The optimal bolus dose of sufentanil for satisfactory laryngeal mask airway (LMA) insertion conditions in chinese pediatric patients: A prospective double-blind randomized controlled trial (CONSORT).

BACKGROUND: This study aimed to estimate the optimal dose of sufentanil, coadministered with 2.5 mg/kg propofol, for satisfactory laryngeal mask airway (LMA) insertion conditions in Chinese children and to determine the optimal bolus dose. METHODS: Seventy-five Chinese children aged 2 to 6 years with the American Society of Anesthesiologists physical status I or II, undergoing elective minor surgery were recruited. They were randomly divided into 5 different dosage groups (0, 0.05, 0.1, 0.15, 0.2 µg/kg). A predetermined sufentanil diluted with 5 mL saline was injected 30 s, 200 s later, followed by 2.5 mg/kg propofol over 10 s. After that the insertion conditions were assessed, using a 6-category score. The duration of apnea was recorded. A Probit analysis was performed to determine the ED50 and ED95 with 95% confidence interval for optimal conditions. RESULTS: There were less hemodynamic changes in all sufentanil groups than propofol-only group, with 0.2 µg/kg patients showing the most stable cardiovascular responses and best insertion conditions. However, the duration of apnea increased with the increasing dosage of sufentanil. From Probit analysis, the ED50 and ED95 of sufentanil for optimum score were 0.064 µg/kg and 0.177 µg/kg, respectively. CONCLUSION: In combination with propofol for anesthesia induction in Chinese children, sufentanil 0.2 µg/kg could prevent patients from dramatic hemodynamic change, providing satisfactory LMA insertion conditions.

Analgesic effect of AG490, a Janus kinase inhibitor, on oxaliplatin-induced acute neuropathic pain.

Neuropathic pain often occurs during chemotherapy with oxaliplatin. AG490 has been shown to exert an antagonistic effect on inflammatory pain, but its effect on oxaliplatin-induced neuropathic pain remains poorly understood. This study sought to observe the analgesic effect of AG490 on acute neuropathic pain induced by a single oxaliplatin treatment and to address the possible mechanism. In this study, we established a model of oxaliplatin-induced acute neuropathic pain by intraperitoneal injection of 6 mg/kg oxaliplatin. On day 2 after injection, models were intraperitoneally injected with 1, 5, or 10 mg/kg AG490. Paw withdrawal threshold to mechanical stimuli and tail withdrawal latency to cold stimuli were determined. Western blot assay was performed to detect the expression of spinal phosphorylated signal transducer and activator of transcription 3 (p-STAT3). Immunohistochemistry was used to determine the immunoreactivity of p-STAT3 and interleukin-6. Results demonstrated that paw withdrawal threshold and tail withdrawal latency were significantly increased by the treatment of AG490 in rats. There was no significant difference in the effect among the different doses of AG490. AG490 10 mg/kg decreased the expression of p-STAT3, the immunoreactivity of p-STAT3 and interleukin-6 in spinal cord of acute neuropathic pain rats. These findings confirm that AG490 can attenuate oxaliplatin-induced acute neuropathic pain and is associated with the inhibition in the JAK/STAT3 signaling pathway.

[Analgesic effect of dexmedetomidine on oxaliplatin-induced neuropathic pain in rats].

OBJECTIVE: To investigate the analgesic effect of dexmedetomidine (Dex) on oxaliplatin-induced neuropathic pain in rats and explore its mechanism. METHODS: SD rats were randomly divided into control, model, Dextreatment, and Dex + atipamezole groups. In the latter 3 groups, rat models of neuropathic pain were established by a single intraperitoneal injection of oxaliplatin. The paw withdrawal threshold (PWT) to mechanical stimuli and tail withdrawal latency (TWL) to thermal stimuli of the rats were determined. Western blotting and immunofluorescence assay were performed to observe the expression of spinal phosphorylated STAT3 (p-STAT3) in the rats. RESULTS: Compared with the rats in the control group, the rats in the model group and Dex+atipamezole group showed significantly decreased PWT and TWL (cold) and increased expression of p-STAT3 in the spinal cord (P < 0.05). In Dex group, PWT and TWL (cold) were significantly increased (P < 0.05) and p-STAT3 expression in the spinal cord was significantly decreased (P < 0.01) 60 to 120 after Dex treatment as compared with those in the model group, and these effects of Dex were significantly attenuated by the administration of atipamezole (P < 0.05). CONCLUSIONS: Dex can alleviate oxaliplatin-induced neuropathic pain in rats by inhibiting the phosphorylation of STAT3 in the spinal cord.