transmission and potentiate the neuromuscular block of muscle relaxants. The purpose of this study was to examine the influence of lidocaine on the onset time of rocuronium and intubating conditions in children. METHODS: 84 children, ASA physical status 1 or 2, were randomly divided into 3 groups (Group 1, 2 and 3). Anesthesia was induced with fentanyl 1 microgram/kg and propofol 3 mg/kg and we maintained anesthetic states with 10 mg/kg/h of propofol. We intravenously injected saline 1.0 ml/kg to Group 1, lidocaine 1.0 mg/kg to Group 2 and lidocaine 1.5 mg/kg to Group 3. After 2 minutes, all patients received rocuronium 0.6 mg/kg. Intubation was performed 2 minutes after the administration of rocuronium, and intubating conditions were evaluated. Neuromuscular blockades were assessed by train-of-four (TOF) at the adductor pollicis muscle with supramaximal stimulation of the ulnar nerve (2 Hz, 0.2 msec) every 15 second. RESULTS: There was no difference between the onset time of Group 1 (107.8 +/- 54.4 sec), Group 2 (112.0 +/- 39.3 sec) and Group 3 (90.0 +/- 39.5 sec). Intubating conditions and hemodynamic response to tracheal intubation were similar in all groups. CONCLUSIONS: Additional 1.5 mg/kg lidocaine to 0.6 mg/kg rocuronium neither influences intubating condition nor accelerate the onset of rocuronium during induction of anesthesia in the children.

Dynorphin A (1-17) was Selective tomicro-Opioid Receptor in Agonist-Stimulated 35S GTPgammaS Binding in Cortical and Thalamic Membranes of Monkey / 대한마취과학회지

BACKGROUND: Dynorphin A (1-17) is conceived as an endogenous opioid peptide with a high degree of selectivity forkappa- opioid receptor even though it has been reported to sometimes act like amicro- opioid agonist. The aim of this study was to investigate [35S] GTPgammaS binding stimulated activation by dynorphin A (1-17) in the cerebral and thalamic membranes of a rhesus monkey. METHODS: The rhesus monkey (Macaca mulatta, male, n = 1) was euthanized for the preparation of the cerebral and thalamic membranes. Protein concentrations were determined by the Bradford method. In the dynorphin A (1-17)-stimulated [35S] GTPgammaS binding dose-response curve, EC50 (effective concentration 50 nM) and maximum stimulation (% over basal) were determined in the absence or presence of themicro-andkappa-opioid receptor antagonists naloxone (20 nM) and norbinaltorphimine (nor-BNI, 3 nM), respectively. E2078-stimulated [35S] GTPgammaS binding was also determined in the absence or presence ofmicro-andkappa-opioid receptor antagonists in the cortical membrane and compared with dynorphin A (1-17). RESULTS: Values of EC50 and maximum stimulation of dynorphin A (1-17)-stimulated [35S] GTPgammaS binding were as follows: cortex (474 nM/32.0%) and thalamus (423 nM/45.3%). Nor-BNI (3 nM) did not antagonize dynorphin A (1-17)-stimulated [35S] GTPgammaS binding at all in cortical or thalamic membrane, but naloxone (20 nM) produced a 12.2 fold rightward shift of the dynorphin A (1-17)-stimulated [35S] GTPgammaS binding dose-response curve in the thalamic membrane. The EC50 and the maximum stimulation of E2078-stimulated [35S] GTPgammaS binding were 65.6 nM and 22.7%, respectively. In E2078-stimulated [35S] GTPgammaS binding, the dose-response curve was antagonized not by nor-BNI but by naloxone but in the cortical membrane (a 14.2 times rightward shift). CONCLUSIONS: Dynorphin A (1-17) is selective formicro-opioid receptor in agonist-stimulated [35S] GTPgammaS binding in the cortical and thalamic membranes of rhesus monkey.