Inhibitory Effects of Propofol Mixed with Lidocaine on Fentanyl Induced Cough Reflex / 대한마취과학회지

BACKGROUND: Propofol and lidocaine have been purported to attenuate bronchoconstriction induced by fentanyl administration during induction of anesthesia. The purpose of the present study was to study the synergic bronchodilation effect of propofol mixed with lidocaine. METHODS: Two hundred and thirty four patients were randomly allocated to five groups: Group 1 (n = 60, normal saline 0.25 ml/kg followed by fentanyl 3ng/kg), Group 2 (n = 30, propofol 2 mg/kg mixed with normal saline 0.05 ml/kg followed by normal saline 0.06 ml/kg), Group 3 (n = 50, propofol 2 mg/kg mixed with normal saline 0.05 ml/kg followed by fentanyl 3ng/kg), Group 4 (n = 33, propofol 2 mg/kg mixed with lidocaine 1 mg/kg followed by normal saline 0.06 ml/kg) and Group 5 (n = 61, propofol 2 mg/kg mixed with lidocaine 1 mg/kg followed by fentanyl 3ng/kg). All patients were injected with fentanyl or normal saline two minutes after administration of propofol premixed with lidocaine or normal saline, respectively. We checked the cough reflex, injection pain, oxygen desaturation and chest wall rigidity. RESULTS: There was a significant difference in the incidence of cough reflex between group 1 and 3 or 5. The incidience of group 5 was significantly lower than in group 3. CONCLUSIONS: This study suggests that a propofol-lidocaine mixture should be considered when patients require bronchodilation during induction of anesthesia.

Morphine Protects Peroxynitrite-induced Cell Death in Primary Rat Neonatal Astrocytes / 대한마취과학회지

BACKGROUND: Astrocytes, representing a major non-neuronal cell population in the central nervous system (CNS), contain opioid receptors and are actively involved in several brain functions. This study is designed to evaluate the effects by which morphine contributes to cytotoxicity of nitric oxide (NO) species including NO and peroxynitrite (ONOO(-)) in primary astrocytes isolated from the cerebral cortexes of 1 - 2 day Sprague-Dawley rats. METHODS: The cultured cells were pretreated with morphine and exposed to 3-morpholinosydnonimine (SIN-1) which simultaneously generates NO and superoxide, thus possibly forming peroxynitrite. The cell damage was assessed by using an MTT (methylthizol-2-yl-2, 5-diphenyl, tetrazolium bromide) assay. Morphological nuclear changes of the cells after exposure to SIN-1 for 24 hours was evaluated by using 4', 6-diamidino-2-phenylindole (DAPI) staining. RESULTS: Morphine significantly protected primary rat astrocytes in a dose-dependent manner from the death mediated by sodium nitroprusside (SNP), a donor of nitric oxide, and SIN-1. Moreover, it was found that naloxone antagonized the protective effect of morphine on SIN-1-induced cell death, revealed as apoptosis by the occurrence of morphological nuclear changes characteristic of apoptosis. Morphine also inhibited the nuclear condensation of SIN-1-treated cells, however the action of morphine was antagonized by pretreatment of naloxone. The protective role of morphine on SIN-1-induced cytotoxicity was inhibited by DL-Buthionine-[S, R]-sulfoximine (BSO). Furthermore, the effects of morphine on SIN-1-induced cytotoxicity were blocked by pretreatment of Gi protein inhibitor, pertussis toxin, and phosphoinositide 3-kinase (PI3 kinase) inhibitors, Wortmannin and LY294002. CONCLUSIONS: These results suggest that morphine may protect primary rat astrocytes from NO species via the signaling cascades involving G-protein and PI3-kinase, and possibly regulates the anti-oxidant, glutathione (GSH).