Diaphragm-sparing efficacy of subparaneural upper trunk block for arthroscopic shoulder surgery: A randomised controlled trial.

BACKGROUND: Inter-scalene block (ISB) is associated with an inevitable risk of hemi-diaphragmatic paresis (HDP). To reduce the risk of HDP, an upper trunk block (UTB) has been proposed at the brachial plexus division level. OBJECTIVE: We hypothesised that UTB would be associated with a lower incidence of HDP than ISB while providing sufficient analgesia following arthroscopic shoulder surgery. DESIGN: Randomised controlled trial. SETTING: A tertiary teaching hospital. PATIENTS: Seventy patients aged 20 to 80 years undergoing arthroscopic rotator cuff repair. INTERVENTION: Ultrasound-guided ISB or UTB was performed with 5 ml 0.75% ropivacaine. MAIN OUTCOME MEASURES: The primary outcome was the incidence of complete HDP, assessed by diaphragm excursion using ultrasound, defined as a decrease to 25% or less of baseline or occurrence of paradoxical movement. Postoperative pulmonary function change, pain scores, opioid consumption and pain-related outcomes were the secondary outcomes. RESULTS: The UTB group had a significantly lower incidence of complete HDP than the ISB group [5.9% (2/34) vs. 41.7% (15/36); absolute difference, 35.8%; 95% confidence interval (CI), 17.8 to 53.7%; P < 0.001]. The postblockade decline in pulmonary function was more pronounced in the ISB group than that in the UTB group. The pain score at 1 h postoperatively was not significantly different between the groups (ISB vs. UTB group: median 0 vs. 1; median difference, -1; 95% CI, -2 to 0.5). No significant difference was observed in any other secondary outcomes. CONCLUSION: UTB was associated with a lower incidence of HDP compared with ISB while providing excellent analgesia in arthroscopic shoulder surgery. TRIAL REGISTRATION: Clinical Trial Registry of Korea (https://cris.nih.go.kr) identifier: KCT0007002. IRB NUMBER: Chungnam National University Hospital Institutional Review Board No. 2021-12-069.

Intraoperative changes in upper extremity perfusion index after thoracic paravertebral and intertransverse process block in patients undergoing lung resection surgery.

Background: Perfusion index (PI) has been used as a surrogate marker of sympathetic blockade. This study evaluated changes in PI of bilateral upper extremity after thoracic paravertebral block (PVB) and intertransverse process block (ITPB). Methods: This pilot study included three groups of patients undergoing elective unilateral pulmonary resection under general anesthesia with PVB (n=11) or ITPB (n=10), or urologic procedures with general anesthesia (control group, n=10). Blockades were performed using 10 mL aliquots of 0.5% ropivacaine administered at T3-4, T5-6, and T7-8 intercostal levels immediately after general anesthesia induction. The PI value of the operating side (PI-O) was divided by the contralateral side (PI-CL), and the relative change to baseline was assessed (relative PI-O/PI-CL), with a 50% increase considered meaningful. Results: In all cases within the PVB and ITPB groups, a significant increase in PI was observed following the blockades. The median (1Q, 3Q) intraoperative relative PI-O/PI-CL values were 0.9 (0.8, 1.4), 2.1 (1.4, 2.5), and 1.4 (0.9, 1.9) in the control, PVB, and ITPB groups (P=0.01), respectively. Pairwise comparison revealed a significant difference only between the control and PVB groups (adjusted P=0.01). While the relative PI-O/PI-CL value in the control group generally remained close to 1, occasional fluctuations exceeding 1.5 were noted. Conclusions: PVB induced a noticeable unilateral increase in upper extremity PI, whereas ITPB tended to result in an inconsistent and lesser degree of increase. Monitoring PI values can serve as an indicator of upper extremity sympathetic blockade, but consideration of potential confounders impacting these observations during surgery is essential. Further research is needed to validate these findings.

Apnea during moderate to deep sedation using continuous infusion of remimazolam compared to propofol and dexmedetomidine: A retrospective observational study.

