高原缺氧对血小板活化的研究进展
摘要
环境和人体的生命健康息息相关,是人类赖以生存和发展的物质基础条件,已有研究表明居住在高原地区的人群,血液系统的改变是缺氧环境下最敏感指标之一,突出的表现在红细胞和血红蛋白增高,血液黏稠度增加上,促使人体的血液处于高凝状态[1],这一改变使得血液流动缓慢、血小板聚集增加,可导致血管内皮细胞的损伤及许多细胞因子和炎症因子的释放,引起血小板活化进而可能引起血栓,其变化与海拔高度、缺氧状态、机体损伤程度等有关[1],本综述旨在提供一个全面系统的分析总结,以期待对后期临床工作及后续研究提供指导性意见。
引文
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[3]尚春香,乌仁塔娜,南星梅,等.慢性低氧暴露对血小板活化及其分泌的炎性因子水平的影响[J].中国高原医院与生物学杂志,2017,(4):262-266.
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[5]肖青林,郜中平,陈广浩,等.高原低氧环境对人血小板功能的影响[J].武警医学,2005,16(10):758-759.
[6]陆建红,陈国军,董长林.不同剂量阿司匹林对阻抗血小板聚集的作用评价[J].武警医学,2004,15(3):220-221.
[7]张红,周旭彬,林壮坚.慢性肺心病患者血小板功能变化[J].广东医学,2001,22(2):151-152.
[8]Mousa SA,Lorelli W,Campochiaro PA.Role of hypoxia and extracel lu-lar matrix-integrin binding in the molulation of angiogenic growth fac-tors secretion by retinal pigmented epi thelial cells[J].J Cell Biochem,1997,74(1):135-143.
[9]Everly G S,Lating J M.A clinical guide to the treatment of the human stress response[J].Springer Sci&Bus Media,2012,161(9):293-315.
[10]Chen S,Du C,Shen M,et al,Sympathetic stimulation facilitates thrombopoiesis by promoting megakaryocyte adhesion,migration,and proplatelet formation[J].Blood,2016,127(8):1024-1035.
[11]Chen S,Hu M,et al.Dopamine induces platelet production from megakaryocytes via oxidative stress-mediated signaling pathways[J].Platelets,2017,11(9)1-7.
[12]Heidt T,sager H B,Courties G,et al.Chronic variable stress activates hematopoietic stem cell[J].Nat Med,2014,20(7):754-758.
[13]Katayama Y,Battisa M,Kao W M,et al.Signals from the sympathetic nervous system regulate hematopoietic stem cell egress from bone marrow[J].Cell,2006,124(2)407-421.
[14]Qian p,He X C,Paulson A,et al.The Dlkl-Gtl2 locus preserves LT-HSCfunction by inhibiting the PI3K-mTOR pathway to restrict mitochondrial metabolism[J].Cell Stem,2016,18(2)214-228.
[2]张博,汤伯基,程守科.冠状循环中血小板活化状态对冠状动脉斑块形成的影响70例临床观察[J].武警医学,1997,8(6):333.
[3]尚春香,乌仁塔娜,南星梅,等.慢性低氧暴露对血小板活化及其分泌的炎性因子水平的影响[J].中国高原医院与生物学杂志,2017,(4):262-266.
[4]张庆成,孟腾涛,司本辉..高原缺氧环境对青年战士血小板活的影响[J].环境与健康杂志,2000,(3):142-144.
[5]肖青林,郜中平,陈广浩,等.高原低氧环境对人血小板功能的影响[J].武警医学,2005,16(10):758-759.
[6]陆建红,陈国军,董长林.不同剂量阿司匹林对阻抗血小板聚集的作用评价[J].武警医学,2004,15(3):220-221.
[7]张红,周旭彬,林壮坚.慢性肺心病患者血小板功能变化[J].广东医学,2001,22(2):151-152.
[8]Mousa SA,Lorelli W,Campochiaro PA.Role of hypoxia and extracel lu-lar matrix-integrin binding in the molulation of angiogenic growth fac-tors secretion by retinal pigmented epi thelial cells[J].J Cell Biochem,1997,74(1):135-143.
[9]Everly G S,Lating J M.A clinical guide to the treatment of the human stress response[J].Springer Sci&Bus Media,2012,161(9):293-315.
[10]Chen S,Du C,Shen M,et al,Sympathetic stimulation facilitates thrombopoiesis by promoting megakaryocyte adhesion,migration,and proplatelet formation[J].Blood,2016,127(8):1024-1035.
[11]Chen S,Hu M,et al.Dopamine induces platelet production from megakaryocytes via oxidative stress-mediated signaling pathways[J].Platelets,2017,11(9)1-7.
[12]Heidt T,sager H B,Courties G,et al.Chronic variable stress activates hematopoietic stem cell[J].Nat Med,2014,20(7):754-758.
[13]Katayama Y,Battisa M,Kao W M,et al.Signals from the sympathetic nervous system regulate hematopoietic stem cell egress from bone marrow[J].Cell,2006,124(2)407-421.
[14]Qian p,He X C,Paulson A,et al.The Dlkl-Gtl2 locus preserves LT-HSCfunction by inhibiting the PI3K-mTOR pathway to restrict mitochondrial metabolism[J].Cell Stem,2016,18(2)214-228.