Warren B A, Philp R B, Inwood M J
Br J Exp Pathol. 1973 Apr;54(2):163-72.
The pathogenesis of the ill effects following air embolism cannot be attributed solely to the space occupying and surface tension effects of the air bubbles altering the normal flow of blood through the vasculature. Decompression sickness was induced in rats and the following features of this process observed by electron microscopy in the vessels of the mesentery: imprisonment of blood elements (especially platelets) took place within the various enclosures created by the boundaries set up by different sized air bubbles between the layer of blood and the vessel walls, and the air/blood interface. Air bubble size and the thickness of the film of blood between bubbles varied enormously. The air/blood interface had the following characteristics: (1) A surface associated protein layer measuring 20 nm which coated the air bubbles and which could slide off the bubble of origin and float freely in the blood. (2) Material morphologically similar to the surface layer was found away from the surface and included small lipid droplets between its layers, and platelets adhered to this to form small aggregates suspended from the interface. (3) The surface layer fused with like laminae and was found within the fluid blood in the vessel, sometimes with adherent platelet aggregates. (4) Platelet adhesion to the bubble interface with the formation of platelet aggregates of an early type i.e. without gross fibrin formation within the aggregates. (5) Pressure damage to underlying endothelial cells by the passage of air bubbles under pressure resulted in herniation of the endothelial cells through fenestrations in the more rigid structures of the vessel wall. (6) Deposits of fibrin on the walls of the vessels were noted after endothelial damage. (7) Lipid droplets were found attached to the surface associated protein on the air side of the air/blood interface and were also found incorporated within it, i.e. covered by this layer on both sides, in which case they took on an ellipsoidal shape. These alterations would account for certain features of decompression sickness, such as the drop in platelets, even when the mechanical blockage by air bubbles was not of great significance.
空气栓塞后不良影响的发病机制不能仅仅归因于气泡的占位效应和表面张力效应,这些效应改变了血液在脉管系统中的正常流动。在大鼠身上诱发了减压病,并通过电子显微镜观察肠系膜血管中这一过程的以下特征:血液成分(尤其是血小板)被困在由不同大小气泡在血液层与血管壁之间以及气/血界面处形成的边界所构成的各种封闭空间内。气泡大小以及气泡之间的血液薄膜厚度差异极大。气/血界面具有以下特征:(1)一个厚度为20纳米的表面相关蛋白层,覆盖着气泡,该层可从起源气泡上滑落并在血液中自由漂浮。(2)在远离表面处发现形态与表面层相似的物质,其层间包含小脂滴,血小板附着于此形成从界面悬垂的小聚集体。(3)表面层与类似薄片融合,并在血管内的流动血液中发现,有时还伴有附着的血小板聚集体。(4)血小板粘附于气泡界面,形成早期类型的血小板聚集体,即聚集体内无明显纤维蛋白形成。(5)气泡在压力下通过导致对下方内皮细胞的压力损伤,致使内皮细胞通过血管壁较坚硬结构中的窗孔疝出。(6)在内皮损伤后,注意到血管壁上有纤维蛋白沉积。(7)发现脂滴附着在气/血界面空气一侧的表面相关蛋白上,也发现其包含在该层内,即两侧均被该层覆盖,在这种情况下它们呈椭圆形。这些改变可以解释减压病的某些特征,例如血小板减少,即使气泡的机械阻塞并不十分严重。