Remimazolam's rapid onset and offset make it an innovative sedative for use during regional anesthesia. However, its respiratory safety profile is not well understood. We compared the continuous infusion of remimazolam with commonly used sedatives, propofol and dexmedetomidine, after regional anesthesia. In this retrospective study, the incidence of apnea (>10 seconds) was assessed in patients who underwent orthopedic surgery under regional anesthesia and received moderate to deep sedation using continuous infusion of remimazolam (group R: 0.1 mg/kg in 2 minutes followed by 0.5 mg/kg/hr). The incidence was compared with that of propofol (group P: 2-3 µg/mL target-controlled infusion) and dexmedetomidine (group D: 1 µg/kg in 10 minutes followed by 0.4-1 µg/kg/hr). Propensity score weighted multivariable logistic regression model was utilized to determine the effects of the sedative agents on the incidence of apnea. A total of 634 (191, 278, and 165 in group R, P, and D) cases were included in the final analysis. The incidence of apnea was 63.9%, 67.3%, and 48.5% in group R, P, and D, respectively. The adjusted odds ratios for apnea were 2.33 (95% CI, 1.50 to 3.61) and 2.50 (95% CI, 1.63 to 3.85) in group R and P, compared to group D. The incidence of apnea in patients receiving moderate to deep sedation using continuous infusion of remimazolam with dosage suggested in the current study was over 60%. Therefore, careful titration and respiratory monitoring is warranted.

Employing the sustained-release properties of poly(lactic-co-glycolic acid) nanoparticles to reveal a novel mechanism of sodium-hydrogen exchanger 1 in neuropathic pain.

Neuropathic pain is caused by injury or disease of the somatosensory system, and its course is usually chronic. Several studies have been dedicated to investigating neuropathic pain-related targets; however, little attention has been paid to the persistent alterations that these targets, some of which may be crucial to the pathophysiology of neuropathic pain. The present study aimed to identify potential targets that may play a crucial role in neuropathic pain and validate their long-term impact. Through bioinformatics analysis of RNA sequencing results, we identified Slc9a1 and validated the reduced expression of sodium-hydrogen exchanger 1 (NHE1), the protein that Slc9a1 encodes, in the spinal nerve ligation (SNL) model. Colocalization analysis revealed that NHE1 is primarily co-localized with vesicular glutamate transporter 2-positive neurons. In vitro experiments confirmed that poly(lactic-co-glycolic acid) nanoparticles loaded with siRNA successfully inhibited NHE1 in SH-SY5Y cells, lowered intracellular pH, and increased intracellular calcium concentrations. In vivo experiments showed that sustained suppression of spinal NHE1 expression by siRNA-loaded nanoparticles resulted in delayed hyperalgesia in naïve and SNL model rats, whereas amiloride-induced transient suppression of NHE1 expression yielded no significant changes in pain sensitivity. We identified Slc9a1, which encodes NHE1, as a key gene in neuropathic pain. Utilizing the sustained release properties of nanoparticles enabled us to elucidate the chronic role of decreased NHE1 expression, establishing its significance in the mechanisms of neuropathic pain.

Errors in pressure measurements due to changes in pressure transducer levels during adult cardiac surgery: a prospective observational study.

BACKGROUND: Blood pressure measurement is an essential element during intraoperative patient management. However, errors caused by changes in transducer levels can occur during surgery. METHODS: This single center, prospective, observational study enrolled 25 consecutive patients scheduled for elective cardiac surgery with invasive arterial and central venous pressure (CVP) monitoring. Hydrostatic pressures caused by level differences (leveling pressure) between a reference point (on the center of the left biceps brachii muscle) and the transducers (fixed on the right side of the operating table) for arterial and central lines were continuously measured using a leveling transducer. Adjusted pressures were calculated as measured pressure - leveling pressure. Hypotension (mean arterial pressure < 80, <70, and < 60 mmHg), and CVP (< 6, ≥6 and < 15, or ≥ 15 mmHg) and pulmonary artery pressure (PAP, mean > 20 mmHg) levels were determined using unadjusted and adjusted pressures. RESULTS: Twenty-two patients were included in the analysis. Leveling pressure ≥ 3 mmHg and ≥ 5 mmHg observed at 46.0 and 18.7% of pooled data points, respectively. Determinations of hypotension using unadjusted and adjusted pressures showed disagreements ranging from 3.3 to 9.4% depending on the cutoffs. Disagreements in defined levels of CVP and PAP were observed at 23.0 and 17.2% of the data points, respectively. CONCLUSIONS: The errors in pressure measurement due to changes in transducer level were not trivial and caused variable disagreements in the determination of MAP, CVP, and PAP levels. To prevent distortions in intraoperative hemodynamic management, strategies should be sought to minimize or adjust for these errors in clinical practice. TRIAL REGISTRATION: cris.nih.go.kr (KCT0006510).

