ABSTRACT
BACKGROUND: Pain 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. METHODS: We 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. RESULTS: THE 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). CONCLUSIONS: Our 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
Apigenin, one of the most common flavonoids, has been shown to possess anti-inflammatory, anticarcinogenic, and free radical-scavenging properties. However, the influence of apigenin on the immunostimulatory effects and maturation of dendritic cells (DC) remains, for the most part, unknown. In this study, we have attempted to ascertain whether apigenin influences the expression of surface molecules, dextran uptake, cytokine production, and T-cell differentiation as well as the signaling pathways underlying these phenomena in murine bone marrow-derived DC. In the presence of apigenin, CD80, CD86, and major histocompatibility complex class I and II molecules, expressions on DC were significantly suppressed, and lipopolysaccharide (LPS)-induced interleukin (IL)-12 expression was impaired. The DC proved highly efficient at antigen capture, as evidenced by the observation of mannose receptor-mediated endocytosis in the presence of apigenin. The LPS-induced activation of mitogen-activated protein kinase, the nuclear translocation of its nuclear factor-kappaB p65 subunit, and the induction of the T-helper 1 response were all impaired in the presence of apigenin, whereas the cell-mediated immune response remained normal. These findings provide new insight into the immunopharmacological functions of apigenin and its effects on DC, and they may also prove useful in the development of adjuvant therapies for individuals suffering from acute or chronic DC-associated diseases.