Time- and dose-dependent correlations between patient-controlled epidural analgesia and intrapartum maternal fever.

BACKGROUND: To investigate the relationship between intrapartum maternal fever and the duration and dosage of patient-controlled epidural analgesia (PCEA). METHODS: This observational study included 159 pregnant women who voluntarily accepted PCEA. During labor, patients with body temperature ≥ 38 °C were classified into the Fever group, (n = 42), and those with body temperature < 38 °C were classified into the No-fever group (n = 117). The outcome measures included the duration of PCEA, number of PCEA, and total PCEA amount. Body temperature and parturient variables, including interpartum fever status and the duration of any fever were monitored. RESULTS: The total PCEA duration and total PCEA amount in the Fever group were significantly higher than the corresponding values in the No-fever group (both, p < 0.05). The duration of fever was weakly correlated with the duration of PCEA (R2 = 0.08) and the total PCEA amount (R2 = 0.05) (both, p < 0.05). The total and effective PCEA were higher in the Fever group than in the No-fever group (both, p < 0.05). The total PCEA duration and total PCEA amount were positively correlated with the incidence of fever (both, p < 0.05). The diagnostic cutoff value for fever was 383 min, with a sensitivity of 78.6% and specificity of 57.3%. The mean temperature-time curves showed that parturients who developed fever had a steeper rise in temperature. CONCLUSIONS: This study showed that there were weak time- and dose-dependent correlations between PCEA and maternal fever during delivery. A total PCEA duration exceeding 6.3 h was associated with an increase in the duration of maternal intrapartum fever.

Effect of caudal ketamine on minimum local anesthetic concentration of ropivacaine in children: a prospective randomized trial.

BACKGROUND: Caudal ketamine has been shown to provide an effective and prolonged post-operative analgesia with few adverse effects. However, the effect of caudal ketamine on the minimum local anesthetic concentration (MLAC) of ropivacaine for intra-operative analgesia is unclear. METHODS: One hundred and sixty-nine children were randomized to five groups: Group C (caudal ropivacaine only), Group K0.25 (caudal ropivacaine plus 0.25 mg/kg ketamine), Group K0.5 (caudal ropivacaine plus 0.5 mg/kg ketamine), Group K0.75 (caudal ropivacaine plus 0.75 mg/kg ketamine), and Group K1.0 (caudal ropivacaine plus 1.0 mg/kg ketamine). The primary outcome was the MLAC values of ropivacaine with/without ketamine for caudal block. RESULTS: The MLAC values of ropivacaine were 0.128% (0.028%) in the control group, 0.112% (0.021%) in Group K0.25, 0.112% (0.018%) in Group K0.5, 0.110% (0.019%) in Group K0.75, and 0.110% (0.020%) in Group K1.0. There were no significant differences among the five groups for the MLAC values (p = 0.11). During the post-operative period the mean durations of analgesia were 270, 381, 430, 494, and 591 min in the control, K0.25, K0. 5, K0.75, and K1.0 groups respectively, which shown that control group is significantly different from all ketamine groups. Also there were significant differences between K0.25 and K0.75 groups, and between K1.0 groups and the other ketamine groups. CONCLUSIONS: Adding caudal ketamine to ropivacaine prolong the duration of post-operative analgesia; however, it does not decrease the MLAC of caudal ropivacaine for intra-operative analgesia in children. CLINICAL TRIAL REGISTRATION: ChiCTR-TRC-13003492. Registered on 13 August 2013.

Relationship Between Body Mass Index and Spread of Spinal Anesthsia in Pregnant Women: A Randomized Controlled Trial.

