Background: The aim of this study was to investigate effect of single- and multiple-dose of parecoxib on shoulder pain after gynecologic laparoscopy.Methods: 126 patients requiring elective gynecologic laparoscopy were randomly allocated to three groups. Group M (multiple-dose): receiving parecoxib 40mg at 30min before the end of surgery, at 8 and 20hr after surgery, respectively; Group S (single-dose): receiving parecoxib 40mg at 30min before the end of surgery and normal saline at the corresponding time points; Group C (control): receiving normal saline at the same three time points. The shoulder pain was evaluated, both at rest and with motion, at postoperative 6, 24 and 48hr. The impact of shoulder pain on patients' recovery (activity, mood, walking and sleep) was also evaluated. Meanwhile, rescue analgesics and complications were recorded.Results: The overall incidence of shoulder pain in group M (37.5%) was lower than that in group C (61.9%) (difference=-24.4%; 95% CI: 3.4~45.4%; P=0.023). Whereas, single-dose regimen (61.0%) showed no significant reduction (difference with control=-0.9%; 95% CI: -21.9~20.0%; P=0.931). Moreover, multiple-dose regimen reduced the maximal intensity of shoulder pain and the impact for activity and mood in comparison to the control. Multiple-dose of parecoxib decreased the consumption of rescue analgesics. The complications were similar among all groups and no severe complications were observed.Conclusions: Multiple-, but not single-, dose of parecoxib may attenuate the incidence and intensity of shoulder pain and thereby improve patients' quality of recovery following gynecologic laparoscopy.
BACKGROUND: Intestinal ischemia/reperfusion (I/R) challenge often results in gut barrier dysfunction and induces distant organ injury. Dexmedetomidine has been shown to protect intestinal epithelial barrier against I/R attack. The present study aims to investigate the degree to which intestinal I/R attack will contribute to gut-vascular barrier (GVB) damage, and to examine the ability of dexmedetomidine to minimize GVB and liver injuries in mice. METHODS: In vivo, intestinal ischemic challenge was induced in mice by clamping the superior mesenteric artery for 45 minutes. After clamping, the mice were subjected to reperfusion for either 2, 4, 6, or 12 hours. Intraperitoneal injection of dexmedetomidine 15, 20, or 25 μg•kg -1 was performed intermittently at the phase of reperfusion. For the in vitro experiments, the challenge of oxygen-glucose deprivation/reoxygenation (OGD/R) was established in cultured vascular endothelial cells, and dexmedetomidine (1 nM) was used to treat the cells for 24 hours. Moreover, in vivo and in vitro, SKL2001 (a specific agonist of β-catenin) or XAV939 (a specific inhibitor of β-catenin) was applied to determine the role of β-catenin in the impacts provided by dexmedetomidine. RESULTS: The attack of intestinal I/R induced GVB damage. The greatest level of damage was observed at 4 hours after intestinal reperfusion. There was a significant increase in plasmalemma vesicle-associated protein-1 (PV1, a specific biomarker for endothelial permeability) expression (5.477 ± 0.718 vs 1.000 ± 0.149; P < .001), and increased translocation of intestinal macromolecules and bacteria to blood and liver tissues was detected (all P < .001). Liver damages were observed. There were significant increases in histopathological scores, serum parameters, and inflammatory factors (all P < .001). Dexmedetomidine 20 μg•kg -1 reduced PV1 expression (0.466 ± 0.072 vs 1.000 ± 0.098; P < .001) and subsequent liver damages (all P < .01). In vitro, dexmedetomidine significantly improved vascular endothelial cell survival (79.387 ± 6.447% vs 50.535 ± 1.766%; P < .001) and increased the productions of tight junction protein and adherent junction protein (all P < .01) following OGD/R. Importantly, in cultured cells and in mice, β-catenin expression significantly decreased (both P < .001) following challenge. Dexmedetomidine or SKL2001 upregulated β-catenin expression and produced protective effects (all P < .01). However, XAV939 completely eliminated the protective effects of dexmedetomidine on GVB (all P < .001).
Intestinal ischaemia/reperfusion (I/R) severely disrupts gut barriers and leads to high mortality in the critical care setting. Transforming growth factor (TGF)‐β1 plays a pivotal role in intestinal cellular and immune regulation. However, the effects of TGF‐β1 on intestinal I/R injury remain unclear. Thus, we aimed to investigate the effects of TGF‐β1 on gut barriers after intestinal I/R and the molecular mechanisms. Intestinal I/R model was produced in mice by clamping the superior mesenteric artery for 1 hr followed by reperfusion. Recombinant TGF‐β1 was intravenously infused at 15 min. before ischaemia. The results showed that within 2 hrs after reperfusion, intestinal I/R disturbed intestinal immunoglobulin A class switch recombination (IgA CSR), the key process of mucosal IgA synthesis, and resulted in IgA dysfunction, as evidenced by decreased production and bacteria‐binding capacity of IgA. Meanwhile, the disruptions of intestinal microflora and mucosal structure were exhibited. Transforming growth factor‐β1 activated IgA CSR as evidenced by the increased activation molecules and IgA precursors. Strikingly, TGF‐β1 improved intestinal mucosal IgA dysfunction, dysbiosis and epithelial damage at the early stage after reperfusion. In addition, SB‐431542, a specific inhibitor of activating mothers against decapentaplegic homologue (SMAD) 2/3, totally blocked the inductive effect of TGF‐β1 on IgA CSR and almost abrogated the above protective effects on intestinal barriers. Taken together, our study demonstrates that TGF‐β1 protects intestinal mucosal IgA immunity, microbiota and epithelial integrity against I/R injury mainly through TGF‐β receptor 1/SMAD 2/3 pathway. Induction of IgA CSR may be involved in the protection conferred by TGF‐β1.
ObjectivesPostlaparoscopic shoulder pain (PLSP) remains a common problem after laparoscopies. The aim of this study was to investigate the correlation between pressure pain threshold (PPT) of different muscles and PLSP after gynecologic laparoscopy, and to explore the effect of parecoxib, a cyclooxygenase-2 inhibitor, on the changes of PPT.Materials and methodsThe patients were randomly allocated into two groups; group P and group C. In group P, parecoxib 40 mg was intravenously infused at 30 minutes before surgery and 8 and 20 hours after surgery. In group C, normal saline was infused at the corresponding time point. PPT assessment was performed 1 day before surgery and at postoperative 24 hours by using a pressure algometer at bilateral shoulder muscles (levator scapulae and supraspinatus) and forearm (flexor carpi ulnaris). Meanwhile, bilateral shoulder pain was evaluated through visual analog scale score at 24 hours after surgery.ResultsPreoperative PPT level of the shoulder, but not of the forearm, was significantly and negatively correlated with the intensity of ipsilateral PLSP. In group C, PPT levels of shoulder muscles, but not of forearm muscles, decreased after laparoscopy at postoperative 24 hours. The use of parecoxib significantly improved the decline of PPT levels of bilateral shoulder muscles (all P<0.01). Meanwhile, parecoxib reduced the incidence of PLSP (group P: 45% vs group C: 83.3%; odds ratio: 0.164; 95% confidence interval: 0.07–0.382; P<0.001) and the intensity of bilateral shoulder pain (both P<0.01).ConclusionPreoperative PPT levels of shoulder muscles are closely associated with the severity of shoulder pain after gynecologic laparoscopy. PPT levels of shoulder muscles, but not of forearm muscles, significantly decreased after surgery. Parecoxib improved the decrease of PPT and relieved PLSP.
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