Is measurement of central venous pressure required to estimate systemic vascular resistance? A retrospective cohort study.

BACKGROUND: The clinical range of central venous pressure (CVP) (typically 5 to 15 mmHg) is much less than the range of mean arterial blood pressure (60 to 120 mmHg), suggesting that CVP may have little impact on estimation of systemic vascular resistance (SVR). The accuracy and feasibility of using an arbitrary CVP rather than actual CVP for the estimation of SVR during intraoperative period is not known. METHODS: Using vital records obtained from patients who underwent neurological and cardiac surgery, the present study retrospectively calculated SVR using fixed values of CVP (0, 5, 10, 15, and 20 mmHg) and randomly changing values of CVP (5 to 15 mmHg) and compared these calculated SVRs with actual SVR, calculated using actual CVP. Differences between actual SVR and SVRs based on fixed and random CVPs were quantified as root mean square error (RMSE) and mean absolute percentage error (MAPE). Bland-Altman analysis and four-quadrant plot analysis were performed. RESULTS: A total of 34 patients are included, including 18 who underwent neurosurgery and 16 who underwent cardiac surgery; 501,380 s (139.3 h) of data was analyzed. The SVR derived from a fixed CVP of 10 mmHg (SVRf10) showed the highest accuracy (RMSE: 115 and 104 [dynes/sec/cm- 5] and MAPE: 6.3 and 5.7% in neurological and cardiac surgery, respectively). The 95% limits of agreement between SVRf10 and actual SVR were - 208.5 (95% confidence interval [CI], - 306.3 to - 148.1) and 242.2 (95% CI, 181.8 to 340.0) dynes/sec/cm- 5 in neurosurgery and - 268.1 (95% CI, - 367.5 to - 207.7) and 163.2 (95% CI, 102.9 to 262.6) dynes/sec/cm- 5 in cardiac surgery. All the SVRs derived from the fixed CVPs (regardless of its absolute value) showed excellent trending ability (concordance rate > 0.99). CONCLUSIONS: SVR can be estimated from a fixed value of CVP without causing significant deviation or a loss of trending ability. However, caution is needed when using point estimates of SVR when the actual CVP is expected to be out of the typical clinical range. TRIAL REGISTRATION: This study was registered Clinical Research Information Service, a clinical trial registry in South Korea ( KCT0006187 ).

Perineural Epinephrine for Brachial Plexus Block Increases the Incidence of Hypotension during Dexmedetomidine Infusion: A Single-Center, Randomized, Controlled Trial.

BACKGROUND: Sedation using dexmedetomidine is frequently associated with hypotension. In contrast, epinephrine, a commonly used adjunctive agent in regional anesthesia, is a potent vasopressor. We hypothesized that perineural epinephrine used in brachial plexus blockade may reduce hypotension during dexmedetomidine infusion. METHODS: Patients scheduled for upper extremity surgery were randomly allocated into a control and an epinephrine group. All patients received brachial plexus blockade, consisting of 25 mL of a 1:1 mixture of 1% lidocaine and 0.75% ropivacaine, with patients in the epinephrine group also receiving 125 µg epinephrine. Intraoperative sedation was induced using dexmedetomidine at a loading dose of 1 µg/kg and maintenance dose of 0.4 µg/kg/hr. The primary outcome was the incidence of intraoperative hypotension or hypotension in the post-anesthesia care unit (PACU). RESULTS: One hundred and thirty patients were included (65 per group). The incidence of hypotension was significantly higher in the epinephrine than in the control group (80.6% vs. 56.9%, p = 0.009). The duration of hypotension and the maximal change in blood pressure were also greater in the epinephrine group. CONCLUSIONS: Perineural epinephrine for brachial plexus blockade does not reduce hypotension due to dexmedetomidine infusion and may actually augment the occurrence of hypotensive events.

