To determine the exact role of various factors in silicone-oil emulsification, we investigated eight different silicone oils with specific physicochemical characteristics in terms of their rate of emulsification. The silicone oils were defined by viscosity, volatility, amount of low-molecular components, electrical resistivity, degree of purification and chemical composition. The viscosities differed between the ranges of 1000 and 10,000 cs. The silicone oils included purified polydimethylsiloxane (PDMS), hydroxyl-enriched PDMS and trimethylsiloxy-terminated polydiphenylsiloxane (PDPS). As emulsifiers we used 0.1% solutions of fibrinogen, fibrin, gamma globulins, acidic alpha-1-glycoprotein, very-low-density lipoprotein and serum dissolved in sterile, distilled water as well as in balanced salt solution. The group of low-viscosity silicone oils (1000 cs) was least stable. The greatest difference in stability was found among purified PDMS, having viscosities between 1000 and 5000 cs. The most stable oil was purified PDMS, whose emulsification rate was almost identical at 5000 and 10,000 cs. High contents of hydroxyl end groups enhanced silicone-oil emulsification to a greater extent than did phenyl side groups. The strongest emulsifiers were fibrinogen, fibrin and serum, followed by gamma globulins, very-low-density lipoprotein and acidic alpha-1-glycoprotein. Balanced salt solution accelerated silicone oil emulsification in all cases. For reduction of emulsification in vivo, purified PDMS of high viscosity should be used. Biologically active emulsifiers found in hemorrhages or inflammatory situations might be lowered in vivo by hemostasis and sufficient postoperative anti-inflammatory therapy.

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Glial cells and newly formed collagen may play an important role in macular hole formation by exerting tangential traction regardless of the underlying disease process. Glial cells, however, may also be involved in healing of the retinal defect and pars plana vitrectomy with peeling of an epiretinal membrane, and/or the ILL may induce directed glial cell proliferation and migration. The similar ultrastructure of epiretinal membranes associated with macular holes and "simple epiretinal membranes" as described by Foos [8] suggests a common pathogenesis for macular holes and macular pucker.

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Various histogenetically different cell types such as macrophages, retinal pigment epithelial cells, glial cells, and fibroblasts are involved in the formation of epiretinal membranes. In the development of such multicellular tissues, cellular adhesion molecules (CAMs) are necessary for cell migration, proliferation, and localization, and the transfer of information between the cells. We investigated the expression of the intercellular adhesion molecule 1 (ICAM-1) and the leukocyte function-associated antigen 1 (LFA-1) in frozen sections of epiretinal membranes in proliferative vitreoretinopathy (PVR), proliferative diabetic retinopathy (PDR), macular pucker, and recurrent membranes after intraocular silicone oil tamponade using the indirect immunoperoxidase method. ICAM-1 forms a receptor-ligand pair with LFA-1 and is involved in a number of significant cellular interactions, e.g. in providing dynamic position-specific information to guide lymphocyte and leukocyte localization in the immune response. ICAM-1 is a member of the immunoglobulin gene super-family of CAMs. LFA-1 is a member of the integrin family of cell membrane receptors. It mediates a wide range of lymphocyte, monocyte, natural killer cell, and granulocyte interactions with other cells in immunity and inflammation, and it is a receptor for ICAM-1. The LFA-1 interaction with its ligand ICAM-1 mediates not only cell adhesion but also signal transduction in immunologic and inflammatory cell responses. Basal ICAM-1 expression is normally low on nonhematopoietic cells, but it can be subject to an up-and-down regulation by various cytokines.(ABSTRACT TRUNCATED AT 250 WORDS)