Assessment of the effect of perineural dexmedetomidine on oxidative stress during peritoneal dialysis catheter insertion: a randomized, controlled trial.

PURPOSE: This study aimed to evaluate the effect of the addition of dexmedetomidine to ropivacaine on oxidative stress during transversus abdominis plane (TAP) and rectus sheath (RS) blockades for patients with end-stage renal disease (ESRD) undergoing peritoneal dialysis (PD) catheter insertion. METHODS: Sixty patients with ESRD undergoing PD catheter insertion to receive left ultrasound-guided TAP and RS blockades were randomly divided into two groups: the dexmedetomidine plus ropivacaine group (25 mL of 0.3% ropivacaine + 1 µg/kg dexmedetomidine) and the ropivacaine group (25 mL of 0.3% ropivacaine). Primary outcomes were oxidative stress marker levels during the procedure. RESULTS: A total of 60 patients (30 patients in each group) were evaluated. Compared with the ropivacaine group, the dexmedetomidine plus ropivacaine group had significantly lower serum malondialdehyde levels (P < 0.05) and increased glutathione peroxidase (P < 0.01) and superoxide dismutase levels at 24 h after the procedure (P < 0.01). CONCLUSION: The addition of 1 µg/kg of dexmedetomidine to ropivacaine for ultrasound-guided TAP and RS blockades could inhibit oxidative stress in patients with ESRD undergoing PD catheter insertion. Trial registration This study was registered at www.chictr.org.cn on June 7, 2021 (ChiCTR2100047050).

Effect of dexmedetomidine administration on analgesic, respiration and inflammatory responses in patients undergoing percutaneous endoscopic lumbar discectomy: a prospective observational study.

BACKGROUND: Local anesthesia has been recommended for percutaneous endoscopic lumbar discectomy (PELD) in recent years; however, the efficacy, including oxidative stress, inflammatory reactions and ventilation effects, when intravenous dexmedetomidine (DEX) is administered during PELD has not been described. METHODS: Sixty adult patients undergoing PELD were randomly allocated to either an intravenous DEX sedation group (Group A) or a normal saline group (Group B). Respiratory data, including minute ventilation (MV), tidal volume (TV), and respiratory rate (RR), were recorded using a respiratory volume monitor (RVM), and peripheral oxygen saturation (SpO2) was monitored by pulse oximetry. The visual analog score (VAS) was used to assess the level of pain. The serum levels of inflammatory biomarkers including interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were to assess inflammatory reactions. The serum levels of oxidative stress biomarkers including malondialdehyde (MDA) and glutathione peroxidase (GSH-PX) were also recorded to evaluate oxidative stress. RESULTS: There were no significant differences in RR, MV, TV and SpO2 between the two groups at any time point (P > 0.05). Group B exhibited lower serum levels of GSH-PX (P < 0.0001) and higher serum levels of MDA (p < 0.0001) than Group A at the end of surgery. Twenty-four hours after surgery, Group B exhibited higher serum levels of IL-6 (P = 0.0033), TNF-α (P = 0.0002), and MDA (P < 0.0001) and lower serum levels of GSH-PX (P < 0.0001) than Group A. In addition, Group A exhibited lower VAS (P < 0.0001) than Group B during surgery. CONCLUSIONS: DEX administration using RVM not only provides analgesia without ventilatory depression but also alleviates oxidative stress and inflammatory reactions in patients undergoing PELD.

Neuroprotective effects of four different fluids on cerebral ischaemia/reperfusion injury in rats through stabilization of the blood-brain barrier.

Protecting the blood-brain barrier (BBB) is a potential strategy to treat cerebral ischaemic injury. We previously reported that hypertonic sodium chloride hydroxyethyl starch 40 (HSH) treatment alleviates brain injury induced by transient middle cerebral artery occlusion (tMCAO). However, other fluids, including 20% mannitol (MN), 3% hypertonic sodium chloride (HTS) and hydroxyethyl starch 130/0.4 solution (HES), have the same effect as HSH in cerebral ischaemia/reperfusion injury (CI/RI) remains unclear. The present study evaluated the protective effects of these four fluids on the BBB in tMCAO rats. Sprague-Dawley (SD) rats were randomly assigned to six groups. A CI/RI rat model was established by tMCAO for 120 min followed by 24 h of reperfusion. The sham and tMCAO groups were treated with normal saline (NS), whereas the other four groups were treated with the four fluids. After 24 h of reperfusion, neurological function, brain oedema, brain infarction volume, permeability of the BBB, cortical neuron loss and protein and mRNA expression were assessed. The four fluids (especially HSH) alleviated neurological deficits and decreased the infarction volume, brain oedema, BBB permeability and cortical neuron loss induced by tMCAO. The expression levels of GFAP, IL-1ß, TNF-α, MMP-9, MMP-3, AQP4, MMP-9, PDGFR-ß and RGS5 were decreased, whereas the expression levels of laminin and claudin-5 were increased. These data suggested that small-volume reperfusion using HSH, HES, MN and HTS ameliorated CI/RI, probably by attenuating BBB disruption and postischaemic inflammation, with HSH exerting the strongest neuroprotective effect.

Celastrol ameliorates inflammatory pain and modulates HMGB1/NF-κB signaling pathway in dorsal root ganglion.

Evidences reported that high mobility group box 1 (HMGB1) played a pivotal role in the modulation of chronic inflammatory pain. Celastrol, a bioactive component extracted from Tripterygium wilfordii Hook, possesses anti-inflammatory activity, but the underlying mechanism remains to be fully clarified. We aim to investigate whether HMGB1 in dorsal root ganglion (DRG) participates in the effect of celastrol on inflammatory pain. Complete Freund's adjuvant (CFA)-induced inflammatory pain rat model was used. Paw withdrawal latency (PWL) was detected to evaluate the effects of celastrol on CFA-evoked inflammatory pain. After application of celastrol (1mg/kg, i.p.) on day 1, 3, 7 and 14 post-CFA injection, the expression levels of HMGB1, NF-κB, some proinflammatory markers, GFAP and CD11b in DRG were determined by qRT-PCR and western blot analysis. These results showed that celastrol significantly suppressed HMGB1, NF-κB and IL-1ß mRNA and protein expression in DRG and alleviated CFA-evoked thermal hyperalgesia. Furthermore, celastrol obviously inhibited COX-2 protein expression and down-regulated IL-6, IL-17, TNF-α, MCP-1, GFAP and CD11b mRNA levels in DRG of CFA rats. Collectively, the present study firstly provide evidences of the anti-inflammatory effect of celastrol via suppressing CFA-induced the activation of HMGB1/NF-κB signaling pathway in DRG, which maybe a potential therapeutic target for celastrol alleviating inflammatory pain.