BackgroundPostoperative nausea and vomiting is a common side effect of general anesthesia. In this study, we performed a meta-analysis on the efficacy and safety of ramosetron versus ondansetron in the prevention of postoperative nausea and vomiting using the most recently published randomized controlled clinical studies.MethodsPubMed and EMBASE were searched for randomized controlled clinical trials comparing the efficacy and safety of ramosetron and ondansetron. The meta-analysis was performed using Review Manager version 5.3 (Cochrane Collaboration, Oxford, UK). Dichotomous outcomes are presented as the relative risk (RR) with a 95% confidence interval (CI).ResultsA total of 898 patients from nine selected studies were treated with antiemetics after surgery, including 450 patients who received ondansetron 4 mg and 448 patients who received ramosetron 0.3 mg. The meta-analysis showed no statistically significant difference between the two groups with regard to prevention of postoperative nausea (PON) during different time periods in the 48 hours after surgery. When comparing the efficacy of ramosetron and ondansetron in the prevention of postoperative vomiting (POV), at various time intervals in the 24 hours after surgery, ramosetron was significantly more efficient than ondansetron: 0–6 hours (RR 0.46, 95% CI 0.24–0.92; P=0.03), 0–24 hours (RR 0.72, 95% CI 0.52–1.00; P=0.05), and 6–24 hours (RR 0.51, 95% CI 0.31–0.84; P=0.008). At other time periods between 24 and 48 hours after surgery, ramosetron did not show better efficacy than ondansetron. When comparing the safety profiles of ramosetron and ondansetron, fewer side effects were recorded in the ramosetron group (RR 0.65, 95% CI 0.47–0.91; P=0.01).ConclusionOur meta-analysis demonstrates that ramosetron was more effective than ondansetron in the prevention of early POV (0–24 hours) with fewer recorded side effects. However, our study did not reveal any statistically significant differences in efficacy between ramosetron and ondansetron in the prevention of PON or late POV (at 24–48 hours).
<b><i>Introduction:</i></b> Isoflurane inhalation leads to apoptotic neurodegeneration and further results in learning and cognitive dysfunction. Notoginsenoside R1 (NGR1), a major ingredient from Radix notoginseng, has been reported to exert neuroprotective effect during brain or neuron injury. This study aimed to investigate the effect of NGR1 on neurological impairment. <b><i>Methods:</i></b> Sixty-four male Sprague Dawley rat pups (15–20 g) of postnatal day 7 were recruited. Spatial learning and memory were assessed by the Morris water maze test, and the neurological severity score was determined. Real-time quantitative PCR was used to detect the expression levels of microRNA (miR)-29a. Enzyme-linked immunosorbent assay was applied to estimate the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in the hippocampal tissues. <b><i>Results:</i></b> NGR1 attenuated neurological impairment induced by isoflurane, shown by the decrease in neurological function score and escape latency and the increase in staying time in the original quadrant in rats. NGR1 reversed the downregulation of miR-29a expression induced by isoflurane treatment. After the treatment of NGR1, the elevated levels of IL-6, TNF-α, and IL-1β induced by isoflurane were all decreased significantly in the hippocampal tissues of rats. Additionally, the repressive action of NGR1 in neurological impairment and neuroinflammation was eliminated by downregulating miR-29a in rats. <b><i>Conclusion:</i></b> NGR1 protects against isoflurane-induced neurological impairment. The protective effect of NGR1 might be achieved by promoting the expression of miR-29a and preventing inflammatory response.
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