Flurbiprofen axetil increases arterial oxygen partial pressure by decreasing intrapulmonary shunt in patients undergoing one-lung ventilation.

PURPOSES: In the present study, we investigated whether flurbiprofen axetil (FA) alleviates hypoxemia during one-lung ventilation (OLV) by reducing the pulmonary shunt/total perfusion (Q s/Q t) ratio, and examined the relationship between the Q s/Q t ratio and the thromboxane B2 (TXB2)/6-keto-prostaglandin F1α (6-K-PGF1α) ratio. METHODS: Sixty patients undergoing esophageal resection for carcinoma were randomly assigned to groups F and C (n = 30 for each group). FA and placebo were administered i.v. 15 min before skin incision in groups F and C, respectively. The partial pressure of arterial oxygen (PaO2) was measured and the Q s/Q t ratio was calculated. Serum TXB2, 6-K-PGF1α, and endothelin (ET) were measured by radioimmunoassay. The relationship between TXB2/6-K-PGF1α and Q s/Q t was investigated. RESULTS: Compared with group C, PaO2 was higher and the Q s/Q t ratio was lower during OLV in group F (P < 0.05). After treatment with FA, both serum TXB2 and 6-K-PGF1α decreased significantly (P < 0.05) but the TXB2/6-K-PGF1α ratio increased significantly (P < 0.01). Increases in the TXB2/6-K-PGF1α ratio were correlated with reductions in the Q s/Q t ratio during OLV in group F (r = -0.766, P < 0.01). There was no significant difference in serum ET between groups F and C. CONCLUSIONS: Treatment with FA reduced the Q s/Q t ratio and further increased the PaO2 level during OLV, possibly due to upregulation of the vasoactive agent TXB2/6-K-PGF1α ratio.

Flurbiprofen axetil enhances analgesic effect of fentanyl associated with increase in ß-endorphin levels.

PURPOSE: To examine the analgesic effect of preoperative administration of flurbiprofen axetil and that of postoperative administration of a combination of flurbiprofen axetil and fentanyl, as well as perioperative plasma ß-endorphin (ß-EP) levels in patients undergoing esophagectomy. METHODS: Forty-five patients were randomly divided into three groups: group A: 100 mg flurbiprofen axetil preoperative, 10 µg/kg fentanyl + 10 ml placebo postoperative; group B: 100 mg flurbiprofen axetil preoperative, 10 µg/kg fentanyl + 100 mg flurbiprofen axetil postoperative; group C: 10 ml placebo preoperative, 10 µg/kg fentanyl + 10 ml placebo postoperative. Postoperative analgesia was achieved by intravenous infusion containing flurbiprofen axetil and/or fentanyl at 2.0 ml/h (total volume, 100 ml) using infusion pumps. The ß-EP was measured at preanesthesia (T(1)), the end of surgery (T(2)), 24 h (T(3)), and 48 h (T(4)) after surgery. Visual analog scale scores (VAS) at T3, T4 (at rest), and rescue analgesic tramadol requirement was recorded. RESULTS: The VAS of group B was significantly lower than group A and C (P < 0.01) at T(3) and T(4). The ß-EP levels at T(2)-T(4) in group A did not differ significantly from those at T(1) (P > 0.05); however, the ß-EP levels in group B at T(3)-T(4) increased significantly (P < 0.05), while those in group C increased at T(2) and decreased at T(4) (P < 0.05). The ß-EP levels in group B at T(3) and T(4) were the highest as compared to its levels in groups A and C (P < 0.01). Tramadol consumption in group B was significantly lower than in groups A and C (P < 0.01). CONCLUSION: These results show that flurbiprofen axetil enhances the analgesic effect of fentanyl associated with increase in ß-EP levels.

Penehyclidine prevents nuclear factor-kappaB activation in acute lung injury induced by lipopolysaccharide.

Penehyclidine (PHCD) has been proposed to reduce lung and lethal toxicity. The present study was undertaken to investigate the mechanisms responsible for the protective effect of PHCD against acute lung injury (ALI) in rats. Tail-vein injection of lipopolysaccharide (LPS; 5 mg kg(-1)) was used to induce ALI in rats. Secondary increases in total protein, lactate dehydrogenase activity in bronchoalveolar lavage fluid and myeloperoxidase in lung tissue were used to evaluate the effects of PHCD on ALI in rats. Activated DNA binding activity and expression of nuclear factor kappaB (NF-kappaB) in lung tissue were measured using electrophoretic mobility shift assays assay and immunohistological staining. Levels and mRNA expression of tumour necrosis factor alpha (TNF-alpha) and interleukin 1beta (IL-1beta) were measured by enzyme-linked immunosorbent assay and reverse transcriptase-polymerase chain reaction. Pretreatment with PHCD (0.03 mg kg(-1), 0.1 mg kg(-1) and 0.3 mg kg(-1) i.p.) significantly attenuated the LPS-induced changes in lung injury parameters and inhibited the activation and expression of NF-kappaB in lung tissue. Furthermore, PHCD also substantially reduced the LPS-induced TNF-alpha and IL-1beta mRNA expression and production in lung tissue and suppressed neutrophil recruitment. The results suggest that PHCD attenuates LPS-induced acute lung responses through inhibition of NF-kappaB activation and LPS-induced TNF-alpha and IL-1beta production and resulting neutrophil recruitment associated with acute lung inflammation and injury. PHCD may be a useful adjuvant to treatment strategies targeting clinical situations of acute inflammation.