BACKGROUND The effect of body mass index (BMI) on the spread of spinal anesthesia is not completely clear. The aim of this study was to determine the dose requirements of ropivacaine and the incidence of hypotension in pregnant women with different BMIs during cesarean delivery. MATERIAL AND METHODS In this double-blind study, 405 women undergoing elective cesarean delivery were allocated to group S (BMI <25), group M (25 ≤BMI <30), or group L (BMI ≥30). Women in each group were further assigned to receive 7, 8, 9, 10, 11, 12, 13, 14, or 15 mg of spinal ropivacaine. RESULTS The ED50 and ED95 values of ropivacaine were 9.487 mg and 13.239 mg in Group S, 9.984 mg and 13.737 mg in Group M, and 9.067 mg and 12.819 mg in Group L. There were no significant differences among the 3 groups (p=0.915). Group L had a higher incidence of hypotension and a greater change in MAP after spinal anesthesia compared to the other 2 groups, and also required more doses of ephedrine than the other 2 groups when a dose of 15 mg ropivacaine was used. The incidence of hypotension had a positive correlation with the dose of ropivacaine (OR=1.453, p<0.001) and gestational age (OR=1.894, p<0.001). CONCLUSIONS Spinal ropivacaine dose requirements were similar in the normal BMI range. However, higher doses of spinal ropivacaine were associated with an increased incidence and severity of hypotension in obese patients compared with that in non-obese patients.

Effect of a bolus dose of fentanyl on the ED50 and ED95 of sevoflurane in neonates.

BACKGROUND: The minimum alveolar concentration (MAC) of sevoflurane in neonates is 3.3%, but this value has not been verified in Chinese neonates and the effect of different doses of fentanyl on MAC in neonates has not been investigated. This study was designed to determine the ED50 and ED95 values of sevoflurane in Chinese neonates with and without fentanyl. MATERIAL AND METHODS: Ninety-three neonates were randomly assigned to receive sevoflurane alone (control group, n=30), 1 µg/kg sevoflurane (group fent1, n=29), or 2 µg/kg fentanyl (group fent2, n=32). Following inhalational induction and tracheal intubation, the end-tidal concentration of sevoflurane was adjusted to achieve the designated concentration, which was determined using the modified Dixon's up-and-down method starting with 3.0% in each group, with a 0.25% step size. Success was defined as no motor response within 60 s of skin incision. RESULTS: The MAC (standard deviation) values of sevoflurane were 2.91% (0.27) in the control group, 2.53% (0.31) in the fent1 group, and 2.34% (0.33) in the fent2 group according to Dixon's up-and-down method. Logistic probit regression analysis revealed that the ED50 and ED95 (95% CI) of sevoflurane in neonates were 2.82% (2.66-2.98) and 3.39% (2.89-3.89), respectively, in the control group; 2.44% (2.19-2.68) and 3.30% (2.51-4.09), respectively, in the fent1 group; and 2.21% (1.97-2.45) and 3.11% (2.35-3.88), respectively, in the fent2 group. CONCLUSIONS: The MAC value of sevoflurane in Chinese neonates was lower than previously reported and was reduced by the addition of fentanyl.

Caudal dexmedetomidine decreases the required concentration of levobupivacaine for caudal block in pediatric patients: a randomized trial.

BACKGROUND AND OBJECTIVES: Dexmedetomidine (D) can prolong the duration of local anesthetics, but the effect of caudal dexmedetomidine on the potency of levobupivacaine (L) for caudal block has not been investigated. This study was designed to determine the effect of caudal dexmedetomidine on levobupivacaine for caudal block in pediatric patients. METHODS: Eighty-nine children scheduled for elective inguinal hernia repair or hydrocele were randomly assigned to one of the three groups: Group L (caudal levobupivacaine), Group LD1 (levobupivacaine plus 1 µg·kg(-1) dexmedetomidine), or Group LD2 (levobupivacaine plus 2 µg·kg(-1) dexmedetomidine). The primary endpoint was the minimum local anesthetic concentration (MLAC), which was determined using the Dixon up-and-down method. The secondary endpoints were the duration of analgesia and sedation. RESULTS: The MLAC values (sd) of caudal levobupivacaine were 0.103 (0.01)%, 0.068 (0.02)%, and 0.055 (0.03)% in Groups L, LD1, and LD2, respectively. The values of EC50 and EC95 (95% CI) of caudal levobupivacaine from logistic regression analysis were 0.094 (0.083-0.105)% and 0.129 (0.1-0.159)%, 0.058 (0.044-0.072)% and 0.106 (0.067-0.144)%, and 0.046 (0.033-0.059)% and 0.091 (0.055-0.127)% in Groups L, LD1, and LD2, respectively. The mean durations of analgesia in the postoperative period were 141, 378, and 412 min in Groups L, LD1, and LD2, respectively (L vs LD1 or LD2, P < 0.001). The mean durations of sedation in both Groups LD1 and LD2 also were significantly prolonged, compared with Group L (P < 0.01). CONCLUSIONS: Caudal dexmedetomidine reduces the MLAC values of levobupivacaine and improves postoperative analgesia in children without any neurological side effects.

