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Background and objective Intravenous lidocaine infusion has been shown to facilitate postoperative recovery after major abdominal surgery. The current randomized controlled study was performed to assess the effect of perioperative intravenous lidocaine infusion on pain intensity, bowel function and cytokine response after larparoscopic cholecystectomy. Methods Eighty patients undergoing laparoscopic cholecystectomy were randomly allocated to receive intravenous lidocaine (bolus injection of 1.5 mg/kg lidocaine at induction of anesthesia, then a continuous infusion of 2 mg/kg/h until the end of surgery) or an equal volume of saline. Patients, anesthesiologists, and study personnel were blinded, and anesthesia and multimodal perioperative analgesia were standardized. Blood cytokines were measured at scheduled times within 48 h. Pain scores, opioid consumption, time to first flatus and time to first bowel movement were also measured after surgery. Results Seventy-one of the 80 patients who were recruited completed the study protocol. Patient demographics were similar in the two groups. Lidocaine significantly reduced pain intensity [visual analogue scale (VAS), 0–10 cm] at 2 h (lidocaine 3.01 ± 0.65 cm vs. placebo 4.27 ± 0.58 cm, p = 0.01) and 6 h (lidocaine 3.38 ± 0.42 cm vs. placebo 4.22 ± 0.67 cm, p = 0.01) and total fentanyl consumption 24 h after surgery (lidocaine 98.27 ± 16.33 μg vs. placebo 187.49 ± 19.76 μg, p = 0.005). Time to first flatus passage (lidocaine 20 ± 11 h vs. placebo 29 ± 10 h, p = 0.01) and time to first bowel movement (lidocaine 41 ± 16 h vs. placebo 57 ± 14 h, p = 0.01) were also significantly shorter in patients who received lidocaine. Intravenous lidocaine infusion experienced less cytokine release than the control group. Conclusions This study indicates that perioperative systemic lidocaine improves postoperative recovery and attenuates the initiation of excessive inflammatory response following laparoscopic cholecystectomy.

Background It has been demonstrated that κ-opioid receptor agonists can reduce hypoxia–ischemia brain injury in animal models. However, it is unclear how the κ-opioid receptor responds to hypoxia–ischemia. In the current study, the authors used an in vitro model of oxygen–glucose deprivation and reoxygenation to explore how κ-opioid receptors respond to hypoxia and reoxygenation. Methods Mouse neuroblastoma Neuro2A cells were stably transfected with mouse κ-opioid receptor–tdTomato fusion protein or Flag-tagged mouse κ-opioid receptor, divided into several groups (n = 6 to 12), and used to investigate the κ-opioid receptor movement. Observations were performed under normal oxygen, at 30 min to 1 h after oxygen–glucose deprivation and at 1 h after reoxygenation using high-resolution imaging techniques including immunoelectronmicroscopy in the presence and absence of κ-opioid receptor antagonist, dynamin inhibitors, potassium channel blockers, and dopamine receptor inhibitor. Results Hypoxic conditions caused the κ-opioid receptor to be internalized into the cells. Inhibition of dynamin by Dyngo-4a prevented the receptor internalization. Interestingly, a specific κ-opioid receptor antagonist norbinaltorphimine blocked internalization, suggesting the involvement of activation of a specific κ-opioid receptor. κ-Opioid receptor internalization appears to be reversed by reoxygenation. Quantities of intracellular κ-opioid receptor-associated gold particles as demonstrated by immunoelectron microscopy were increased from 37 to 85% (P < 0.01) after oxygen–glucose deprivation. Potassium channel blockers and dopamine receptor inhibitor failed to block hypoxia-induced κ-opioid receptor internalization. Conclusions Hypoxia induces reversible κ-opioid receptor internalization, which was inhibited by selective κ-opioid receptor antagonists or dynamin inhibitor, and can be reversed by reoxygenation in neuroblastoma cells, indicating the modulating effects between κ-opioid receptor and hypoxia via κ-opioid receptor activation and the dynamin-dependent mechanism.