Does Demineralized Bone Matrix Enhance Tendon-to-Bone Healing after Rotator Cuff Repair in a Rabbit Model?

BACKGROUD: The purpose of this study was to compare the histologic outcomes of rotator cuff (RC) repair with demineralized bone matrix (DBM) augmentation and those without DBM augmentation and to evaluate the role of DBM for tendon-to-bone (TB) healing in a rabbit model. METHODS: Twenty-six adult male New Zealand white rabbits were randomly allocated to the control group (n = 13) or the DBM group (n = 13). Repair was performed 8 weeks after complete transection of the right supraspinatus tendon of all rabbits. In the control group, RC repair was achieved by a standard transosseous technique. In the DBM group, RC repair was achieved using the same technique, and DBM was interposed between the cuff and bone. After 8 weeks, the RC tendon entheses from all rabbits were processed for gross and histologic examination. RESULTS: On gross TB healing, 2 of 11 specimens in the control group were unhealed and no specimen was grossly unhealed in the DBM group (p = 0.421). In the control group, the tendon midsubstance was disorganized with randomly and loosely arranged collagen fibers and rounded fibroblastic nuclei. The TB interface was predominantly fibrous with small regions of fibrocartilage, especially mineralized fibrocartilage. In the DBM group, the tendon midsubstance appeared normal and comprised densely arranged collagen fibers, with orientated crimped collagen fibers running in the longitudinal direction of the tendon. These fibers were interspersed with elongated fibroblast nuclei. The TB interface consisted of organized collagen fibers with large quantities of fibrocartilage and mineralized fibrocartilage. CONCLUSIONS: The use of DBM for TB interface healing in rabbit experiments showed good results in gross and histologic analysis. However, it is difficult to draw a solid conclusion because the sample size is small. Further evaluation in the in vivo setting is necessary to determine clinical recommendations.

NFAT5 Deficiency Alleviates Formalin-Induced Inflammatory Pain Through mTOR.

Nuclear factor of activated T cells (NFAT5) is a well-known transcription factor that regulates the expression of genes involved in osmotic stress. However, the role of NFAT5 in inflammatory pain remains unknown. Here, we studied the function of NFAT5 in inflammatory pain using NFAT5-heterozygous (Het) mice. To study inflammatory pain, we injected 10 µL of 2% formalin into the right hind paws of mice and monitored pain behaviors, such as licking, lifting, and flinching, for 60 min. After the first 15 min (phase I), there were no significant differences in pain behaviors between wild-type (WT) and NFAT5-Het mice. However, from 15-60 min (phase II), NFAT5-Het mice displayed significantly fewer pain behaviors compared to WT mice. Further, the expression levels of inflammatory-pain-related factors, including c-Fos, phosphorylated extracellular signal-regulated kinase (p-ERK), and phosphorylated n-methyl-D-aspartate receptor subunit 2B (p-NR2B), were significantly elevated in the spinal dorsal neurons of formalin-treated WT mice but was not elevated in NFAT5-Het mice. Similarly, c-Fos, p-ERK, and p-NR2B levels were significantly higher in glutamate-treated PC12 neuronal cells but were not affected by Nfat5 silencing in glutamate-treated PC12 cells. Altogether, our findings suggest that NFAT5 deficiency may mitigate formalin-induced inflammatory pain by upregulating mammalian target of rapamycin (mTOR) expression and downregulating its downstream factors in spinal dorsal neurons. Therefore, NFAT5 is a potential therapeutic target for the treatment of inflammatory pain.

Circadian regulation of chemotherapy-induced peripheral neuropathic pain and the underlying transcriptomic landscape.