Prophylactic Epidural Blood Patch or Prophylactic Epidural Infusion of Hydroxyethyl Starch in Preventing Post-Dural Puncture Headache - A Retrospective Study.

BACKGROUND: Post-dural puncture headache (PDPH) is particularly likely to happen in patients under obstetric care due to an unintentional dural puncture (UDP). There is as yet no ideal strategy for preventing UDP-induced PDPH. OBJECTIVES: The primary objective of this study was to assess whether a prophylactic epidural blood patch (EBP) or prophylactic epidural infusion of hydroxyethyl starch (HES) is effective in preventing PDPH for parturients with UDP compared with conservative treatments. STUDY DESIGN: Retrospective analysis from a single center's inpatient data. SETTING: Department of Anesthesiology at a single center. METHODS: A retrospective study was conducted of a single center's inpatient data from January 2017 through March 2020. The study included parturients with UDP during neuraxial anesthesia. The interventions of UDP included conservative treatment, prophylactic EBP, and prophylactic epidural infusion of HES. The incidence of PDPH, the use of intravenous aminophylline, therapeutic EBP, symptom onset, duration of headache, and duration of hospital stay were compared. RESULTS: A total of 85 patients were analyzed. The incidences of PDPH were 84%, 52.6% and 54.5% with conservative, prophylactic EBP, and prophylactic epidural HES treatments, respectively. Compared with the conservative treatment, prophylactic EBP and prophylactic epidural HES treatment significantly reduced the incidence of PDPH (P < 0.05). No significant difference was found between the prophylactic EBP and prophylactic epidural HES groups. Compared with the conservative treatment group, therapeutic EBP was significantly less used in the prophylactic EBP and prophylactic epidural HES groups (P < 0.05). Prophylactic EBP shortened the length of hospital stay of parturients with UDP (P < 0.05) while prophylactic epidural HES showed no statistical difference compared with conservative treatment. No severe complications, such as central nervous system and puncture site infection or nerve injury, were found in those patients. LIMITATIONS: Retrospective nature and single center data with a relatively small sample size. CONCLUSIONS: Prophylactic management with EBP and epidural infusion of HES has an effect in preventing the occurrence of PDPH; prophylactic EBP significantly shortened hospital stay length in parturients with UDP. KEY WORDS: Unintentional dural puncture, epidural blood patch, hydroxyethyl starch, post-dural puncture headache, parturient.

[Effect of dexmedetomidine on postoperative analgesia and sedation in pediatric patients undergoing cleft lip and palate repair].

OBJECTIVE: To explore the effect of different doses of dexmedetomidine on the sedation of recovery period and the postoperative early pain scores in pediatric patients undergoing cleft lip and palate repair. METHODS: A total of 100 American Society of Anesthesiologists (ASA) I-II pediatric patients undergoing cleft lip and palate repair were randomly divided into 5 groups (D1, D2, D3, D4 and C, n = 20 each). Groups D1-D4 received a continuous pump infusion of dexmedetomidine at 0.25, 0.5, 0.75, 1.0 µg × kg(-1)× h(-1) respectively for 1 h before the completion of operation. Then an intravenous injection of 1 µg/kg was prescribed over 10 min as a loading dose. Group C, taken as control, received an equal volume of normal saline. Propofol 2 mg/kg was added for the occurrence of emergence agitation. Mean arterial pressure (MAP), heart rate (HR), respiratory rate (RR), partial pressure of end-tidal carbon dioxide (P(ET)CO(2)), Riker sedation-agitation scale, times of additional propofol requirements, times of additional artificial ventilation, extubation time, discharge time, side effects and face, legs, activity, cry and consolability (FLACC) scale were observed and recorded. RESULTS: The Riker sedation-agitation scale were 5.3 ± 0.9, 4.3 ± 0.8, 3.5 ± 0.8, 2.6 ± 0.6 and 6.1 ± 0.7, times of additional propofol requirements were 4.7 ± 1.7, 2.5 ± 1.4, 0.8 ± 0.9, 0.1 ± 0.4 and 5.7 ± 0.7 in groups D1, D2, D3, D4 and C respectively. In short, group D4 ≈ group D3 < group D2 < group D1 < group C (P < 0.05). As compared with group D4, the extubation time and discharge time significantly increased in groups D1, D2, D3 and C (P < 0.05). The FLACC scales in groups D2, D3 and D4 were lower than those in groups D1 and C. Side effects: 2 cases developed sinus bradycardia in group D4 and heart rate returned to normal after treatment. CONCLUSION: At a load dosage of 1 µg/kg and a maintenance dosage of 0.75 µg × kg(-1)× h(-1), dexmedetomidine shows excellent effects on the recovery period of cleft lip and palate repairing in pediatric patients. The FLACC scale decreases with fewer side effects, but extubation time and discharge time increase.