Background Simulation-based training (SBT) has become a standard for medical education. However, the efficacy of simulation based training in airway management education remains unclear. Methods The aim of this study was to evaluate all published evidence comparing the effectiveness of SBT for airway management versus non-simulation based training (NSBT) on learner and patient outcomes. Systematic review with meta-analyses were used. Data were derived from PubMed, EMBASE, CINAHL, Scopus, the Cochrane Controlled Trials Register and Cochrane Database of Systematic Reviews from inception to May 2016. Published comparative trials that evaluated the effect of SBT on airway management training in compared with NSBT were considered. The effect sizes with 95% confidence intervals (CI) were calculated for outcomes measures. Results Seventeen eligible studies were included. SBT was associated with improved behavior performance [standardized mean difference (SMD):0.30, 95% CI: 0.06 to 0.54] in comparison with NSBT. However, the benefits of SBT were not seen in time-skill (SMD:-0.13, 95% CI: −0.82 to 0.52), written examination score (SMD: 0.39, 95% CI: −0.09 to 0.86) and success rate of procedure completion on patients [relative risk (RR): 1.26, 95% CI: 0.96 to 1.66]. Conclusion SBT may be not superior to NSBT on airway management training.

Opioid receptors and their ligands produce powerful analgesia that is effective in perioperative period and chronic pain managements accompanied with various side effects including respiratory depression, constipation and addiction etc. Opioids can also interfere with the immune system, not only participating in the function of the immune cells, but also modulating innate and acquired immune responses. The traditional notion of opioids is immunosuppressive. Recent studies indicate that the role of opioid receptors on immune function is complicated, working through various different mechanisms. Different opioids or opioids administrations show various effects on the immune system: immunosuppressive, immunostimulatory, or dual effect. It is important to elucidate the relationship between opioids and immune function, since immune system plays critical role in various physiological and pathophysiological processes, including the inflammation, tumor growth and metastasis, drug abuse, and so on. This review article tends to have an overview of the recent work and perspectives on opioids and the immune function.

Postoperative pain management remains a significant challenge after abdominal surgery.The aim of this meta-analysis was to evaluate the efficacy of systemic lidocaine for postoperative pain management and recovery after abdominal surgery.Data were derived from Medline (1966-2010), CINAHL, The Cochrane Central Register of Controlled Trials, and Scopus.Randomized controlled trials of systemic administration of lidocaine for postoperative analgesia and recovery after abdominal surgery in adults, ie,18 years, were considered.Combined data were analyzed with use of a random-effects model.Data on opioid consumption, postoperative pain intensity, opioid-related side effects, time to first flatus, time to first bowel movement, and length of hospital stay were extracted.Twenty-one trials comparing systemic lidocaine with placebo or blank control for postoperative analgesia and recovery after abdominal surgery were included in this meta-analysis. Weighted mean difference for cumulative analgesic opioid (morphine) consumption 48 hours after surgery was -7.04 mg (95% CI: -10.40, -3.68, I2= 46.1%).Systemic lidocaine also significantly reduced postoperative pain intensity(visual analog scale, 0-100 mm) 6 hours after surgery at rest (weighted mean difference: -8.07 mm (95% CI: -14.69, -1.49); I2 = 90.6%) and during activity (weighted mean difference: -10.56 mm (95% CI: -16.89, -4.23), I2 = 82%). The time to first flatus and bowel movement was significantly shortened with lidocaine intervention by 6.92 hours (95% CI: -9.21, -4.63, I2 = 62.8%) and 11.74 hours (95% CI:-16.97, -6.51, I2 = 0). Moreover, systemic lidocaine also reduced hospital length of stay following the open procedure (weighted mean difference: -0.71 days (95% CI: -1.35, -0.07); I2 = 37.3%).Heterogeneity of study results is the main limitation of this meta-analysis.Perioperative systemic lidocaine may be a useful adjunct for postoperative pain management by decreasing postoperative pain intensity, reducing opioid consumption, facilitating GI function, and shortening length of hospital stay.

