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目的 探讨血小板膜糖蛋白CD31、CD61和CD62p表达在减压病发病机制中的作用。方法 1 4只雌性昆明种小鼠随机分为减压病组和正常对照组。减压病组经 60 0kPa压缩空气暴露后 ,用 1min快速减压至常压。在减压后 60min时 ,用流式细胞术检测小鼠血小板膜糖蛋白CD31、CD61和CD62p表达。结果 减压病组小鼠血小板膜糖蛋白CD31的平均荧光强度 (1 8.64± 1 .0 1 )高于正常对照组 (1 6 .89± 1 .69) ,差异有显著性 (P <0 .0 5) ;减压病组小鼠血小板膜糖蛋白CD61的平均荧光强度 (2 71 .0 6± 2 4 .2 5)和CD62p的阳性百分数 (4.48%± 0 .43 % )均高于正常对照组 (分别为 2 34 .0 9± 1 5 .96、3 .0 0 %± 0 .66 % ) ,差异有非常显著性 (P <0 .0 1 )。结论 不适宜的快速减压可增强血小板膜糖蛋白CD31、CD61和CD62p的表达 ,促使血栓形成
Objective To investigate the role of platelet membrane glycoproteins CD31, CD61 and CD62p in the pathogenesis of decompression sickness. Methods A total of 4 female Kunming mice were randomly divided into decompression sickness group and normal control group. Decompression sickness group after 60 0kPa compressed air exposure, with 1min rapid decompression to atmospheric pressure. At 60min after decompression, the expression of platelet membrane glycoproteins CD31, CD61 and CD62p in mice was detected by flow cytometry. Results The mean fluorescence intensity of platelet membrane glycoprotein CD31 in the decompression sickness group was significantly higher than that in the normal control group (16.89 ± 1.69) (P <0.05). The mean fluorescence intensity of platelet membrane glycoprotein CD61 in mice with decompression sickness was significantly higher than that of normal (2.71.06 ± 2.42.5) and CD62p (4.48% ± 0.43%) Control group (respectively, 2 34 .0 9 ± 1 5 .96,3 .0 0% ± 0 .66%), the difference was significant (P <0. Conclusion Inappropriate rapid decompression can enhance the expression of platelet membrane glycoproteins CD31, CD61 and CD62p, promote thrombosis