The anti-inflammatory actions of sevoflurane postconditioning are suggested as an important mechanism of sevoflurane postconditioning-induced neuroprotection against cerebral ischemia. Here, we determined whether the anti-inflammatory effects of sevoflurane postconditioning were mediated via inhibition of the toll-like receptor (TLR)-4/nuclear factor kappa B (NF-κB) pathway after global transient cerebral ischemia in rats. Forty-five rats were randomly assigned to five groups as follows: (1) control (10 min of ischemia, n = 10); (2) sevoflurane postconditioning (two periods of sevoflurane inhalation after ischemia for 10 min with a wash period of 10 min, n = 10); (3) resatorvid (intraperitoneal injection of a selective TLR-4 antagonist (3 mg/kg) 30 min before ischemia, n = 10); (4) sevoflurane postconditioning plus resatorvid (n = 10), and sham (n = 5). The numbers of necrotic and apoptotic cells in the hippocampal CA1 region, the expression levels of TLR-4, NF-κB, cleaved caspase-3, and tumor necrosis factor alpha (TNF-α) in the anterior part of each brain, and the serum levels of TNF-α, interleukin 6 (IL-6), and interleukin 1 beta (IL-1β) were assessed 1 day after ischemia. The necrotic cell counts and expression levels of TLR-4, NF-κB, caspase-3, and TNF-α in brain tissue as well as serum levels of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) were significantly higher in the control group than in the other groups. Our findings suggest that the anti-inflammatory actions of sevoflurane postconditioning via inactivation of the TLR-4/NF-κB pathway and subsequent reduction in pro-inflammatory cytokine production, in part, contribute to sevoflurane postconditioning-induced neuroprotection after global transient cerebral ischemia in rats.
20 May 2002 in Acta Anaesthesiologica Scandinavica
Craniotomy patients have a high incidence of postoperative nausea and vomiting (PONV). This prospective, randomized, double-blind, multi-center study was performed to evaluate the efficacy of prophylactic ramosetron in preventing PONV compared with ondansetron after elective craniotomy in adult patients. A total of 160 American Society of Anesthesiologists physical status I–II patients aged 19–65 years who were scheduled to undergo elective craniotomy for various intracranial lesions were enrolled in this study. All patients received total intravenous anesthesia (TIVA) with propofol and remifentanil. Patients were randomly allocated into three groups to receive ondansetron (4 mg; group A, n = 55), ondansetron (8 mg; group B, n = 54), or ramosetron (0.3 mg; group C, n = 51) intravenously at the time of dural closure. The incidence of PONV, the need for rescue antiemetics, pain score, patient-controlled analgesia (PCA) consumption, and adverse events were recorded 48 h postoperatively. Among the initial 160 patients, 127 completed the study and were included in the final analysis. The incidences of PONV were lower (nausea, 14% vs. 59% and 41%, respectively; P < 0.001; vomiting, P = 0.048) and the incidence of complete response was higher (83% vs. 37% and 59%, respectively; P < 0.001) in group C than in groups A and B at 48 h postoperatively. There were no significant differences in the incidence of PONV or need for rescue antiemetics 0–2 h postoperatively, but significant differences were observed in the incidence of PONV and complete response among the three groups 2–48 h postoperatively. No statistically significant intergroup differences were observed in postoperative pain, PCA consumption, or adverse events. Intravenous administration of ramosetron at 0.3 mg reduced the incidence of PONV and rescue antiemetic requirement in craniotomy patients. Ramosetron at 0.3 mg was more effective than ondansetron at 4 or 8 mg for preventing PONV in adult craniotomy patients. Clinical Research Information Service (CRiS) Identifier: KCT0000320 . Registered 9 January 2012.
1 February 2016 in Canadian Journal of Anesthesia/Journal canadien d'anesthésie
Catheter-related bladder discomfort (CRBD) due to an indwelling urinary catheter can cause postoperative distress, and the mechanism underlying CRBD is linked to the activation of muscarinic receptors. Inhalation of anesthetic agents, such as sevoflurane and desflurane, has differential inhibitory effects on muscarinic receptors. We aimed to compare the effect of intraoperative sevoflurane vs desflurane inhalation on postoperative CRBD. Eighty-nine patients undergoing transurethral resection of a bladder tumour (TURBT) were randomly allocated to two groups. The sevoflurane group (n = 45) and the desflurane group (n = 44) received the respective inhalational agents for maintenance of general anesthesia. The incidence and severity (mild/moderate/severe) of CRBD were assessed at zero, one, six, and 24 hr postoperatively. Catheter-related bladder discomfort during the first 24 hr postoperatively occurred in 34/45 (76%) patients receiving sevoflurane compared with 41/44 (93%) patients receiving desflurane [absolute difference 18%; 95% confidence interval [CI], 2 to 33; P = 0.039]. The differences in the rate of CRBD between the sevoflurane and desflurane groups at zero, one, and six hours postoperatively were 24% (95% CI, 7 to 40; P = 0.012), 33% (95% CI, 15 to 49; P = 0.001), and 26% (95% CI, 6 to 43; P = 0.019), respectively. The incidence of moderate to severe CRBD and the number of patients treated with tramadol for CRBD were comparable between the two groups. As a maintenance agent of general anesthesia, sevoflurane reduced the incidence of early postoperative CRBD in patients undergoing TURBT when compared with desflurane. The protocol for this clinical trial was registered at ClinicalTrials.gov (NCT02096224).
26 July 2005 in Acta Anaesthesiologica Scandinavica