During the perinatal period, the pharmacokinetics and pharmacodynamics of drugs may be altered. Data about the neurotoxicity of intrathecal local anesthetics in the peripartum period are lacking. So we hypothesized that the neurotoxicity of intrathecal lidocaine during perinatal period may be changed. Therefore, we designed the present study to determine whether the neurotoxicity of intrathecal lidocaine in postpartum rats would be different from that in nonpregnant, virgin rats. Postpartum and nonpregnant rats randomly received an intrathecal infusion of lidocaine 50 mg/mL in saline, lidocaine 20 mg/mL in saline, or saline for 1 h at a rate of 1 μL/min. Four days after drug infusion, the rats were assessed for persistent impairment of sensory and motor function (MF) using the tail-flick (TF) test, paw pressure test, and MF score. Spinal cords and nerve roots were obtained for light and electron microscopic examinations, and the injury scores were compared between groups. The TF latencies and the mean nerve injury scores of the postpartum group were significantly higher than those of nonpregnant group. Lidocaine induced a dose-dependent impairment in TF latencies and nerve injury scores. There was no significant interaction between postpartum and the drug. Our results suggest that the neurotoxicity of intrathecal lidocaine is enhanced in rats during the early postpartum period compared with nonpregnant, virgin rats.

Propofol and ketamine may provide certain degree of neuroprotection, but the underlying mechanism remains unclear to date. The cAMP response element-binding protein (CREB) was proposed that its phosphorylation at Ser133 (P-CREB) constituted a convergence point involved in neuroprotection. The purpose of this study was to determine whether different dosages of propofol and ketamine could provide neuroprotection against permanent middle cerebral artery occlusion (MCAO)-induced ischemic injuries and the involvement of P-CREB. Eighty adult male BALB/c mice that underwent 6 h MCAO were randomly divided into eight groups: Sham-operation; MCAO + saline; MCAO + 25, 50, 100 mg/kg propofol; and MCAO + 25, 50, 100 mg/kg ketamine (intraperitoneal injection 30 min following MCAO). We found that 50, 100 (not 25) mg/kg propofol, and 25 (not 50 and 100) mg/kg ketamine could significantly reduce the infarct volume, edema ratio and neurological deficit (n = 10 per group) as well as inhibit the decrease of P-CREB level in peri-infarct region when compared with that of MCAO + saline group (n = 6 per group). In addition, the results of double-labeled immunofluorescent staining showed that P-CREB co-localized with neuron-specific marker, NeuN, in the peri-infarct region of 50 mg/kg propofol and 25 mg/kg ketamine treated 6 h MCAO mice (n = 4 per group). These results suggested that inhibition of neuron-specific P-CREB dephosphorylation in the peri-infarct region is involved in high dose propofol and low dose ketamine-induced neuroprotection of 6 h MCAO mice.

Adenosine monophosphate-activated protein kinase (AMPK) orchestrates the regulation of energy-generating and -consuming pathways, and protects the heart against ischemic injury and apoptosis. Recent progress shed light on various factors, including adiponectin, MIF, H11K, and metformin in the activation of AMPK. It is uncertain whether the activation of AMPK is contributed to cardioprotection of opioids. Here we show that morphine, an exogenous non-peptide opioid receptor agonist, can modulate the activation of the cardioprotective AMPK pathway during ischemia and exert anti-apoptotic effects through AMPK.Isolated rat hearts were perfused on a constant pressure Langendorff system and subjected to 30 min of global ischemia followed by 60 min of reperfusion. The hearts received vehicles, morphine, a combination of morphine and compound C, a combination of morphine and STO609, a combination of morphine and BAPTA-AM at the onset of ischemia. Hemodynamics parameters, infarct size, release of intracellular creatine kinase, expression of AMPK, and terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling staining were analyzed.Morphine significantly increased phosphorylation level of Thr172 site on AMPK, left ventricular function, and reduced infarct size as a percentage of the area at risk (IS/AAR from 63% ± 7% to 40% ± 5%), release of intracellular creatine kinase (from 319 ± 46 to 156 ± 42IU/60 min/gdw), apoptosis ratio (from 16% ± 2% to 5% ± 1.4%) during reperfusion in comparison with the control group. A inhibitor of AMPK, compound C abrogated phosphorylation of AMPK induced by morphine, the improvement in myocardial function, and the reduction of IS/AAR (58% ± 6%), release of intracellular creatine kinase (270 ± 40IU/60 min/gdw), apoptosis ratio (13% ± 1.5%). A Ca(2+)/calmodulin-dependent protein kinase kinase inhibitor STO609 and a chelator of intracellular Ca(2+) stores BAPTA-AM also abolished the cardioprotection of morphine.Morphine can ameliorate myocardial contractile dysfunction and limit infarct size following ischemia and reperfusion by a mechanism involving activation of AMPK, and activate AMPK by Ca(2+)-CaMKKβ-dependent phosphorylation.