[Retracted] miR­218 suppresses tumor growth and enhances the chemosensitivity of esophageal squamous cell carcinoma to cisplatin.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the western blotting data shown in Fig. 6 and the tumor images shown in Fig. 7A were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Oncology Reports 33: 981­989, 2015; DOI: 10.3892/or.2014.3657].

Using intranasal dexmedetomidine with buccal midazolam for magnetic resonance imaging sedation in children: A single-arm prospective interventional study.

Objective: Although numerous intravenous sedative regimens have been documented, the ideal non-parenteral sedation regimen for magnetic resonance imaging (MRI) has not been determined. This prospective, interventional study aimed to investigate the efficacy and safety of buccal midazolam in combination with intranasal dexmedetomidine in children undergoing MRI. Methods: Children between 1 month and 10 years old requiring sedation for MRI examination were recruited to receive buccal midazolam 0.2 mg⋅kg-1 with intranasal dexmedetomidine 3 µg⋅kg-1. The primary outcome was successful sedation following the administration of the initial sedation regimens and the completion of the MRI examination. Results: Sedation with dexmedetomidine-midazolam was administered to 530 children. The successful sedation rate was 95.3% (95% confidence interval: 93.5-97.1%) with the initial sedation regimens and 97.7% (95% confidence interval: 96.5-99%) with a rescue dose of 2 µg⋅kg-1 intranasal dexmedetomidine. The median sedation onset time was 10 min, and a significant rising trend was observed in the onset time concerning age (R = 0.2491, P < 0.001). The wake-up and discharge times significantly correlated with the duration of the procedure (R = 0.323, P < 0.001 vs. R = 0.325, P < 0.001). No oxygen deficiency nor medication intervention due to cardiovascular instability was observed in any of the patients. History of a prior failed sedation was considered a statistically significant risk factor for failed sedation in the multivariate logistic regression model [odds ratio = 4.71 (95% confidence interval: 1.24-17.9), P = 0.023]. Conclusion: In MRI examinations, the addition of buccal midazolam to intranasal dexmedetomidine is associated with a high success rate and a good safety profile. This non-parenteral sedation regimen can be a feasible and convenient option for short-duration MRI in children between 1 month and 10 years.

A Comparison of Intranasal Dexmedetomidine and Dexmedetomidine Plus Buccal Midazolam for Non-painful Procedural Sedation in Children with Autism.

Children with autism often need sedation for diagnostic procedures and they are often difficult to sedate. This prospective randomized double-blind control trial evaluates the efficacy and safety using intranasal dexmedetomidine with and without buccal midazolam for sedation in children with autism undergoing computerized tomography and/or auditory brainstem response test. The primary outcome is the proportion of children attaining satisfactory sedation. One hundred and thirty-six children received intranasal dexmedetomidine and 139 received intranasal dexmedetomidine with buccal midazolam for sedation. Combination of intranasal dexmedetomidine and buccal midazolam was associated with higher sedation success when compared to intranasal dexmedetomidine. Since intranasal and buccal sedatives required little cooperation this could be especially useful technique for children with autism or other behavioral conditions.

miR-132 targeting E2F5 suppresses cell proliferation, invasion, migration in ovarian cancer cells.

