摘要
目的探讨动物急性潜水减压病时微血管形态功能改变特点及其高压氧暴露后的效用。方法大鼠、豚鼠和家兔87只 ,随机分成对照组、减压损伤组和高压氧暴露组。检测了动物快速减压微血管结构与功能的改变。结果快速减压后可见微循环气泡栓塞 ,血管痉挛 ,毛细血管开放减少 ,局部组织出现大片缺血区。在微血管内 ,可见内皮细胞与白细胞、血小板黏附 ,血栓形成 ,血液瘀滞 ,血流动力减弱 ,并出现组织渗出。减压应激损伤动物 ,经用0.25mPa高压氧暴露60min后 ,红细胞聚集程度减轻 ,血流动力改善 ,微血管充盈良好 ,毛细血管开放数量明显增加 ,组织血液灌注改善。微血管中减压气泡缩小或开始消散 ,未见新的微小血栓形成 ,亦未见微血管内皮细胞与血细胞发生黏附。显示高压氧暴露对减压应激损伤所致的内皮细胞损伤具有保护作用。结论 (1)减压应激损伤后不仅在微血管内存在气泡 ,同时还引起微血管痉挛、毛细血管开放数量减少、白细胞和血小板活化和血栓形成等多因素发病的特点。(2)高压氧暴露可通过增加白细胞、血小板稳定性 ,改善微血流动力 。
Objective To probe morphologic and functional change characteristic of microvessel and effect after hyperbaric oxygen(HBO)exposure during acuter decompression illness.Methods87rats,guinea pig and rabbits,which were divided into control group,decompression injury group and HBO exposure group.Microvessel morphologic and functional changes were measured after rapid decompression in animals.Results After rapid deˉcomprssion bubble forming,spasm and capillary decreasing were found in microcirculation.There are ischemic arˉeas in tissue.Leucocyte and platelet were activated and adhered to endothlial cell to form thrombosis in microvesˉsels,so that blood was sluggish and permeable.After HBO exposure at0.25mPa for60min,blood flow dynamics increased,RBC aggregated improved,microvessel was full,capillary opening number increased.Ischemic areas were perfused well.Meanwhile,bubbles reduced or dissipated.There was no thrombosis,leucocyte and platelet were not adhered to endothelial cell.Results showed that HBO has a protective role on endothelial cell injury caused by decompression stress injury.Conclusions(1)After the decompression stress injury,bubbles not only exist in the microvessels,but also the effects occur,including the spasm of the microvessels,the reduction of the number of capillary vessels,the activation of white blood cells and the platelets,which are the characters capable of causing diseases.(2)The role of HBO therapy was realized by leucocyte and platelet stability,increasing blood flowdynamics and so on.