β-Amyloid protein (Aβ) accumulation, caspase activation, apoptosis, and hypoxia-induced neurotoxicity have been suggested to be involved in Alzheimer disease neuropathogenesis. Aβ is produced from amyloid precursor protein through proteolytic processing by the aspartyl protease β-site amyloid precursor protein-cleaving enzyme (BACE) and γ-secretase. Inhaled anesthetics have long been considered to protect against neurotoxicity. However, recent studies have suggested that the inhaled anesthetic isoflurane may promote neurotoxicity by inducing caspase activation and apoptosis, and by increasing levels of BACE and Aβ. We therefore sought to determine whether isoflurane can induce concentration-dependent dual effects on hypoxia-induced caspase-3 activation and increases in BACE levels: protection versus promotion.H4 human neuroglioma cells were treated with hypoxia (3% O(2)) alone, different concentrations of isoflurane (0.5% and 2%), and the combination of hypoxia and 0.5% or 2% isoflurane. The levels of caspase-3 cleavage (activation), BACE, and Bcl-2 were determined by Western blot analysis.We show for the first time that treatment with 0.5% isoflurane for 8 hours attenuated, whereas treatment with 2% isoflurane for 8 hours enhanced, hypoxia-induced caspase-3 activation and increases in BACE levels. The 2% isoflurane treatment also enhanced a hypoxia-induced decrease in Bcl-2 levels.These results suggest a potential concept that isoflurane has dual effects (protection versus promotion) on hypoxia-induced toxicity, which may act through Bcl-2 family proteins. These findings could lead to more systematic studies to determine the potential dual effects of anesthetics on Alzheimer disease-associated neurotoxicity.

Sedation induces changes in electroencephalography (EEG) dynamics. However, the distinct EEG dynamic characteristics at comparable sedation levels have not been well studied, resulting in potential interpretation errors in EEG monitoring during sedation. We aimed to analyze the EEG dynamics of dexmedetomidine and propofol at comparable sedation levels and to explore EEG changes with increased sedation levels for each agent. We measured the Bispectral Index (BIS) and 20-channel EEG under dexmedetomidine and propofol sedation from wakefulness, moderate sedation, and deep sedation to recovery in healthy volunteers (n = 10) in a randomized, 2-day, crossover study. Observer's Assessment of Alertness and Sedation (OAA/S) score was used to assess sedation levels. Despite similar changes in increased delta oscillations, multiple differences in the EEG spatiotemporal dynamics were observed between these two agents. During moderate sedation, both dexmedetomidine and propofol induced increased spindle power; however, dexmedetomidine decreased the global alpha/beta/gamma power, whereas propofol decreased the alpha power in the occipital area and increased the global spindle/beta/gamma power. During deep sedation, dexmedetomidine was associated with increased fronto-central spindle power and decreased global alpha/beta/gamma power, but propofol was associated with increased theta/alpha/spindle/beta power, which was maximized in the frontal area. The transition of topographic alpha/spindle/beta power distribution from moderate sedation to deep sedation completely differed between these two agents. Our study demonstrated that there was a distinct hierarchy of EEG changes with increased sedation depths by propofol and dexmedetomidine. Differences in EEG dynamics at the same sedation level might account for differences in the BIS value and reflect the different sedation mechanisms. EEG-based clinical sedation monitoring should consider the effect of drug types on EEG dynamics.