Accumulating evidence showed that microRNA-132 (miR-132) are involved in development and progression of several types of cancers, however, the function and underlying molecular mechanism of miR-132 in ovarian cancer remains unclear. In this study we investigated the biological roles and molecular mechanism of miR-132 in ovarian cancer. Here, we found that that the expression levels of miR-132 were dramatically decreased in ovarian cancer cell lines and clinical ovarian cancer tissue samples. Then, we found that introduction of miR-132 significantly suppressed the proliferation, colony formation, migration and invasion of ovarian cancer cells. Mechanism investigation revealed that miR-132 inhibited the expression of transcription factor E2F5 by specifically targeting its mRNA 3'UTR. Moreover, the expression level of E2F5 was significantly increased in ovarian cancer tissues than in the adjacent normal tissues, and its expression was inversely correlated with miR-132 expression in clinical ovarian cancer tissues. Additionally, silencing E2F5 was able to inhibit the proliferation, colony formation, migration and invasion of ovarian cancer cells, parallel to the effect of miR-132 overexpression on the ovarian cancer cells. Meanwhile, overexpression of E2F5 reversed the inhibition effect mediated by miR-132 overexpression. These results indicate that miR-132 suppresses the cell proliferation, invasion, migration in ovarian cancer cells by targeting E2F5.

Activation of α2 adrenoceptor attenuates lipopolysaccharide-induced hepatic injury.

Sepsis induces hepatic injury but whether alpha-2 adrenoceptor (α2-AR) modulates the severity of sepsis-induced liver damage remains unclear. The present study used lipopolysaccharide (LPS) to induce hepatic injury and applied α2-AR agonist dexmedetomidine (DEX) and/or antagonist yohimbine to investigate the contribution of α2-AR in LPS-induced liver injury. Our results showed that LPS resulted in histological and functional abnormality of liver tissue (ALT and AST transaminases, lactate), higher mortality, an increase in proinflammatory cytokines (IL-1ß, IL-6 & TNF-α), as well as a change in oxidative stress (MDA, SOD). Activation of α2-AR by dexmedetomidine (DEX) attenuated LPS-induced deleterious effects on the liver and block of α2-AR by yohimbine aggravated LPS-induced liver damage. Our data suggest that α2-AR plays an important role in sepsis-induced liver damage and activation of α2-AR with DEX could be a novel therapeutic avenue to protect the liver against sepsis-induced injury.

A prospective study comparing the onset and analgesic efficacy of different concentrations of levobupivacaine with/without dexmedetomidine in young children undergoing caudal blockade.

STUDY OBJECTIVE: To investigate the onset and analgesic effect of adding dexmedetomidine to levobupivacaine for caudal block in young children. DESIGN: Randomized, prospective, double-blind study. SETTING: Women and Children Medical Center and university hospital. PATIENTS: Two hundred twelve children, American Society of Anesthesiologists physical status I or II, aged between 1 and 3 years and weighing between 8 and 18 kg, who were scheduled for elective inguinal hernia repair or hydrocele. INTERVENTIONS: Children were randomly allocated, using a computer-generated sequence of numbers, into 1 of 3 groups: caudal 0.25% levobupivacaine (Group L(0.25)), caudal 0.20% levobupivacaine (Group L(0.20)), or caudal 0.20% levobupivacaine plus 2 µg/kg dexmedetomidine (Group LD). MEASUREMENTS AND MAIN RESULTS: The primary end point of the study was the onset time of caudal levobupivacaine in children. The secondary end points of the study were the duration of analgesia and the degree of motor block in children. The 50% and 95% effective onset time (95% confidence interval) values of levobupivacaine were 8.19 minutes (7.30-9.08) and 11.17 minutes (9.44-12.91) in Group L(0.25), 10.16 minutes (8.90-11.41) and 15.85 minutes (13.14-18.57) in Group L(0.20), and 9.91 minutes (8.55-11.28) and 16.39 minutes (13.32-19.46) in Group LD, respectively. The mean durations of analgesia in these children were 7.23, 5.84, and 19.6 hours in Groups L(0.25), L(0.20), and LD, respectively. There were no significant differences in postoperative residual motor block among the 3 groups. CONCLUSIONS: Dexmedetomidine added to levobupivacaine does not have a significant effect on the onset time; however, it prolongs the duration of analgesia during caudal block in children.

Serious anaphylactic shock induced by hemocoagulase agkistrodon during anesthesia in a 5-year-old child.

