Analgesic Effect of Intrathecal Morphine Combined with Low-Dose Bupivacaine on Postoperative Analgesia after Liver Resection: A Randomized Controlled Study.

Although intrathecal morphine and bupivacaine are increasingly implemented in effective postoperative pain control, there is a lack of consensus on the dosage as high doses of bupivacaine may inadvertently cause unwanted side effects. The purpose of this study was to compare the effects of intrathecal morphine injection and low-dose bupivacaine with morphine injection. In total, 90 patients were divided into 3 groups: (1) sham injection for the control group; (2) morphine 400 mcg for the morphine group (M); and (3) morphine 400 mcg and bupivacaine 5 mg for the morphine and bupivacaine group (M + B). Our primary outcome was time to first rescue analgesic. The VAS (visual analogue scale) pain score was compared until POD (postoperative day)1. Total fentanyl dose was compared until POD2. Side effects were monitored until POD3. Although time to first rescue was significantly shorter in the control group compared to group M and group M + B (p < 0.001), both groups (M and M + B) were comparable to each other. There was a significant decrease in the VAS score and total fentanyl administration in group M and group M + B compared to the control group. Pruritus and tingling were more prevalent in the M + B group (p = 0.023; p = 0.010). The addition of 5 mg bupivacaine may be insufficient in providing further analgesic benefits; however, higher doses may aggravate side effects.

Beneficial effect of intravenous magnesium during endoscopic submucosal dissection for gastric neoplasm.

BACKGROUND: Endoscopic submucosal dissection (ESD) has been revealed as an effective treatment of early gastric neoplasm and should be performed under sedation with adequate pain control. Magnesium sulfate has analgesic, sedative, and sympatholytic properties. This study examined the effects of intravenous magnesium 50 mg/kg administered before ESD for gastric neoplasm on analgesic and sedative consumptions during ESD and pain after ESD. METHODS: In this randomized, double-blind, and prospective study, patients undergoing ESD randomly received either intravenous magnesium sulfate 50 mg/kg (magnesium group n = 30) or the same volume of normal saline (control group n = 30) over 10 min before the start of sedation. Fentanyl consumption during ESD was the primary end point. Hemodynamics was recorded during the procedure, and abdominal pain was evaluated at 30 min, 6 h, and 24 h after ESD. RESULTS: During ESD, fentanyl consumption was 24% less in the magnesium group than in the control group (96 ± 27 vs. 126 ± 41 µg, mean ± SD; p = 0.002), although there was no significant difference in propofol consumption (p = 0.317). In addition, magnesium attenuated the elevation of mean blood pressure at the time of epinephrine submucosal injection (p = 0.038) and 5 min after submucosal dissection (p = 0.004). Less patients of the magnesium group compared to the control group requested for additional analgesics in the recovery room (14 vs. 38 %, p = 0.043), and the intensity of abdominal pain was lower at 30 min after ESD in the magnesium group (p = 0.034). CONCLUSIONS: A single-dose intravenous administration of magnesium 50 mg/kg before sedation reduced analgesic requirements both during and after ESD for gastric neoplasm without adverse effects. In addition, magnesium contributed to stable hemodynamics throughout the procedure.

Extracellular vesicles derived from gut microbiota, especially Akkermansia muciniphila, protect the progression of dextran sulfate sodium-induced colitis.

Gut microbiota play an important part in the pathogenesis of mucosal inflammation, such as inflammatory bowel disease (IBD). However, owing to the complexity of the gut microbiota, our understanding of the roles of commensal and pathogenic bacteria in the maintenance of immune homeostasis in the gut is evolving only slowly. Here, we evaluated the role of gut microbiota and their secreting extracellular vesicles (EV) in the development of mucosal inflammation in the gut. Experimental IBD model was established by oral application of dextran sulfate sodium (DSS) to C57BL/6 mice. The composition of gut microbiota and bacteria-derived EV in stools was evaluated by metagenome sequencing using bacterial common primer of 16S rDNA. Metagenomics in the IBD mouse model showed that the change in stool EV composition was more drastic, compared to the change of bacterial composition. Oral DSS application decreased the composition of EV from Akkermansia muciniphila and Bacteroides acidifaciens in stools, whereas increased EV from TM7 phylum, especially from species DQ777900_s and AJ400239_s. In vitro pretreatment of A. muciniphila-derived EV ameliorated the production of a pro-inflammatory cytokine IL-6 from colon epithelial cells induced by Escherichia coli EV. Additionally, oral application of A. muciniphila EV also protected DSS-induced IBD phenotypes, such as body weight loss, colon length, and inflammatory cell infiltration of colon wall. Our data provides insight into the role of gut microbiota-derived EV in regulation of intestinal immunity and homeostasis, and A. muciniphila-derived EV have protective effects in the development of DSS-induced colitis.