BackgroundPain on propofol injection is a well-known adverse effect. We evaluated the clinical factors that affect the pain on injection of propofol to develop a strategy to prevent or reduce pain.MethodsWe conducted a prospective, observational study of 207 adult patients (ASA I-II), and the patients were classified according to gender, age, the body mass index (BMI), the IV site and the side of the IV site. During the 10 seconds after propofol injection, pain intensity was measured on an 11-point numerical rating scale (0 = no pain and 10 = worst possible pain). Pain in excess of 3 on the numerical scale was regarded as moderate to severe pain.ResultsThe subgroups of gender (female: 55.6% vs. male: 25.0%; P < 0.01) and the IV site (dorsum of hand: 61.2% vs. wrist: 40.0% vs. antecubital fossa: 22.5%; P < 0.01) had significantly different frequencies for the incidence of pain on injection on the univariate and multivariate analyses. For the subgroup of females, the incidence of pain was statistically different according to the age group (20-40 yr: 71.0% vs. 41-60: 54.8% vs. 61-80: 38.5%; P = 0.014).ConclusionsOur results showed that the younger age patients, the patients with a peripheral IV site and female patients are more sensitive to pain on the injection of propofol.
Abstract. This study investigated the inhibitory effects and underlying mechanisms of Fructus sophorae, the dried ripe fruit of Styphnolobium japonicum (L.) Schott, on the production of proinflammatory molecules in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. The results indicated that pretreatment with noncytotoxic concentrations of Fructus sophorae extract (FSE) significantly inhibited the release of the proinflammatory mediators nitric oxide (NO) and prostaglandin E 2 , which were associated with the downregulation of both mRNA and protein for inducible NO synthase and cyclooxygenase-2, respectively, in LPS-challenged RAW 264.7 cells. FSE also blocked the LPS-induced expression of the proinflammatory cytokines interleukin (IL)-6 and IL-1β. Furthermore, the results showed that FSE efficiently attenuated the LPS-induced nuclear translocation of nuclear factor-kappa B (NF-κB) and phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) but not p38 MAPK. These results suggest that FSE exhibits anti-inflammatory activity by inhibiting proinflammatory mediators and cytokines through the inactivation of NF-κB, ERK and JNK, and it may offer therapeutic potential for treating inflammatory diseases accompanied with macrophage activation.
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