Growing evidence demonstrates circadian rhythms of pain hypersensitivity in various chronic disorders. In chemotherapy-induced peripheral neuropathy (CIPN), agents such as paclitaxel are known to elicit chronic neuropathic pain in cancer patients and seriously compromise their quality of life. Here, we report that the mechanical threshold for allodynia in paclitaxel-treated rats exhibited a robust circadian oscillation, reaching the nadir during the daytime (inactive phase). Using Per2::LucSV circadian reporter mice expressing a PER2::LUC fusion protein, we isolated dorsal root ganglia (DRG), the primary sensory cell body for peripheral nerve injury generated hypersensitivity, and monitored ex vivo reporter bioluminescence. We observed strong circadian reporter rhythms in DRG neurons which are highly entrainable by external cues. Paclitaxel treatment significantly lengthened DRG circadian periods, with little effects on the amplitude of oscillation. We further observed the core protein BMAL1 and PER2 in DRG neurons and satellite cells. Using DRG and dorsal horn (DH; another key structure for CIPN pain response) tissues from vehicle and paclitaxel treated rats, we performed RNA-sequencing and identified diurnal expression of core clock genes as well as clock-controlled genes in both sites. Interestingly, 20.1% and 30.4% of diurnal differentially expressed genes (DEGs) overlapped with paclitaxel-induced DEGs in the DRG and the DH respectively. In contrast, paclitaxel-induced DEGs displayed only a modest overlap between daytime and nighttime (Zeitgeber Time 8 and 20). Furthermore, paclitaxel treatment induced de novo diurnal DEGs, suggesting reciprocal interaction of circadian rhythms and chemotherapy. Our study therefore demonstrates a circadian oscillation of CIPN and its underlying transcriptomic landscape.

Long-term efficacy and feasibility of levonorgestrel-releasing intrauterine device use in patients with adenomyosis.

To evaluate the efficacy and feasibility of levonorgestrel-releasing intrauterine device (LNG-IUD) use longer than 5 years in women with adenomyosis.Data were retrospectively collected from patients who were treated with LNG-IUD longer than 5 years at the Chungnam National University hospital for adenomyosis diagnosed with ultrasonography from January 2006 to November 2013.A total of 131 patients who were diagnosed with adenomyosis had treated with LNG-IUD longer than 5 years. The mean duration of keeping 1 device without replacement was 58.35 ±â€Š15.98 months, and total duration of LNG-IUD treatment was 83.86 ±â€Š23.88 months. A total of 51 patients stopped using LNG-IUD after 5 years and the mean age at the time of LNG-IUD removal was 52.46 ±â€Š6.9. LNG-IUD treatment had a significant effect on both menorrhagia and dysmenorrhea starting from the first month of insertion (P < .01), which persisted until 6 years when the effect started to plateau. The decrease in uterine volume was not consistent during the treatment period. The uterine volume decreased significantly only in the first and second year of LNG-IUD treatment and then from eighth to tenth year of LNG-IUD treatment (P < .05). Adverse events after insertion of LNG-IUD decreased significantly after 5 years.LNG-IUD treatment longer than 5 years is an effective and feasible method for patients diagnosed with adenomyosis.

BMAL1 Suppresses Proliferation, Migration, and Invasion of U87MG Cells by Downregulating Cyclin B1, Phospho-AKT, and Metalloproteinase-9.

Several studies have shown that brain and muscle aryl hydrocarbon receptor nuclear translocator-like 1 (BMAL1), an important molecule for maintaining circadian rhythms, inhibits the growth and metastasis of tumor cells in several types of cancer, including lung, colon, and breast cancer. However, its role in glioblastoma has not yet been established. Here, we addressed the function of BMAL1 in U87MG glioblastoma cells with two approaches-loss and gain of function. In the loss of function experiments, cell proliferation in U87MG cells transfected with small interfering RNA (siRNA) targeting BMAL1 was increased by approximately 24% (small interfering (si)-NC 0.91 ± 0.00 vs. si-BMAL1 1.129 ± 0.08) via upregulation of cyclin B1. In addition, cell migration and invasion of BMAL1 siRNA-treated glioblastoma cells were elevated by approximately 20% (si-NC 51.00 ± 1.53 vs. si-BMAL161.33 ± 0.88) and 209% (si-NC 21.28 ± 1.37 vs. si-BMAL1 44.47 ± 3.48), respectively, through the accumulation of phosphorylated-AKT (p-AKT) and matrix metalloproteinase (MMP)-9. Gain of function experiments revealed that adenovirus-mediated ectopic expression of BMAL1 in U87MG cells resulted in a 19% (Adenovirus (Ad)-vector 0.94± 0.03 vs. Ad-BMAL1 0.76 ± 0.03) decrease in cell proliferation compared with the control via downregulation of cyclin B1 and increased early and late apoptosis due to changes in the levels of BCL2-associated X protein (BAX), B-cell lymphoma 2 (BCL-2), and cleaved caspase-3. Likewise, cell migration and invasion were attenuated by approximately 24% (Ad-vector 55.00 ± 0.00 vs. Ad-BMAL1 41.83 ± 2.90) and 49% (Ad-vector 70.01 ± 1.24 vs. Ad-BMAL1 35.55 ± 1.78), respectively, in BMAL1-overexpressing U87MG cells following downregulation of p-AKT and MMP-9. Taken together, our results suggest that BMAL1 acts as an anti-cancer gene by altering the proliferation, migration, and invasion of glioblastoma cells. Therefore, the BMAL1 gene could be a potential therapeutic target in the treatment of glioblastoma.

