Foam bubble size is significantly influenced by sclerosant concentration for polidocanol but not sodium tetradecyl sulphate.

OBJECTIVES: To determine the effect of liquid gas fraction (LGF), sclerosant type and concentration, and filter use on foam bubble size and count. METHODS: Sclerosant foam microstructure was investigated using light microscopy for a range of LGFs (1 + 2, 1 + 4 and 1 + 8), for both sodium tetradecyl sulphate (STS) and polidocanol (POL), at a range of concentrations (0.5-3%), with and without the addition of micro-filters. Foam was generated using a modified Tessari method and placed into wells for analysis by light microscopy. Foam microscopic morphology was photographically documented, and bubble diameters and counts were quantified. RESULTS: Spherical bubbles were observed at lower LGF and a trend towards polyhedral morphology was observed at the higher LGF of (1 + 8). The higher gas content in LGF led to larger but fewer bubbles. POL bubble diameters appeared to be more influenced by concentration than STS with smaller bubbles observed at higher concentrations of POL. The mean bubble diameters were slightly larger for STS than POL at the highest concentration of 3% but smaller at lower concentrations of 1% and 1.5%. CONCLUSIONS: LGF is the primary determinant of bubble diameter and count. In contrast to STS, POL concentration influences the foam bubble size with smaller bubbles generated at higher concentrations of POL and larger bubbles appearing at low concentrations of this agent.

Heme oxygenase-1 deficiency alters erythroblastic island formation, steady-state erythropoiesis and red blood cell lifespan in mice.

Heme oxygenase-1 is critical for iron recycling during red blood cell turnover, whereas its impact on steady-state erythropoiesis and red blood cell lifespan is not known. We show here that in 8- to 14-week old mice, heme oxygenase-1 deficiency adversely affects steady-state erythropoiesis in the bone marrow. This is manifested by a decrease in Ter-119(+)-erythroid cells, abnormal adhesion molecule expression on macrophages and erythroid cells, and a greatly diminished ability to form erythroblastic islands. Compared with wild-type animals, red blood cell size and hemoglobin content are decreased, while the number of circulating red blood cells is increased in heme oxygenase-1 deficient mice, overall leading to microcytic anemia. Heme oxygenase-1 deficiency increases oxidative stress in circulating red blood cells and greatly decreases the frequency of macrophages expressing the phosphatidylserine receptor Tim4 in bone marrow, spleen and liver. Heme oxygenase-1 deficiency increases spleen weight and Ter119(+)-erythroid cells in the spleen, although α4ß1-integrin expression by these cells and splenic macrophages positive for vascular cell adhesion molecule 1 are both decreased. Red blood cell lifespan is prolonged in heme oxygenase-1 deficient mice compared with wild-type mice. Our findings suggest that while macrophages and relevant receptors required for red blood cell formation and removal are substantially depleted in heme oxygenase-1 deficient mice, the extent of anemia in these mice may be ameliorated by the prolonged lifespan of their oxidatively stressed erythrocytes.