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A Sondén

Publications and source records attributed to A Sondén.

2 recordsLinked to original sources

Laser-induced shock wave endothelial cell injury.

BACKGROUND AND OBJECTIVE: Several laser procedures, extracorporeal lithotripsies (ESWL), and high-velocity missile trauma generate pressure transients that are transmitted through the tissues. Despite several publications demonstrating shock wave-induced tissue injury, little is known about its pathophysiology. This study introduces an in vitro model for studying shock wave effects on endothelial cell (EC) monolayers. STUDY DESIGN/MATERIALS AND METHODS: A Nd:YAG laser-driven flyer-plate technique was used to generate shock waves. Physical characteristics were determined with a pressure transducer, a high-speed video camera, and sequential photography. Biological effects were studied with phase contrast and lightfield microscopy, computerized morphometry, immunocytochemistry, spectrophotometry, and enzyme-linked immunosorbent assay (ELISA). RESULTS: The shock waves generated were highly reproducible. Cavitation was verified and quantified, and its extent could be varied in the vials. Exposed cultures exhibited areas with cell membrane damage and cell detachment. Release of LD was elevated (P < 0.01) in exposed vials. The EC lesions were larger (>P < 0.01) in cultures submitted to high vs. low extent of cavitation. CONCLUSION: The flyer-plate model can be used to subject cell monolayers to defined and reproducible shock waves causing immediate cell injury similar to the previously reported vascular lesions associated with ESWL, pulsed lasers, and blast trauma. With the flyer-plate model, such lesions may be further studied on the cellular and subcellular levels.

Aluminum Silicates↗

Hydrogen peroxide induces endothelial cell atypia and cytoskeleton depolymerization.

Reactive oxygen intermediates induce cell injury in a variety of pathophysiological conditions. Human umbilical cord vein endothelial cell (HUVEC) cultures were exposed to 1 or 200 microM H2O2 for 15 min, and observed after 15 min, or 1, 4, 24, or 120 h. Factor VIII and the cytoskeletal proteins vimentin and tubulin were visualized immunocytochemically. Release of lactate dehydrogenase (indices of cell membrane injury) did not increase after H2O2 exposure; nor was cellular expression of factor VIII affected. 200 microM H2O2 induced cell contraction after 15 min which disappeared after 1 and 4 h, but was evident again after 24 h. Immediately after exposure, the filamentous structure of vimentin and tubulin disappeared, but normalized after 1 h. After 120 h, the cytoskeleton filaments were coarsened and disorganized, and an abundance of multinucleated giant cells were observed. Catalase (150 U/ml) abolished all effects of H2O2. One microM H2O2 did not induce any changes in HUVEC. Thus, the present concentrations of H2O2 did not induce cell necrosis or altered expression of factor VIII. Early, reversible cell contraction and depolymerization of cytoskeletal proteins were observed, followed by a delayed contraction and cell atypia after 200 microM H2O2.

Antibodies, Monoclonal↗