血栓弹力图评价急性创伤患者早期血小板功能的改变

目的 用血栓弹力图（TEG）血小板图分析急性创伤后血小板抑制功能的改变。方法 用TEG检测51例急诊创伤患者及48例健康人全血血小板二磷酸腺苷（ADP）抑制率及花生四烯酸（AA）抑制率,并用logistic回归分析创伤患者的高危风险因素。结果 创伤患者平均二磷酸腺苷（ADP）抑制率（%）为85.9（38.4,97.6）、平均花生四烯酸（AA）抑制率（%）为44.7（26.4,59.1）,健康人平均ADP抑制率（%）为4.4（0,18.1）、平均AA抑制率（%）为0.7（0,3.03）,创伤组与健康人对照组血小板抑制率差异有统计学意义（P〈0.01）。以ADP抑制率是否大于75%为cut off值,患者碱缺失（BD）〉6 m Eq/L（OR=3.21,95%CI：1.45~9.31）和6 h内至少输注血浆200 m L（OR=4.9,95%CI：0.89~28.8）为患者的高危风险因素;以ADP抑制率是否大于90%为cut off值,患者收缩压〈70 mm Hg（OR=12.4,95%CI：1.8~91.4）和患者6 h内至少输注红细胞悬液2 U（OR=8.7,95%CI：1.8~46.5）为患者的高危风险因素。结论 创伤患者血小板AA及ADP抑制率明显升高,血小板活化功能降低;血制品输注增加创伤患者风险。

两种CPG血小板聚集试验在血小板捐献者筛查中的应用

目的探讨以阳离子没食子酸丙酯(CPG)为血小板激活剂的血小板聚集实验在单采血小板献血者血小板功能筛查应用中的可行性,并对血小板聚集仪法和薄片法(SPAT)进行比较。方法(1)以CPG为血小板激活剂,分别用血小板聚集仪法和薄片法测定30名自愿者服用阿司匹林前和服药24h后的血小板聚集功能,以确定服药与否的临界值;(2)应用血小板聚集仪法和薄片法同时检测483例单采血小板捐献者的血小板聚集功能,调查血小板献血者血小板功能缺陷的发生率。结果(1)服用阿司匹林的自愿者服药24h后,CPG诱导的血小板聚集率(聚集仪法)均显著降低,尤以180s时的血小板聚集率减低最为显著,由服药前的45.4%±9.5%降低为10.1%±5.0%(P<0.001)。23例自愿者服药24h后血小板聚集时间(薄片法)显著延长,由服药前的(64.5±13.9)s延长为(178.8±16.3)s(P<0.001)。血小板功能缺陷的临界值(cutoff)确定为:血小板聚集仪法为测定时间180s时的血小板聚集率小于20%;薄片法为血小板聚集时间≥150s;(2)483例血小板捐献者中,血小板聚集仪法检出血小板聚集功能不良者25例(5.18%);薄片法为5例(1.03%)。结论以CPG为激活剂的血小板聚集实验能有效检出阿司匹林服药者或其他因素导致的血小板聚集功能不良者,适用于单采血小板捐献者血小板功能筛查,以血小板聚集仪法优于薄片法。

A Decreased Responsiveness of Platelet to Nitric Oxide in Cholesterol-Fed Rabbits

Objective:To determine whether endothelial dysfunction leads to an abnormal responsiveness of platelet to nitric oxide(NO)during the development of atherosclerosis. Methods:Rabbits were fed a 1% cholesterol chow for 12 weeks to induce atherosclerosis.Serum NOx levels and the responsiveness of platelet to NO donor SNP were determined every 4 weeks during maintaining on a chow containing 1% cholesterol.The measurement of serum lipids and the examination of morphological feature and endothelial-dependent relaxation of aorta were performed after 12 weeks of cholesterol diet. Results:Cholesterol diet significantly increased serum levels of cholesterol and LDL,caused a remarkable platelet hyperaggregability,and produced an evident endothelial dysfunction as indicated by the diminished vasorelaxation induced by acetylcholine and endothelial cell lesion as exhibited by scanning electron microscope examination.The percentage of inhibition of ADP-induced platelet aggregation by NO donor SNP was significantly smaller in cholesterol chow group than that in normal chow group although no significant difference in serum NOx levels between normal and cholesterol chow group was observed throughout the development of atherosclerosis. Conclusion:The present study suggests that the endothelial dysfunction caused by enhanced serum cholesterol and LDL levels induces a decreased responsiveness of platelet to NO.