Effect of serotonin-norepinephrine reuptake inhibitors for patients with chemotherapy-induced painful peripheral neuropathy: A meta-analysis.

BACKGROUND: To compare the efficacy of serotonin-norepinephrine reuptake inhibitors (SNRIs) treatment for chemotherapy-induced peripheral neuropathy (CIPN) METHODS:: Two authors independently searched MEDLINE, Embase, Cochran Library, and Web of Science to identify and review articles published from January 1998 until December 2018 according to selection criteria. Outcomes were expressed as mean difference, the pooled odds ratio, or relative risk in a meta-analysis model. RESULTS: A total of 10 studies were included in this meta-analysis: 6 randomized-controlled studies and 4 observational studies. Meta-analysis showed that CIPN was improved after treatment with SNRI (standardized mean difference = 2.20; 95% confidence interval, 0.90-3.49; I = 93% in 3 randomized controlled studies). Somnolence and insomnia occurred in <15% of patients. Incidence of somnolence was lower than with pregabalin treatment, and insomnia was comparable to that in expectant management or pregabalin treatment. Incidence of nausea and vomiting was higher than in expectant management, but no significant difference was found when compared to expectant management. CONCLUSION: From the several available studies suitable for indirect comparison, SNRI shows excellent efficacy and tolerability to CIPN. SNRI could provide an important treatment option for CIPN.

Evans Blue Reduces Neuropathic Pain Behavior by Inhibiting Spinal ATP Release.

Upon peripheral nerve injury, vesicular ATP is released from damaged primary afferent neurons. This extracellular ATP subsequently activates purinergic receptors of the spinal cord, which play a critical role in neuropathic pain. As an inhibitor of the vesicular nucleotide transporter (VNUT), Evans blue (EB) inhibits the vesicular storage and release of ATP in neurons. Thus, we tested whether EB could attenuate neuropathic pain behavior induced by spinal nerve ligation (SNL) in rats by targeting VNUT. An intrathecal injection of EB efficiently attenuated mechanical allodynia for five days in a dose-dependent manner and enhanced locomotive activity in an SNL rat model. Immunohistochemical analysis showed that EB was found in VNUT immunoreactivity on neurons in the dorsal root ganglion and the spinal dorsal horn. The level of ATP in cerebrospinal fluid in rats with SNL-induced neuropathic pain decreased upon administration of EB. Interestingly, EB blocked ATP release from neurons, but not glial cells in vitro. Eventually, the loss of ATP decreased microglial activity in the ipsilateral dorsal horn of the spinal cord, followed by a reduction in reactive oxygen species and proinflammatory mediators, such as interleukin (IL)-1ß and IL-6. Finally, a similar analgesic effect of EB was demonstrated in rats with monoiodoacetate-induced osteoarthritis (OA) pain. Taken together, these data demonstrate that EB prevents ATP release in the spinal dorsal horn and reduces the ATP/purinergic receptor-induced activation of spinal microglia followed by a decline in algogenic substances, thereby relieving neuropathic pain in rats with SNL.

Analgesic Effect of Toll-like Receptor 4 Antagonistic Peptide 2 on Mechanical Allodynia Induced with Spinal Nerve Ligation in Rats.