Background The mechanism of general anesthesia (GA) has been explored for hundreds of years, but unclear. Previous studies indicated a possible correlation between NREM sleep and GA. The purpose of this study is to compare them by in vivo human brain function to probe the neuromechanism of consciousness, so as to find out a clue to GA mechanism. Methods 24 healthy participants were equally assigned to sleep or propofol sedation group by sleeping ability. EEG and Ramsay Sedation Scale were applied to determine sleep stage and sedation depth respectively. Resting-state functional magnetic resonance imaging (RS-fMRI) was acquired at each status. Regional homogeneity (ReHo) and seed-based whole brain functional connectivity maps (WB-FC maps) were compared. Results During sleep, ReHo primarily weakened on frontal lobe (especially preoptic area), but strengthened on brainstem. While during sedation, ReHo changed in various brain areas, including cingulate, precuneus, thalamus and cerebellum. Cingulate, fusiform and insula were concomitance of sleep and sedation. Comparing to sleep, FCs between the cortex and subcortical centers (centralized in cerebellum) were significantly attenuated under sedation. As sedation deepening, cerebellum-based FC maps were diminished, while thalamus- and brainstem-based FC maps were increased. Conclusion There’re huge distinctions in human brain function between sleep and GA. Sleep mainly rely on brainstem and frontal lobe function, while sedation is prone to affect widespread functional network. The most significant differences exist in the precuneus and cingulate, which may play important roles in mechanisms of inducing unconciousness by anesthetics. Trial registration Institutional Review Board (IRB) ChiCTR-IOC-15007454.

Background and Objectives Potentially, perioperative regional anesthesia and analgesia (RA) could influence the outcomes of patients with cancer. The aim of this systematic review and meta-analysis was to evaluate the effects of perioperative RA on survival and cancer recurrence after oncologic surgery. Methods The authors searched computerized databases (from inception to December 2014) and reference lists and considered all studies comparing the effects of RA on cancer recurrence or overall survival with that of general anesthesia (GA). Risk estimates were pooled to determine the effects of RA on risks of cancer recurrence and mortality. Twenty eligible studies were included. Results Perioperative RA use was associated with improved overall survival (Hazard ratio [HR] = 0.84, 95% CI, 0.75 − 0.94; I2 =41%), but not with reduced cancer recurrence (HR=0.91, 95% CI, 0.70 − 1.18; I2=83%). Conclusions Our meta-analysis suggests that RA may improve overall survival but not reduce cancer recurrence after oncologic surgery.

To compare paravertebral block under thoracoscopy with wound infiltration at an early stage after video-assisted thoracic lobectomy surgery.A prospective, randomized, triple-blinded, placebo-controlled trial.A single-center university hospital.Patients scheduled for video-assisted thoracic lobectomy surgery between February 20, 2014 and June 1, 2014 randomly were allocated into paravertebral block (PVB) (n = 35) and infiltration (n = 35) groups.In the PVB group, 0.5% ropivacaine was injected into the paravertebral space by the surgeon under direct vision with placebo infiltration of saline in the wounds. In the infiltration group, the wounds were infiltrated with 0.5% ropivacaine by the surgeon with a placebo paravertebral block. Subsequently, patient-controlled intravenous morphine analgesia and paracoxib were administered.The primary endpoints were visual analog scale (VAS) pain scores at rest and on cough 0, 2, 6, and 24 hours after surgery. The secondary endpoints were the total morphine during postoperative 0 hours to 24 hours, adverse events, and patient satisfaction with the analgesia. Sixty-one patients completed the study. VAS score on cough at each time point was significantly lower (p0.05) and median (25th, 75th) morphine consumption was lower in the PVB group than in the infiltration group (26 [10, 35] mg and 42 [29, 58] mg, p0.001, respectively). There was no difference in VAS score at rest. Patients in the PVB group had higher satisfaction with analgesia than in the infiltration group (p = 0.003).As part of the multimodal postoperative analgesia, intraoperative paravertebral block provided better dynamic pain relief and reduced morphine consumption compared with local wound infiltration.

