24:I[63208,["8920","static/chunks/8920-efbff8517d590b7e.js","9097","static/chunks/9097-7e60ff382fede0de.js","5914","static/chunks/5914-356082358a498a0b.js","9903","static/chunks/9903-11222066602aad8e.js","5438","static/chunks/5438-cfc6cd3ec63ed58c.js","3851","static/chunks/3851-d9d99b9df58ccefb.js","4621","static/chunks/4621-60797c2425663d2a.js","6871","static/chunks/6871-85cb03c97585f46a.js","6736","static/chunks/6736-932312a004c99faf.js","4550","static/chunks/4550-0bf059e3050c08b3.js","688","static/chunks/688-a6a2ac7bff269cd3.js","3984","static/chunks/3984-063c0b62f32133c7.js","7038","static/chunks/7038-4f87670d4e55ef18.js","9039","static/chunks/9039-75366c62dc7d0d0e.js","4563","static/chunks/4563-ad980d1babbf7b0b.js","6761","static/chunks/6761-0c10d1446de7ae1c.js","744","static/chunks/744-1e76229abb9e297b.js","7342","static/chunks/7342-1586df78600bf911.js","3617","static/chunks/3617-1f62a097637f4747.js","5895","static/chunks/5895-caa6c774914eb108.js","7481","static/chunks/7481-3b84c503a2ebfb3f.js","3668","static/chunks/3668-7dab69e4121c33af.js","39","static/chunks/39-e93a27d0920e6d92.js","2881","static/chunks/2881-445cc2384af2c6f9.js","2364","static/chunks/2364-e83d52fb21729d99.js","3208","static/chunks/3208-e65462d166bd3688.js","7582","static/chunks/app/toc/%5Btla%5D/%5Bvolume%5D/%5Bissue%5D/page-694a0e465c2c1334.js"],"default"] 25:T46a,

The effect of laminar flow on the regulation of von Willebrand Factor (vWF) of cultured human umbilical vein endothelial cells (HUVECs) was studied. Confluent endothelial monolayers were exposed to shear stresses (0.2 and 1.0 Pa) from 2 to 24 h. vWF was labelled with indirect immunofluorescence method and observed with 3D fluorescence microscopy. The distribution of vWF and the cytoskeleton organization were observed simultaneously by double fluorescence labelling. More actin stress fibers and an increased release of vWF appeared in the cells exposed to flow at the same time. The qualitative and quantitative results showed that there was not only a shear‐dependent regulation but also a time‐dependent modification. For a short‐time shear stimulation, both 0.2 Pa and 1.0 Pa shear stresses induced a release of vWF from the endothelial cells. In contrast, after 24 h exposure to 1.0 Pa shear flow, vWFs were much more in the cells than that in the cells exposed to 0.2 Pa for 24 h (p<0.01) or that in the control cells (p<0.05). TNF‐α caused a decrease of vWF and Weibel–Palade bodies in the cells.

26:T51b,

The effects of two oxygen radical generating systems (H₂O₂ and ascorbate/Fe⁺²) on erythrocyte deformability, osmotic fragility, lipid peroxidation and protein degradation were studied. Incubation of erythrocytes with different concentrations of H₂O₂ (5–20 mM) or ascorbate/Fe⁺² (10/0.1–40/0.4 mM) caused a loss of deformability and increased osmotic fragility. The loss of deformability has occurred in a dose‐dependent fashion and was proportional to the extent of malonyldialdehyde (an indicator of lipid peroxidation) and alanine production (an indicator of protein degradation). Prior exposure of the erythrocytes to carbon monoxide (known to inhibit heme‐protein degradation) prevented almost completely the loss in deformability caused by H₂O₂, indicating that the loss in deformability was due mainly to protein degradation rather than to lipid peroxidation. Erythrocytes incubated with either of the two systems have also shown morphologic changes characterized by a dose‐dependent increase in echinocyte formation. The results indicate the importance of oxidatively damaged proteins in compromising the rheologic behaviour of the erythrocytes, particularly when the free radicals are involved.

27:T5db,