Savion N, Alhalel A, Treister G, Bartov E
Maurice and Gabriela Goldschleger Eye Research Institute, Sackler, Faculty of Medicine, Tel Aviv University, Sheba Medical Center, Tel-Hashomer, Israel.
Invest Ophthalmol Vis Sci. 1996 Dec;37(13):2694-9.
To develop an in vitro model for silicone oil emulsification and to explore the blood components involved in this process.
The capacity of various blood components to support silicone oil (1000 CS) emulsification was studied by applying 0.5 ml oil on top of 0.5 ml saline containing various blood components. Each tube was sonicated for 150 seconds and centrifuged at 5000 g for 20 minutes. Three phases were noted in the tube: At the top was clear silicone oil, in the middle was emulsified silicone oil, and at the bottom was aqueous solution. The tubes were photographed, and the percentage of the phase length containing emulsified silicone oil (middle) of the total length of the three phases was calculated from the projected image of each tube.
Emulsified silicone oil in plasma or serum was initiated after 100 seconds of sonication and quickly reached maximum (approximately 80%) at 120 seconds. The size of these oil droplets prepared in vitro was 0.0467 +/- 0.028 mm, closely resembling that observed in oil samples removed from a patient's anterior chamber (0.038 +/- 0.018 mm). Under these conditions, silicone oil emulsified in the presence of whole blood cells occurred only at a concentration of 120 micrograms protein/ml; in the presence of red blood cell membranes, it occurred at a concentration of 60 micrograms protein/ml. Lipoprotein-deficient serum failed to support emulsification; however, samples of high-density lipoprotein and low-density lipoprotein supported this process. Purified high-density lipoprotein-apolipoproteins supported oil emulsification. The addition of phosphatidylcholine further enhanced this process, but phosphatidylcholine alone failed to support emulsification.
A simple and fast in vitro model to study factors affecting silicone oil emulsification was developed. Using this model, red blood cell membranes, plasma lipoproteins, and purified HDL-apolipoproteins supported silicone oil emulsification. Lipids did not, but they had the capacity to enhance the apolipoprotein-supported emulsification.
建立硅油乳化的体外模型，并探索参与该过程的血液成分。
通过在含有各种血液成分的0.5 ml盐溶液上方加入0.5 ml硅油（1000 CS），研究各种血液成分支持硅油乳化的能力。每管超声处理150秒，然后以5000 g离心20分钟。管中可见三相：顶部为澄清的硅油，中间为乳化硅油，底部为水溶液。对管进行拍照，并根据每根管的投影图像计算包含乳化硅油（中间相）的相长度占三相总长度的百分比。
血浆或血清中的硅油在超声处理100秒后开始乳化，并在120秒时迅速达到最大值（约80%）。体外制备的这些油滴大小为0.0467±0.028 mm，与从患者前房取出的油样中观察到的大小（0.038±0.018 mm）非常相似。在这些条件下，全血细胞存在时硅油乳化仅在蛋白质浓度为120微克/毫升时发生；红细胞膜存在时，在蛋白质浓度为60微克/毫升时发生。缺乏脂蛋白的血清不能支持乳化；然而，高密度脂蛋白和低密度脂蛋白样品支持该过程。纯化的高密度脂蛋白-载脂蛋白支持油乳化。添加磷脂酰胆碱进一步增强了该过程，但单独的磷脂酰胆碱不能支持乳化。
建立了一种简单快速的体外模型来研究影响硅油乳化的因素。使用该模型，红细胞膜、血浆脂蛋白和纯化的高密度脂蛋白-载脂蛋白支持硅油乳化。脂质不支持，但它们有增强载脂蛋白支持的乳化的能力。