The commonly used inhaled anesthetic isoflurane has been shown to induce caspase-3 activation. However, the underlying mechanism(s) and targeted intervention(s) remain largely to be determined. Isoflurane may induce caspase-3 activation via causing accumulation of reactive oxygen species (ROS), mitochondrial dysfunction, and reduction in adenosine triphosphate (ATP) levels. Therefore, we performed a hypothesis-generation study to determine whether glucose could attenuate isoflurane-induced caspase-3 activation, ROS accumulation, mitochondrial dysfunction, and ATP reduction in cultured cells.H4 human neuroglioma cells (H4 cells) were treated with 2% isoflurane or the control condition plus saline or 50 mM glucose for 6 or 3 hours. Caspase-3 activation, cell viability, levels of ROS and ATP, and mitochondrial membrane potential were determined at the end of the experiments by Western blot analysis and fluorescence assay.We found that the glucose treatment might attenuate isoflurane-induced caspase-3 activation and reduction of cell viability in H4 cells. Moreover, the glucose treatment mitigated the isoflurane-induced increase in ROS levels and reduction in ATP levels in H4 cells. Unexpectedly, we observed that the glucose treatment might not inhibit the isoflurane-induced decrease in mitochondrial membrane potential in H4 cells.Pending further studies, these results suggested that glucose might attenuate isoflurane-induced caspase-3 activation through a mitochondria-independent reduction in ROS levels and enhancement in ATP levels. These findings have established a system and suggest that it is worth performing more research to further investigate whether glucose can attenuate anesthesia neurotoxicity.

An estimated 234 million patients worldwide undergo anesthesia and surgery each year. Even though the incidence of Alzheimer disease (AD) may not be increased by anesthesia,1 the age of AD onset was reported to be inversely related to cumulative exposure to anesthesia and surgery before the age of 50 yrs.2 Several other studies have also suggested general anesthesia as one of the risk factors for AD.3,4 Opposing findings, however, do exist,5–7 and therefore more research, especially human studies aimed to define the role of anesthesia in AD neuropathogenesis, is necessary.8,9 Excessive production and/or accumulation of β-amyloid protein (Aβ), predominantly including Aβ40 and Aβ42, plays a fundamental role in the neuropathogenesis of AD.10–13 In addition, recent studies have suggested the contribution of Aβ40 in AD neuropathogenesis.14,15 Furthermore, Aβ40 has been shown to induce caspase activation and apoptosis16–18 and to impair synaptic plasticity and memory function..19,20 In addition to Aβ, the accumulation, abnormal aggregation, and deposition of tau play a key role in AD neuropathogenesis.21 As the major protein component of intraneuronal neurofibrillary tangles, elevation of total tau levels (two- to threefold) is seen in the cerebrospinal fluid (CSF) of AD patients compared to nondemented elderly adults.22,23 Moreover, a reduced ratio of Aβ42 to tau in the CSF has been suggested as one of the biomarkers of AD.23,24 Several studies have suggested that the commonly used inhalation anesthetic isoflurane can increase Aβ accumulation in cultured cells, neurons, and animals.9,25–29 The isoflurane has been shown to increase levels of phosphorylated, but not total, tau in brain tissues of mice.30 In contrast, another commonly used inhalation anesthetic desflurane has been shown not to increase Aβ levels in cultured cells.31 However, the in vivo relevance of these acute effects of isoflurane on Aβ levels in humans has not yet been assessed. In this study, we set out to determine the effects of surgery under spinal (S) anesthesia alone, spinal plus desflurane (SD) anesthesia, and spinal plus isoflurane (SI) anesthesia on the acute changes in CSF Aβ levels in human participants. We also assessed the effects of surgery under S, SD, and SI anesthesia on total tau levels in human CSF and calculated the ratios of Aβ40 or Aβ42 to tau. We hypothesized, based on the in vitro and animal studies, that isoflurane, but not desflurane, would increase the human CSF Aβ levels.