Neuroinflammation is one of the key mechanisms of neuropathic pain, which is primarily mediated by the Toll-like receptor 4 (TLR4) signaling pathways in microglia. Therefore, TLR4 may be a reasonable target for treatment of neuropathic pain. Here, we examined the analgesic effect of TLR4 antagonistic peptide 2 (TAP2) on neuropathic pain induced by spinal nerve ligation in rats. When lipopolysaccharide (LPS)-stimulated BV2 microglia cells were treated with TAP2 (10 µM), the mRNA levels of proinflammatory mediators, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-6, cyclooxygenase (COX)-2, and inducible nitric oxide synthase (iNOS), were markedly decreased by 54-83% as determined by quantitative PCR (qPCR) analysis. Furthermore, when TAP2 (25 nmol in 20 µL PBS) was intrathecally administered to the spinal nerve ligation-induced rats on day 3 after surgery, the mechanical allodynia was markedly decreased for approximately 2 weeks in von Frey filament tests, with a reduction in microglial activation. On immunohistochemical and qPCR analyses, both the level of reactive oxygen species and the gene expression of the proinflammatory mediators, such as TNF-α, IL-1ß, IL-6, COX-2, and iNOS, were significantly decreased in the ipsilateral spinal dorsal horn. Finally, the analgesic effect of TAP2 was reproduced in rats with monoiodoacetate-induced osteoarthritic pain. The findings of the present study suggest that TAP2 efficiently mitigates neuropathic pain behavior by suppressing microglial activation, followed by downregulation of neuropathic pain-related factors, such as reactive oxygen species and proinflammatory molecules. Therefore, it may be useful as a new analgesic for treatment of neuropathic pain.

Effect of an epinephrine mixture for interscalene block on hemodynamic changes after the beach chair position under general anesthesia: a retrospective study.

BACKGROUND: The beach chair position (BCP) can cause significant hypotension. Epinephrine is used to prolong the duration of local anesthetics; it is also absorbed into blood and can exert systemic effects. This study determined the effects of epinephrine mixed with ropivacaine for an interscalene block (ISB) on hemodynamic changes related to BCP. METHODS: Patient data collected from March 2013 to August 2014 were used retrospectively. We divided the patients into three groups: 1) ISB only, 2) I+G (general anesthesia after ISB without epinephrine), and 3) I+E+G (general anesthesia after ISB with epinephrine). Mean blood pressure (MBP) and heart rate (HR) were measured for 30 minutes at 5-minute intervals. RESULTS: The study analyzed data from 431 patients. MBP tended to decrease gradually in the groups I+G and I+E+G. There were significant differences in MBP between the groups I+G and I, and between the groups I+G and I+E+G. Group I+E+G showed a significant increase in HR compared with the other two groups. CONCLUSIONS: ISB with an epinephrine mixture did not prevent hypotension caused by the BCP after general anesthesia. HR increased only in response to the epinephrine mixture. A well-planned prospective study is required to compare hemodynamic changes in that context.

Effects of nicardipine on the onset time and intubation conditions of rocuronium-induced neuromuscular blockade.

STUDY OBJECTIVE: The objective of this study was to identify the effects of nicardipine on neuromuscular blockade of rocuronium, such as the onset time and intubation conditions, using a nicardipine dose that attenuates cardiovascular responses during endotracheal intubation. DESIGN: Randomized, double-blinded, placebo-controlled clinical comparison was used as the design of this study SETTING: The study was conducted at the operating room of a university hospital. PATIENTS: Participants of this study comprise 78 American Society of Anesthesiologists physical status 1 and 2 patients, aged 18 to 60 years who were undergoing elective surgery under general anesthesia. INTERVENTIONS: The nicardipine group was given an intravenous bolus of 20 µg/kg nicardipine before tracheal intubation: the control group was given an intravenous bolus of a comparable volume of normal saline before tracheal intubation. MEASUREMENTS: Using a TOF-Watch SX monitor, the time from the end of the injection of rocuronium to maximum depression of T1 (onset time) was measured. Intubation was performed 1 minute after rocuronium administration, and the status of the intubation conditions was assessed. The mean blood pressure and heart rate were each measured after endotracheal intubation. Rate pressure product values were also calculated. MAIN RESULTS: Intubation conditions were clinically acceptable in 37 (94.9%) of 39 patients in group N compared with 29 (74.4%) of 39 in group C (P < .05). The onset time of rocuronium was significantly faster in group N than in group C (P < .05). The mean blood pressure was significantly lower in group N than in group C (P < .05). The heart rate was significantly higher in group N than in group C (P < .05). Rate pressure product values showed no significant difference between the two groups (P > .05). CONCLUSIONS: Pretreatment with 20 µg/kg nicardipine improves intubation conditions, shortens the onset time of rocuronium, and attenuates cardiovascular responses to tracheal intubation.

