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作 者:罗晨芳[1] 高婉菱[1] 张富程[2] 黑子清[1]
机构地区:[1]中山大学附属第三医院麻醉科,广东广州510630 [2]中山大学附属第三医院中心实验室
出 处:《中国输血杂志》2013年第4期346-348,共3页Chinese Journal of Blood Transfusion
基 金:广东省卫生厅基金项目(A2009197)
摘 要:目的观察重型肝炎患者血小板形态学及线粒体膜电位的变化,探讨血小板功能缺陷的可能机制。方法重型肝炎及健康自愿者各20名,观测2组血小板形态学参数(Plt、体积、血小板分布宽度、血小板压积)及血小板线粒体膜电位水平。肝脏损害的相关指标及凝血功能亦被观测。结果重型肝炎患者凝血酶原时间(25.08±7.45)、活化部分凝血活酶时间(56.42±12.50)明显延长。与正常对照组相比,重型肝炎患者Plt(79.3±44.0 vs222.5±47.9)、血小板压积(0.08±0.04 vs 0.22±0.05)明显降低,但平均血小板体积(11.19±1.02 vs 9.89±0.90)增大;重型肝炎患者血小板线粒体膜电位水平(0.72±0.19)较正常对照组(0.59±0.16)增高。结论重型肝炎患者血小板减少,其形态学及线粒体膜电位水平与正常对照组显著不同;血小板线粒体膜电位水平增高可能是血小板功能缺陷的机制之一。Objective To study the alterations of mitochondrial membrane potential and morphological parameters in platelets of severe hepatitis patients and to explore the possible mechanisms underlying the defective platelet functions. Methods The examination was completed in the group of 20 severe hepatitis patients and 20 healthy individuals. Platelet count( Pit), mean platelet volume( MPV), platelet distribution width( PDW), platelet crit(PCT) and mitochondrial membrane potential were measured. Biochemical parameters of liver damage( alanine aminotransferase,aspartate amin- otransferase, albumin and bilirubin) as well as coagulation disorders were observed in the study. Results The prothrombin time (PT), and activated partial thromboplastin time (APTT) were significantly prolonged in severe hepatitis patients, which was (25.08 ±7.45) and (56. 42 ± 12. 50) ,respectively. Plt(79. 3 ±44. 0 vs 222. 5±47. 9)and PCT (0. 08 ±0. 04 vs 0. 22± 0. 05 ) decreased significantly when compared to the normal healthy volunteers. There was a significant increase ( P 〈 0.05 ) in the levels of mitochondrial membrane potential in the severe hepatitis group when compared to the healthy individuals, which was (0.72 v0. 19)vs(0. 59 ±0. 16) (P 〈0.05). Conclusion The Ph,MPV and mitochondrial membrane potential in platelets of severe hepatitis patients are different with that of normal healthy volunteers. The increase in the mitochondrial membrane potential may play a role in the pathological process of platelet function defects.
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