A single dose of dezocine suppresses emergence agitation in preschool children anesthetized with sevoflurane-remifentanil.

BACKGROUND: Emergence agitation (EA) is a common phenomenon in preschool children during emergence from general anesthesia. This study evaluated the safety and efficacy of dezocine for emergence agitation in preschool children anesthetized with sevoflurane-remifentanil. METHODS: A total of 100 preschool children, scheduled for elective laparoscopic repair of an inguinal hernia by high ligation of the hernia sac under sevoflurane-remifentanil anesthesia were randomized into two groups: Group C (n = 50) received Ringer's lactate 10 mL and Group D received Ringer's lactate 10 mL containing dezocine 0.1 mg/kg, postoperatively. RESULTS: Incidence of EA, defined as a score ≥ 3 on Aono's four point scale or Pediatric Anesthesia Emergence Delirium (PAED) score ≥ 10 in the PACU (10% vs. 76%) and the percentage of patients with severe EA (PAED score ≥ 13) (12% vs. 76%) were significantly lower in Group D compared to Group C (P < 0.05). Mean Children and Infants Postoperative Pain Scale (CHIPPS) score was significantly lower in Group D compared to Group C (1.2 ± 0.5 vs. 5.2 ± 0.6; P < 0.05). Patients need for fentanyl (18% vs. 4%) or propofol rescue (20% vs. 0) was significantly greater in Group C compared to Group D. No significant differences in other relative aspects after surgery between groups. CONCLUSION: Administration of dezocine 0.1 mg/kg decreased the incidence and severity of EA in preschool children that had undergone laparoscopic repair of an inguinal hernia by high ligation of the hernia sac under sevoflurane-remifentanil anesthesia. TRIAL REGISTRATION: A single dose of dezocine suppresses emergence agitation in preschool children anesthetized with sevoflurane-remifentanil effectively: A double-blind, prospective, randomized, controlled study, Chinese Clinical Trial Registry (ID: ChiCTR-IOR-16010033), retrospectively registered on November 21, 2016.

Magnesium sulfate inhibits sufentanil-induced cough during anesthetic induction.

Sufentanil-induced cough is a common phenomenon during the induction of anesthesia. This double-blind, randomized, and placebo-controlled study was designed to investigate the effects of prophylactic magnesium sulfate (MgSO4) on the incidence and severity of sufentanil-induced cough. A total of 165 patients who were scheduled for elective surgery under general anesthesia were allocated into three groups (I, II, and III; n = 55 each) that were injected with either 50 ml of normal saline, 30 or 50 mg/kg of MgSO4 (diluted with normal saline into 50 ml). One minute following the injection, all patients were injected with 1.0 µg/kg of sufentanil within 5 s. The incidence and severity of cough were recorded 30 s after the sufentanil injection. The hemodynamic parameters and plasma magnesium concentration of the patients were also noted. Three patients dropped out the study due to an obvious burning sensation during the injection of 50 mg/kg of MgSO4. Although the injection of 50 mg/kg of MgSO4 increased the plasma magnesium level, the increase remained within the therapeutic range (2-4 mmol/L). The incidence of cough was much higher in group I than in groups II and III (47.1% vs. 16.4% and 7.6%, respectively, P < 0.05). Compared with group I, group III had the lowest incidence of mild cough and both groups II and III had lower incidence of moderate and severe cough (P < 0.05). There were no differences in the hemodynamic data at three timepoints among the three groups. In conclusion, sufentanil-induced cough may be suppressed effectively and safely by prophylactic use of 30 mg/kg of MgSO4 during anesthetic induction.

Magnesium sulphate suppresses fentanyl-induced cough during general anesthesia induction: a double-blind, randomized, and placebo-controlled study.

Fentanyl-induced cough is a common phenomenon during anesthesia induction. Magnesium sulphate (MgSO4) is reported to have a powerful relaxation of airway smooth muscle. This study is to investigate the effects of prophylactic MgSO4 on the incidence and severity of fentanyl-induced cough. A total of 120 patients, scheduled for elective surgery under general anesthesia, were randomly allocated into three groups (n = 40, each group) and injected with 50 ml normal saline, 30 mg/kg and 50 mg/kg of MgSO4 (diluted with normal saline into 50 ml) in groups I, II and III, respectively. One minute later all patients were injected with 5.0 µg/kg of fentanyl within 5 s. The incidence and severity of cough were recorded 30 s after fentanyl injection. Hemodynamic parameters and plasma magnesium concentration of the patients were also noted. Three patients dropped off the study due to obvious burning sense during injection of 50 mg/kg of MgSO4. Injection with 50 mg/kg of MgSO4 increased plasma magnesium level at the end of its infusion, but the latter still remained within therapeutic range (2-4 mmol/L). The incidence of cough in group I was much higher than those in groups II and III (45.0% vs. 15.0% and 8.1%, P < 0.05). Compared with the group I, both the groups II and III had lower incidence of moderate cough (P < 0.05). There were no differences in the hemodynamic data at three timepoints among the three groups. In conclusion, fentanyl-induced cough may be suppressed effectively and safely by prophylactic 30 mg/kg of MgSO4 during anesthetic induction.

Identification and characterization of reactive metabolites in myristicin-mediated mechanism-based inhibition of CYP1A2.

Myristicin belongs to the methylenedioxyphenyl or allyl-benzene family of compounds, which are found widely in plants of the Umbelliferae family, such as parsley and carrot. Myristicin is also the major active component in the essential oils of mace and nutmeg. However, this compound can cause adverse reactions, particularly when taken inappropriately or in overdoses. One important source of toxicity of natural products arises from their metabolic biotransformations into reactive metabolites. Myristicin contains a methylenedioxyphenyl substructure, and this specific structural feature may allow compounds to cause a mechanism-based inhibition of cytochrome P450 enzymes and produce reactive metabolites. Therefore, the aim of this work was to identify whether the role of myristicin in CYP enzyme inhibition is mechanism-based inhibition and to gain further information regarding the structure of the resulting reactive metabolites. CYP cocktail assays showed that myristicin most significantly inhibits CYP1A2 among five CYP enzymes (CYP1A2, CYP2D6, CYP2E1, CYP3A4 and CYP2C19) from human liver microsomes. The 3.21-fold IC50 shift value of CYP1A2 indicates that myristicin may be a mechanism-based inhibitor of CYP1A2. Next, reduced glutathione was shown to block the inhibition of CYP1A2, indicating that myristicin utilized a mechanism-based inhibition. Phase I metabolism assays identified two metabolites, 5-allyl-1-methoxy-2,3-dihydroxybenzene (M1) and 1'-hydroxymyristicin or 2',3'-epoxy-myristicin (M2). Reduced glutathione capturing assays captured the glutathione-M1 adduct, and the reactive metabolites were identified using UPLC-MS(2) as a quinone and its tautomer. Thus, it was concluded that myristicin is a mechanism-based inhibitor of CYP1A2, and the reactive metabolites are quinone tautomers. Additionally, the cleavage process of the glutathione-M1 adduct was analyzed in further detail. This study provides additional information on the metabolic mechanism of myristicin inhibition and improves risk evaluation for this compound.