During the perinatal period, the pharmacokinetics and pharmacodynamics of drugs may be altered. Data about the neurotoxicity of intrathecal local anesthetics in the peripartum period are lacking. So we hypothesized that the neurotoxicity of intrathecal lidocaine during perinatal period may be changed. Therefore, we designed the present study to determine whether the neurotoxicity of intrathecal lidocaine in postpartum rats would be different from that in nonpregnant, virgin rats. Postpartum and nonpregnant rats randomly received an intrathecal infusion of lidocaine 50 mg/mL in saline, lidocaine 20 mg/mL in saline, or saline for 1 h at a rate of 1 μL/min. Four days after drug infusion, the rats were assessed for persistent impairment of sensory and motor function (MF) using the tail-flick (TF) test, paw pressure test, and MF score. Spinal cords and nerve roots were obtained for light and electron microscopic examinations, and the injury scores were compared between groups. The TF latencies and the mean nerve injury scores of the postpartum group were significantly higher than those of nonpregnant group. Lidocaine induced a dose-dependent impairment in TF latencies and nerve injury scores. There was no significant interaction between postpartum and the drug. Our results suggest that the neurotoxicity of intrathecal lidocaine is enhanced in rats during the early postpartum period compared with nonpregnant, virgin rats.

The chronic intrathecal catheterization of the subarachnoid space in the rat is a very useful model in the research of neuroscience, anesthesiology, neurotoxicity, and etc. To avoid high postoperative mortality and neurological impairment, the catheterization from the lumbar interspace has been widely used in recent years. But one of the most discouraging disadvantages is that the external portion of the chronic indwelling catheters is easily damaged by rats. Besides, the short length of catheter left in the subarachnoid space in addition to its slimness makes it difficult for proper fixation. To improve the abovementioned situations, we designed a protector to protect the external portion of the catheters and developed a simple method for better fixation. Results suggest that this is an excellent method for protecting and fixing the lumbar catheters placed in the subarachnoid space of rats, and this method did not affect the sensory and motor function of the rat. The general conditions of the rats were unswayed.

Ca/calmodulin-dependent protein kinase II (CaMKII) activation through autophosphorylation at threonine 286 was involved in the modulation of neuronal excitability and neurotransmission. Both propofol and ketamine may affect the intracellular Ca levels through N-methyl-D-aspartate receptors or voltage-dependent Ca channels, but they have different mechanisms in general anesthesia. The purpose of this study was to investigate the effects of propofol and ketamine on CaMKII total protein and phosphorylation (p-CaMKII) levels in the brain of rats. We found that both propofol and ketamine could induce a decrease of p-CaMKII, not CaMKII total protein, in an anesthetic depth-dependent manner, whereas only ketamine caused a dose (50, 100, and 150 mg/kg)-dependent depression of p-CaMKII in hippocampus and frontal cortex of rats after intraperitoneal injections for 30 minutes. The significant depressions of p-CaMKII started at 5 minutes both in hippocampus and frontal cortex of rats after 100 mg/kg propofol treatment, whereas 100 mg/kg ketamine-induced significant depression of p-CaMKII initiated at 30 minutes in hippocampus and 5 minutes (no reduction observed at 15 min) in frontal cortex of rats. The maximum reduction of p-CaMKII with both drugs was at 60 minutes, and then restored to control level at 240 minutes. In addition, we confirmed the depression of p-CaMKII in hippocampus and frontal cortex of rats after 100 mg/kg of propofol or ketamine treatment for 60 minutes by using immunostaining. These results suggested that decreased p-CaMKII levels correlate with anesthetic depths achieved by propofol and ketamine, which may be related to the effects of propofol and ketamine on central nervous system function and their clinical effect.

Background/Objective Inadvertent intraoperative hypothermia (core temperature 2 h (OR = 3.44, 95% CI 1.90–6.22,), and intravenous un-warmed fluid (OR = 2.45, 95% CI 1.45–4.12) significantly increased the risk of hypothermia. Conclusions The incidence of inadvertent intraoperative hypothermia in Beijing is high, and the rate of active warming of patients during operation is low. Concern for the development of intraoperative hypothermia should be especially high in patients undergoing major operations, requiring long periods of anesthesia, and receiving un-warmed intravenous fluids.