We report a case of serious anaphylactic shock in a 5-year-old child undergoing scheduled surgery blank space of a right femoral intramedullary nail removal. The boy had undergone right femoral elastic intramedullary nail fixation surgery 14 months prior, but had no history of allergies. Within 5 minutes of intravenous bonus injection of hemocoagulase agkistrodon (HCA) 1 unit, a widespread transient diffuse erythema was seen on the front of his chest. After 20 minutes, sudden, profound cardiovascular collapse occurred. The child was treated effectively and sent to a ward 5 hours later. In this period, he received intravenously infused 200 ml hydroxyethyl starch solution and epinephrine at a rate of 0.05-0.01 µg kg(-1) min(-1). Total amount of dexamethasone sodium phosphate 14 mg was used. To the best of our knowledge, few case reports of HCA-induced anaphylactic shock in children exist. Our report will, therefore, increase awareness of the allergic potential of HCA among pediatric anesthesiologists.

miR-218 suppresses tumor growth and enhances the chemosensitivity of esophageal squamous cell carcinoma to cisplatin.

A growing body of evidence suggests that microRNA-218 (miR-218) acts as a tumor suppressor and is involved in tumor progression, development and metastasis and confers sensitivity to certain chemotherapeutic drugs in several types of cancer. However, our knowledge concerning the exact roles played by miR-218 in esophageal squamous cell carcinoma (ESCC) and the underlying molecular mechanisms remain relatively unclear. Thus, the aims of this study were to detect the expression of miR-218 in human ESCC tissues and explore its effects on the biological features and chemosensitivity to cisplatin (CDDP) in an ESCC cell line (Eca109), so as to provide new insights for ESCC treatment. Here, we found increased expression of miR-218 in the ESCC tissues compared with that in the matched non-tumor tissues, and its expression level was correlated with key pathological characteristics including clinical stage, tumor depth and metastasis. We also found that enforced expression of miR-218 significantly decreased cell proliferation, colony formation, migration and invasion, induced cell apoptosis and arrested the cell cycle in the G0/G1 phase, as well as suppressed tumor growth in a nude mouse model. In addition, our results showed that miR-218 mimics increased the sensitivity to the antitumor effect of CDDP in the human Eca109 cells. Importantly, this study also showed that miR-218 regulated the expression of phosphorylated PI3K, AKT and mTOR, which may contribute to suppressed tumor growth of ESCC and enhanced sensitivity of ESCC cells. These findings suggest that miR-218 is a potential therapeutic agent for the treatment of ESCC.

Hyperbaric oxygen treatment at various stages following chronic constriction injury produces different antinociceptive effects via regulation of P2X4R expression and apoptosis.

PURPOSE: The aims of this study were to investigate the effect of hyperbaric oxygen (HBO) treatment at various stages following chronic constriction injury (CCI) and to explore the underlying mechanisms of HBO treatment. METHODS: Forty adult male Sprague-Dawley rats were randomly assigned to five groups (n = 8 for each group): the sham group, CCI group, HBO1 group, HBO2 group, and HBO3 group. Neuropathic pain was induced by CCI of the sciatic nerve. HBO treatment began on postoperative days 1, 6, and 11 and continued for 5 days. The mechanical withdrawal threshold and thermal withdrawal latency were tested on preoperative day 3 and postoperative days 1, 3, 5, 7, 10, 14, and 21. The expression of P2X4R was determined by immunohistochemistry and western blot analysis. Cell apoptosis was measured using TUNEL staining. The expression of caspase 3 was measured using reverse transcription polymerase chain reaction (RT-PCR). Electron microscopy was used to determine the ultrastructural changes. RESULTS: Early HBO treatment beginning on postoperative day 1 produced a persistent antinociceptive effect and inhibited the CCI-induced increase in the expression of P2X4R without changing CCI-induced apoptosis. In contrast, late HBO treatment beginning on postoperative day 11 produced a persistent antinociceptive effect and inhibited CCI-induced apoptosis and upregulation of caspase-3 without changing the expression of P2X4R. In addition, late HBO treatment reduced CCI-induced ultrastructural damage. However, HBO treatment beginning on postoperative day 6 produced a transient antinociceptive effect without changing the expression of P2X4R or CCI-induced apoptosis. CONCLUSION: HBO treatment at various stages following CCI can produce antinociceptive effects via different mechanisms. Early HBO treatment is associated with inhibition of P2X4R expression, and late HBO treatment is associated with inhibition of cell apoptosis.