Ultrastructural localization of factor VIII procoagulant antigen in human liver hepatocytes

Factor VIII is generally believed to circulate in blood as a multimeric complex of two glycoproteins which are physiologically and immunologically distinct. One component of the factor VIII complex is factor VIII procoagulant activity (FVIII:C) which is associated with factor VIII/procoagulant antigen (FVIII:Ag, formerly FVIII/CAg). The second, larger unit of the complex is factor VIII/von Willebrand factor (vWF:Ag, formerly factor VIII-related antigen or FVIIIRAg). FVIII:C has anti-haemophilic activity and is defective or deficient in patients with classical haemophilia, and vWF:Ag is absent in patients with von Willebrand disease. FVIII:Ag was demonstrated recently in endothelial cells lining hepatic sinusoids, by using immunoperoxidase staining and light microscopy, whereas biochemical data had indicated its presence predominantly in the hepatocyte fractions and in lesser amounts in endothelial cells. Moreover, recent hybridization experiments detected FVIII:C messenger RNA in liver and kidney tissues. Despite several efforts, the cells responsible for FVIII:C synthesis have not been unequivocally identified. Here we use protein A-gold complex labelling to demonstrate the ultrastructural localization of FVIII:C in human liver cells; the results indicate that hepatocytes may synthesize FVIII:Ag.     

Ultrastructural localization of choline acetyltransferase in vascular endothelial cells in rat brain

Furchgott and Zawadski have shown that acetylcholine (ACh) does not act directly on the smooth muscle of blood vessel walls, but rather via receptors on the endothelial cells lining the lumen, to release an endothelium-derived relaxing factor (EDRF). As it is very unlikely that neurotransmitter released from the periarterial nerves, which are confined to the adventitial-medial border, diffuses all the way through the medial muscle coat before acting on endothelial cells to release EDRF to produce vasodilatation, this discovery has been regarded as an indication of a pathophysiological mechanism, rather than a physiological one (see refs 2, 3). ACh is rapidly degraded in the blood by acetylcholinesterase, so that ACh must be released locally to be effective on endothelial cells. Here we demonstrate the immunocytochemical localization of choline acetyltransferase in endothelial cells of small brain vessels, which is consistent with the view that the ACh originates from endothelial cells that can synthesize and store it. We suggest that release of ACh following damage to endothelial cells during ischaemia contributes to a pathophysiological mechanism of vasodilation which protects that segment of vessel from further damage as well as brain cells from hypoxia.     

开口箭对小鼠5-羟色胺分泌的影响

目的:采用灌胃、石蜡切片、免疫组化染色和ELISA等方法,探讨开口箭对小鼠5-羟色胺(5-HT)分泌的影响.方法选取20²2g健康昆明小鼠20只,均分成A,B,C,D 4组,分别以蒸馏水和0.25、0.50、1.00mg/mL的开口箭灌胃,0.20mL/次/d,连续灌胃7d.第8d对全部小鼠摘眼球取血,ELISA检测血清5-HT质量浓度;取血后立即处死小鼠,取十二指肠,4%甲醛固定,石蜡切片,免疫组化染色,镜下统计5-HT阳性细胞数量.结果与A组相比,B,C,D组小鼠血液5-HT质量浓度逐渐降低,十二指肠肠壁组织中5-HT阳性细胞数也明显减少.结论开口箭会下调小鼠5-HT的分泌.