Chilling induces shape changes in platelets from disks to spheres with abundant filopodia. Such changes were time-dependent and correlated well with the phosphorylation of 20-kDa myosin light chain (LC20). Both the shape changes and the phosphorylation were reversible. After the platelets had been chilled, myosin became incorporated into the Triton X-insoluble fraction. When the chilled platelets were immunocytochemically stained, anti-myosin antibody was localized with filamentous structures inside the filopodia. These results suggest that LC20 phosphorylation and subsequent interactions with actin filaments play a crucial role in the cold-induced changes in platelet shape and in the formation of filopodia.

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In order to understand the pathology of varicose veins, we prospectively collected a total of 23 vein specimens both from the normal proximal thigh long saphenous vein (LSV) in 3 young trauma patients and from the unstripped proximal LSV near the sapheno-femoral junction and the distal calf blowouts in 10 primary varicose veins patients. Ultra-thin sections were examined under the transmission electron microscope (TEM). Compared with the normal control LSV, varicose vein sections showed increase in the diameter of the lumen, hypertrophy of the wall and elongation and invagination of the intima. Smooth muscle cells (SMCS) lost their normal fusiform shape and were widely separated by increased amounts of extra-cellular collagen fibers. The cells underwent marked degeneration, vacuolization and disintegration into fiber-like material and small separated fragments. SMCs were seen in the subintimal tissue and some of them were lost into tile lumen. SMCs also showed marked phagocytic activity, engulfing not only collagen and elastic fibers, but also other smooth muscle cells. Although these changes were more marked and advanced in the distal calf blowouts, they were also present in the proximal, clinically non-dilated LSV. In conclusion, SMCs of varicose veins show severe degeneration in both the distal calf blowouts and the proximal, clinically non-varicose LSV. It appears that they both form and phagocytose collagen and elastic fibers and play a major role in the pathogenesis of varicose veins.

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