Glomus tumor causing anterior thigh pain: a case report.

Glomus tumors are a rare, benign neoplasm and 75% exist in the subungual region. Extradigital glomus tumors are much more difficult to diagnose because of their atypical location and symptoms. Furthermore, if their symptoms are similar to neuropathic pain, the patient can suffer from misdirected treatment due to misdiagnosis. It is essential to perform careful evaluation of the lesion itself in order to reduce misdiagnosis. Ultrasonography is a useful, non-invasive method that can be easily performed in the pain clinic for local evaluation and diagnosis. We report a case of misdiagnosed glomus tumor in the thigh which was properly diagnosed after ultrasonography.

Vomiting after a pediatric adenotonsillectomy: comparison between propofol induced sevoflurane-nitrous oxide maintained anesthesia and TIVA with propofol-remifentanil.

BACKGROUND: Anesthesia methods and drugs affect postoperative nausea and vomiting. Propofol is known to have antiemetic effects. We compared the incidence of postoperative vomiting (POV) in children undergoing an adenotonsillectomy; anesthesia in one group was induced with propofol and maintained with sevoflurane and nitrous oxide, and the other group received total intravenous anesthesia (TIVA) with propofol-remifentanil. METHODS: Ninety children, ASA physical status I, were assigned randomly to one of two groups. In the PSN group, anesthesia was maintained with 2-3 vol% sevoflurane and 50% nitrous oxide. In the PR group, anesthesia was maintained with 10 mg/kg/h propofol and 0.25 µg/kg/min remifentanil. In both groups, anesthesia was induced with 0.5 µg /kg remifentanil and 2 mg/kg propofol. The incidence of POV and the need for rescue antiemetics were assessed in the postanesthesia care unit at 6, 12, and 24 hours postoperatively. RESULTS: The total incidence of POV was not significantly different between the groups; POV occurred in eight (17.7%) and three (6.7%) children in the PSN and PR groups, respectively. Postoperative frequency of retching in the recovery room was significantly higher in the PSN group, with four children (8.9%) in the PSN group compared to none (0%) in the PR group (P = 0.041). The frequency of POV 24 hrs after exiting the recovery room tended to be higher in the PSN group than the PR group, but no statistically significant difference was observed. CONCLUSIONS: If the development of POV in the early anesthetic recovery phase of children undergoing adenotonsillectomy is adequately prevented, propofol-induced anesthesia maintained with sevoflurane-nitrous oxide is as safe as TIVA with propofol-remifentanil.

The effects of paracetamol, ketorolac, and paracetamol plus morphine on pain control after thyroidectomy.

BACKGROUND: The aim of this study was to compare the efficacy of ketorolac, paracetamol, and paracetamol plus morphine on pain relief after thyroidectomy. METHODS: Eighty patients were randomly allocated to one of the 4 groups: normal saline (group C), ketorolac 30 mg (group K), paracetamol 1 g (group P), and paracetamol 700 mg plus morphine 3 mg (group PM). Each regimen was administered intravenously (IV) 30 min. before the end of surgery. If pain was not relieved, patients received an IV bolus of pethidine hydrochloride 25 mg. Pain intensity using a visual analogue scale (VAS) was recorded at 0.5, 1, 2, 4, and 6 hr after the end of surgery. RESULTS: VAS at 0.5 and 1 hr after the end of surgery were significantly lower in group K, group P, and group PM than in group C (P < 0.05). The number of patients receiving pethidine hydrochloride at 0.5 and 1 hr after the end of surgery was significantly lower in group K, group P, and group PM than in group C (P < 0.05). There was no significant difference among the groups in the incidences of adverse events associated with study medications and patient satisfaction (P > 0.05). CONCLUSIONS: Paracetamol 1 g IV possesses a similar analgesic efficacy to ketorolac 30 mg IV after thyroidectomy. Paracetamol may represent an alternative to ketorolac for pain prevention after mildly to moderately painful surgery in situations where the use of NSAIDs is unsuitable.