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Objective/Hypothesis: Fentanyl is commonly administered toward the end of tonsillectomy to prevent emergence delirium and reduce postoperative pain. However, it can delay emergence from anesthesia and increase the risk of postoperative nausea and vomiting (PONV). The goal of our study was to compare the risk of PONV based on the timing of fentanyl administration at the end of tonsillectomy in children. Study Design: Prospective, double‐blind, randomized controlled trial. Methods: One hundred forty patients aged 3 to 7 years undergoing tonsillectomy were divided into two groups. Fentanyl (1 μg/kg) was administered at the end of surgery in group 1 (n = 70) and at 10 to 15 minutes before the end of surgery in group 2 (n = 70). Time to regular breathing and time to emergence from anesthesia were measured from the end of surgery. PONV and pediatric anesthesia emergence delirium scale scores were assessed every 10 minutes after admission to the postanesthesia care unit. Results: Incidences of PONV (2.9% vs. 2.9%, P >.99) and emergence delirium (11.4% vs. 5.7%, P =.23) were not significantly different between the two groups. Time to regular breathing (mean difference = 2.3 minutes; 95% confidence interval [CI]: 0.9 to 3.7 minutes) and time to emergence (median difference = 6.5 minutes; 95% CI, 2.5 to 10.5 minutes) were significantly longer in group 1 than in group 2. Conclusions: Although there was no beneficial effect on PONV, recovery of regular breathing and consciousness was quicker with earlier fentanyl administration. Emergence delirium was well‐controlled, similar to that with fentanyl administration at the end of surgery. Level of Evidence: 1b Laryngoscope, 2020 [ABSTRACT FROM AUTHOR]

Artemin, one of the glial cell line-derived neurotrophic factor (GDNF) family, enhances the generation and survival of early sympathetic neurons and superior cervical ganglion (SCG) neurons. Src-family kinases (SFK) are involved in the growth and differentiation of cells, which are composed of unique Src homology 2 (SH2), Src homology 3 (SH3) and kinase domains. Various extra-cellular molecules containing growth factors and G-protein coupled receptors stimulate SFK. In this report, artemin is shown to have a significant effect on the neurite growth of dorsal root ganglia (DRG) neurons. Also, artemin triggers Src-family kinase activation and the phosphorylation of extra-cellular signal-regulated kinases (ERK) mitogen-activated protein kinase (MAPK). Artemin also regulated actin polymerization. There are several indications that another SH3-containing protein, Hck, and an SH3-containing adaptor protein, Nck1, play an important role in the organization of the actin cytoskeleton by cellular signalling. These findings suggest that the exploration of binding partners for the SH3 domain could provide an insight into regulation between the microtubule and actin networks. The binding partners for the SH3 domains of Nck, Src and Hck that we identified were Smc chromosome segregation ATPases, FOG Zn-finger protein and the FYVE zinc-binding domain, respectively. Copyright © 2007 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

The article reports a successful nasotracheal intubation using two different-sized fibreoptic bronchoscopes (FOBs) in a small infant with Pierre Robin syndrome. A 6-month-old-female child (6 kg, 60 cm) with Pierre Robin syndrome was scheduled for external distraction device application. She had micrognathia and glossoptosis, which are the characteristic features of Pierre Robin syndrome. Her mouth opening was limited to 1 cm. She snored while asleep, but showed no signs of dyspnoea. To perform the spray-as-you-go technique in infants to prevent cough reflex and laryngospasm during fibreoptic intubation, a FOB has to be small enough to pass through the small tracheal tube and has to have a working channel to spray local anaesthetics.

Background: Naloxone, an opioid antagonist, has a cardiovascular pressor effect and has been used in various types of shock states. The aim was to determine the non-opioid effect on direct cardiac muscle contractility and explore the mechanism using guinea pig right ventricular papillary muscles., Methods: With institutional approval, isometric contractile force was measured in modified normal and 26 mM K+ Tyrode solution at various stimulation rates. The effects of naloxone on sarcoplasmic recticulum function were evaluated by measuring rested-state contraction in low Na+ (25 mM) Tyrode solution and rapid cooling contracture in modified normal Tyrode solution. Normal and slow action potentials (APs) were measured using conventional microelectrode technique. Patch clamp study was performed to examine the direct effect on Ca2+ current in cardiac ventricular myocytes., Results: Naloxone (50, 100, and 200 microM) caused a concentration-dependent depression of peak force and maximal rate of force development. Modest depression, approximately 20%, was shown in rested-state contraction in low Na+ Tyrode solution. Naloxone (100 microM) modestly depressed the rapid cooling contracture to 80 +/- 3% of baseline, accompanied by prolongation of time to peak contracture by approximately 37%. In 26 mM K+ Tyrode solution, naloxone (100 microM) markedly and selectively depressed the late force development. While naloxone (100 microM) did not alter the amplitude and dV/dt-max in normal and slow APs at 0.25 Hz, AP duration was prolonged significantly. In patch clamp experiment, naloxone (50 microM) depressed Ca2+ current by approximately 50%., Conclusions: The direct myocardial depressant effect of naloxone appeared to be in part caused by depression of Ca2+ influx through cardiac membrane. Sarcoplasmic reticulum function appeared to be modestly depressed.