BackgroundRemote ischemic preconditioning (RIPC) and postconditioning (RpostC) have protective effects on ischemia and reperfusion injury. The effects have been reported to activate heme oxygenase-1 (HO-1) and attenuate nuclear factor kappa B (NF-κB) and subsequently reduce systemic inflammation. Ischemic preconditioning prevented inflammatory responses by modulating HO-1 expression in endotoxic shock model. Therefore, we investigated whether RpostC could have protective effects on lipopolysaccharide (LPS)-induced systemic inflammation.MethodsThe LPS-induced sepsis mice received LPS (20 mg/kg) intraperitoneally. Remote ischemic conditioning was induced with three 10-min ischemia/10-min reperfusion cycles of the right hind limbs using tourniquet before LPS injection (RIPC) or after LPS injection (RpostC). The effects of RIPC and RpostC were examined for the survival rate, serum cytokines, NF-κB, HO-1 and liver pathology in the LPS injected mice.ResultsSurvival rate within 120 hours significantly increased in the LPS injected and remote ischemic conditioned mice than in LPS only injected mice (60-65% vs 5%, respectively, p < 0.01). Tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6) increased markedly in the LPS only injected mice, however, remote ischemic conditioning suppressed the changes (p < 0.05). Interleukin-10 (IL-10) level was significantly higher in the LPS injected and RpostC treated mice than in the LPS only injected mice (p = 0.014). NF-κB activation was significantly attenuated (p < 0.05) and HO-1 levels were substantially higher in the LPS injected and remote ischemic conditioned mice than in the LPS only injected mice. Neutrophil infiltration was significantly attenuated in the LPS injected and remote ischemic conditioned mice than in the only LPS injected mice (p < 0.05).ConclusionsRpostC attenuated inflammatory responses and improved survival outcomes of mice with LPS-induced systemic inflammation. The mechanism may be caused by modifying NF-κB mediated expression of cytokines.

ObjectiveThis retrospective case series study of the effectiveness of electroconvulsive therapy (ECT) augmentation on clozapine-resistant schizophrenia was conducted by EMR review.MethodsClozapine-resistance was defined as persistent psychotic symptoms despite at least 12 weeks of clozapine administration with blood levels over 350 ng/mL in order to rule out pseudo-resistance. Seven in-patients who were taking clozapine and treated with ECT were selected. We analyzed the psychopathology and subscales changed by ECT.ResultsThe average number of ECT sessions was 13.4 (±4.6). Total Positive and Negative Syndrome Scale (PANSS) score was significantly reduced by 17.9 (±12.8) points (p=0.0384) on average, which represented a reduction of 25.5% (±14.3). 71.4% (5/7) of patients were identified as clinical remission, with at least a 20% reduction in PANSS score. PANSS reduction was associated with number of ECT sessions, stimulus level in the final session, and blood clozapine levels before ECT. However, the negative subscale on the PANSS were not reduced by ECT in any patient. We did not observe any persistent adverse cognitive effects.ConclusionThis study supports that ECT augmentation on clozapine-resistant schizophrenia reveals clinically effective and safe. Further research should be done involving a larger number of patients to investigate the effectiveness of clozapine/ECT combination therapy.

BackgroundWe purposed to systemically review studies investigating the prophylactic effect of both pharmacological and non-pharmacological modalities against rocuronium induced withdrawal movement (RIWM) in the Korean population.MethodsLiterature search was performed using MEDLINE, EMBASE, CENTRAL, Koreamed, KMBASE, KISS and RISS up to March 2014. Randomized controlled trials (RCTs) comparing pharmacological and non-pharmacological interventions with placebo aimed for the Korean population were included. Outcome measures were the incidence and severity of RIWM. We conducted subgroup analyses according to each intervention method.ResultsData were analyzed from 41 RCTs totaling 4,742 subjects. The overall incidence of RIWM was about 80% (range 56-100%). Incidence and severity of RIWM were significantly reduced with lidocaine (risk ratio [RR] 0.60, 95% CI 0.49-0.74; standardized mean difference [SMD] -0.74, 95% CI -1.05 to -0.44), opioids (RR 0.28, 95% CI 0.18-0.44; SMD -1.71, 95% CI -2.09 to -1.34) and hypnotics (RR 0.36, 95% CI 0.25-0.52; SMD -2.20, 95% CI -2.62 to -1.79). Regardless of tourniquet use, lidocaine showed a prophylactic effect against incidence and severity of RIWM: tourniquet (RR 0.36, 95% CI 0.21-0.62; SMD -1.51, 95% CI -2.15 to -0.86); non-tourniquet (RR 0.58, 95% CI 0.47-0.71; SMD -0.74, 95% CI -1.05 to -0.44). Dilution and slow injection of rocuronium decreased incidence and severity of RIWM: dilution (RR 0.47, 95% CI 0.39-0.56; SMD -1.64, 95% CI -2.47 to -0.81); slow injection (RR 0.34, 95% CI 0.17-0.70; SMD -2.13, 95% CI -2.74 to -1.51).ConclusionsThe greater part of pharmacological and non-pharmacological interventions showed prophylactic effect against the incidence and severity of RIWM in the Korean population.

BackgroundThe regional cerebral oxygen saturation (rSO2) decreases significantly during ordinary anesthetic recovery in pediatric patients anesthetized with sevoflurane or desflurane. The present study examined the relationship between rSO2 and the clinical parameters associated with the degree of anesthetic recovery.MethodsTwelve pediatric patients with American Society of Anesthesiologists physical status 1 were assigned randomly to receive anesthesia with sevoflurane or desflurane. All children underwent general anesthesia for minor surgery. After surgery, the rSO2, the age-adjusted MAC fraction of anesthetic concentration (FE), and the bispectral index (BIS) were recorded over a 10-minute period. The correlations between rSO2 and candidate predictors, such as FE, BIS, anesthetic, and duration of anesthesia, were analyzed.ResultsAll children recovered uneventfully. The lowest observed rSO2 reached 63% and the maximum decrease in rSO2 was 24%. The mean blood pressure and heart rate were maintained within clinical ranges. The decrease in rSO2 correlated positively with the FE (r = 0.25, P = 0.00) and the duration of anesthesia (r = 0.24, P = 0.01), and inversely with the use of sevoflurane (r = -0.30, P = 0.00).ConclusionsDespite normal parameters, cerebral desaturation occurred during the emergence of ordinary general anesthesia even without hemodynamic compromise or arterial desaturation. Cerebral desaturation might be associated with the degree of anesthetic recovery and the use of sevoflurane.