Prevention of emergence agitation in seven children receiving low-dose ketamine and propofol total intravenous anesthesia

Emergence agitation (EA) can be a distressing side effect of pediatric anesthesia. We observed no recurrence of EA after a low-dose ketamine infusion was added to propofol total intravenous anesthesia in a series of seven pediatric oncology patients repetitively anesthetized for radiation therapy. EA had been documented in all seven patients but did not recur in any of 122 subsequent anesthetics in which this technique was used. Based on these findings, we recommend the addition of low-dose ketamine to propofol infusions for total intravenous anesthesia in order to prevent EA in children with a history of EA

Influence of the priming technique on pharmacodynamics and intubating conditions of cisatracurium

Study Objectives: To determine the effects of the priming technique on the intubating conditions and pharmacodynamics of different doses of cisatracurium. Design: Open-label, randomized study. Setting: Operating room of a university-affiliated hospital. Patients: 60 ASA physical status I, II, and III female patients. Interventions: Patients were randomly assigned to one of four groups. Patients from Groups 1, 2, and 3 received 0.01 mg/kg cisatracurium as a priming dose, and patients from Group 4 received placebo. Four minutes later, patients from Groups 1, 2, 3, and 4 received the following intubating doses of cisatracurium: 0.09 mg/kg, 0.14 mg/kg, 0.19 mg/kg, and 0.2 mg/kg, respectively. Anesthesia was induced with thiopental sodium, sufentanil, droperidol, and nitrous oxide (N2O; 6 L/min) in oxygen (O2; 4 L/min) and maintained with isoflurane up to 0.7%, N2O in O2, and sufentanil. Mechanomyography assessed the neuromuscular function of the adductor pollicis with train-of-four supramaximal impulses. The trachea was intubated when the amplitude of the first twitch decreased to 10% to 15% of control. Measurements and Main Results: There were no significant differences among the groups regarding the demographic data, the value of the first twitch at 60 seconds, the time to 90% block, and the onset time. Clinical duration of cisatracurium was significantly different between Group 3 and Groups 1 and 2, whereas Group 4 differed significantly from Group 1. Intubating conditions did not differ significantly among the groups. Conclusion: When primed, cisatracurium 0.09 mg/kg and 0.14 mg/kg produced an onset time comparable with that of 0.2 mg/kg and allowed an earlier spontaneous recovery (p < 0.05). In this study, there was no benefit in priming cisatracurium 0.19 mg/kg

Nitrous Oxide Induces Prominent Cell Proliferation in Adult Rat Hippocampal Dentate Gyrus

The identification of distinct and more efficacious antidepressant treatments is highly needed. Nitrous oxide (N2O) is an N-methyl-D-aspartic acid (NMDA) antagonist that has been reported to exhibit antidepressant effects in treatment-resistant depression (TRD) patients. Yet, no studies have investigated the effects of sub-anesthetic dosages of N2O on hippocampal cell proliferation and neurogenesis in adult brain rats. In our study, adult male Sprague-Dawley rats were exposed to single or multiple exposures to mixtures of 70% N2O and 30% oxygen (O2). Sham groups were exposed to 30% O2 and the control groups to atmospheric air. Hippocampal cell proliferation was assessed by bromodeoxyuridine (BrdU) incorporation, and BrdU-positive cells were counted in the dentate gyrus (DG) using confocal microscopy. Results showed that while the rates of hippocampal cell proliferation were comparable between the N2O and sham groups at day 1, levels increased by 1.4 folds at day 7 after one session exposure to N2O. Multiple N2O exposures significantly increased the rate of hippocampal cell proliferation to two folds. Therefore, sub-anesthetic doses of N2O, similar to ketamine, increase hippocampal cell proliferation, suggesting that there will ultimately be an increase in neurogenesis. Future studies should investigate added N2O exposures and their antidepressant behavioral correlates

Image_1_Nitrous Oxide Induces Prominent Cell Proliferation in Adult Rat Hippocampal Dentate Gyrus.TIF

<p>The identification of distinct and more efficacious antidepressant treatments is highly needed. Nitrous oxide (N₂O) is an N-methyl-D-aspartic acid (NMDA) antagonist that has been reported to exhibit antidepressant effects in treatment-resistant depression (TRD) patients. Yet, no studies have investigated the effects of sub-anesthetic dosages of N₂O on hippocampal cell proliferation and neurogenesis in adult brain rats. In our study, adult male Sprague-Dawley rats were exposed to single or multiple exposures to mixtures of 70% N₂O and 30% oxygen (O₂). Sham groups were exposed to 30% O₂ and the control groups to atmospheric air. Hippocampal cell proliferation was assessed by bromodeoxyuridine (BrdU) incorporation, and BrdU-positive cells were counted in the dentate gyrus (DG) using confocal microscopy. Results showed that while the rates of hippocampal cell proliferation were comparable between the N₂O and sham groups at day 1, levels increased by 1.4 folds at day 7 after one session exposure to N₂O. Multiple N₂O exposures significantly increased the rate of hippocampal cell proliferation to two folds. Therefore, sub-anesthetic doses of N₂O, similar to ketamine, increase hippocampal cell proliferation, suggesting that there will ultimately be an increase in neurogenesis. Future studies should investigate added N₂O exposures and their antidepressant behavioral correlates.</p

Image_2_Nitrous Oxide Induces Prominent Cell Proliferation in Adult Rat Hippocampal Dentate Gyrus.TIFF

<p>The identification of distinct and more efficacious antidepressant treatments is highly needed. Nitrous oxide (N₂O) is an N-methyl-D-aspartic acid (NMDA) antagonist that has been reported to exhibit antidepressant effects in treatment-resistant depression (TRD) patients. Yet, no studies have investigated the effects of sub-anesthetic dosages of N₂O on hippocampal cell proliferation and neurogenesis in adult brain rats. In our study, adult male Sprague-Dawley rats were exposed to single or multiple exposures to mixtures of 70% N₂O and 30% oxygen (O₂). Sham groups were exposed to 30% O₂ and the control groups to atmospheric air. Hippocampal cell proliferation was assessed by bromodeoxyuridine (BrdU) incorporation, and BrdU-positive cells were counted in the dentate gyrus (DG) using confocal microscopy. Results showed that while the rates of hippocampal cell proliferation were comparable between the N₂O and sham groups at day 1, levels increased by 1.4 folds at day 7 after one session exposure to N₂O. Multiple N₂O exposures significantly increased the rate of hippocampal cell proliferation to two folds. Therefore, sub-anesthetic doses of N₂O, similar to ketamine, increase hippocampal cell proliferation, suggesting that there will ultimately be an increase in neurogenesis. Future studies should investigate added N₂O exposures and their antidepressant behavioral correlates.</p