Efficiency and safety: comparison between preoperative analgesia and postoperative analgesia using non-steroidal anti-inflammatory drugs in patients receiving arthroscopic knee surgery in a multicenter, randomized, controlled study.

BACKGROUND: This study aimed to compare the efficiency regarding postoperative pain control, consumption of rescue drug, patients' satisfaction and the safety of preoperative analgesia versus postoperative analgesia using non-steroidal anti-inflammatory drugs (NSAIDs) in patients who received arthroscopic knee surgery (AKS). METHODS: Four hundred and sixty-four patients who received AKS were recruited in this multicenter, randomized, controlled study. Subsequently, they were randomized into PRE group (N = 232) and POST group (N = 232). In PRE group, patients received celecoxib, meloxicam or rofecoxib from 2 h pre-operation (Pre (- 2 h)) to 48 h post-operation for analgesia. In POST group, patients received celecoxib, meloxicam or rofecoxib from 4 to 48 h post-operation for analgesia. RESULTS: h and 12 h; pain VAS at passive movement was reduced in PRE group than POST group at 6 h, 12 h and 24 h. Additionally, consumption of rescue drug (pethidine) was decreased, while overall satisfaction was increased in PRE group compared to POST group. As for adverse events, the incidences of nausea, vomiting, constipation, drowsiness and dizziness were similar between PRE group and POST group. In subgroup analysis, the pain VAS score at passive movement at 6 h and nausea and constipation incidences were distinctive among subgroups categorized by meloxicam, celecoxib and rofecoxib administration. However, no difference of other assessments was found among subgroups categorized by meloxicam, celecoxib and rofecoxib administration. CONCLUSION: Preoperative analgesia using NSAIDs is more efficient and equivalently tolerable compared to postoperative analgesia using NSAIDs in patients who receive AKS.

Treatment of bilateral idiopathic trigeminal neuralgia by radiofrequency thermocoagulation at different temperatures.

Radiofrequency thermocoagulation (RFT) is an effective treatment for trigeminal neuralgia, but consensus regarding an optimal treatment temperature is lacking. While treatment temperatures ranging from 60°C to 95°C have been reported, RFT at too high a temperature is often followed by serious complications, and comparative evaluations of RFT at different temperatures in a single study are rare.This current prospective cohort study was to compare immediate and long-term outcomes of RFT at varying temperatures in patients with bilateral idiopathic trigeminal neuralgia (ITN) of maxillary division of trigeminal nerve (V2), mandibular division of trigeminal nerve (V3), and V2+V3, including pain relief, complications, recurrence rate, and patient satisfaction. From May 2011 to April 2016, 62 consecutive patients with bilateral ITN of V2, V3, and V2+V3 were enrolled in the study. These patients underwent bilateral RFT at 68°C and 75°C, respectively, using the same RF parameters. Side-to-side results, including pain relief, complications, and patient satisfaction, were compared during a 5-year follow-up period.Overall pain relief was satisfactory after RFT. The rate of pain relief after treatment at 75°C was slightly higher than at 68°C (P > 0.05). The pain-free rate was 95.1% at 75°C and 93.5% at 68°C at 1 year, 84.3% and 78.1% at 3 years, and 80.7% and 74.4% at 5 years. There were 10 and 13 cases of recurrence, respectively, and 6 cases of bilateral recurrence. The incidence and severity of complications were greater at 75°C (P < 0.05) than at 68°C, and therefore the patient satisfaction at the higher temperature was lower (P < 0.05).Patients with bilateral ITN who underwent RFT at different temperatures had consistent pain relief after RFT at both 75°C and 68°C, but there were fewer and less severe complications at 68°C, which was accompanied by greater patient satisfaction. This suggests that RFT at lower temperatures may be preferable, and that a temperature of 68°C can be recommended.

Protection of donor lung inflation in the setting of cold ischemia against ischemia-reperfusion injury with carbon monoxide, hydrogen, or both in rats.

AIMS: Lung ischemia-reperfusion injury (IRI) may be attenuated through carbon monoxide (CO)'s anti-inflammatory effect or hydrogen (H2)'s anti-oxidant effect. In this study, the effects of lung inflation with CO, H2, or both during the cold ischemia phase on graft function were observed. MATERIALS AND METHODS: Rat donor lungs, inflated with 40% oxygen (control group), 500ppm CO (CO group), 3% H2 (H2 group) or 500ppm CO+3% H2 (COH group), were kept at 4°C for 180min. After transplantation, the recipients' artery blood gas and pressure-volume (P-V) curves were analyzed. The inflammatory response, oxidative stress and apoptosis in the recipients were assessed at 180min after reperfusion. KEY FINDINGS: Oxygenation in the CO and H2 groups were improved compared with the control group. The CO and H2 groups also exhibited significantly improved P-V curves, reduced lung injury, and decreased inflammatory response, malonaldehyde content, and cell apoptosis in the grafts. Furthermore, the COH group experienced enhanced improvements in oxygenation, P-V curves, inflammatory response, lipid peroxidation, and graft apoptosis compared to the CO and H2 groups. SIGNIFICANCE: Lung inflation with CO or H2 protected against IRI via anti-inflammatory, anti-oxidant and anti-apoptotic mechanisms in a model of lung transplantation in rats, which was enhanced by combined treatment with CO and H2.

SH2-B beta expression in alveolar macrophages in BAL fluid of asthmatic guinea pigs and its role in NGF-TrkA-mediated asthma.

BACKGROUND AND OBJECTIVE: Nerve growth factor (NGF)/tyrosine kinase receptor A (TrkA) signalling may play an important role in the pathogenesis of asthma, and SH2-B beta, a TrkA-binding protein, modulates the NGF signalling pathway. In this study, SH2-B beta expression in alveolar macrophages (AM) in guinea pig BAL fluid and its role in asthma pathogenesis through the NGF-TrkA signalling pathway were investigated. METHODS: Guinea pigs were randomized into five groups: control, a model of asthma, anti-SH2-B beta antibody treatment, anti-NGF antibody treatment and anti-TrkA antibody treatment. The asthmatic model was established in guinea pigs by inhalation of ovalbumin. Specific anti-SH2-B beta, anti-NGF and anti-TrkA antibodies were administered and AM were isolated from BAL fluid to assess SH2-B beta expression using an immunofluorescence assay. SH2-B beta and TrkA protein expression were determined by western blotting, IL-1 beta and IL-4 levels in the BAL fluid supernatants were determined by ELISA, and pathological changes in the bronchi and lung tissues were examined by HE staining. RESULTS: Lymphocyte, eosinophil and total inflammatory cell numbers in BAL fluid were significantly higher in the asthma model group than in the other groups (P < 0.01). NGF expression in the asthma model group was significantly higher than that in the PBS control group (P < 0.01). SH2-B beta was expressed in AM of control animals and expression was significantly higher in the asthma model than in the other groups (P < 0.01). TrkA protein expression was significantly higher in the asthma model group than in the PBS group (P < 0.01), and treatment with anti-NGF antibody resulted in significant reduction of TrkA expression (P < 0.01). CONCLUSIONS: SH2-B beta is expressed in AM of normal guinea pigs, and SH2-B beta may participate in asthma pathogenesis through the NGF-TrkA signalling pathway.