摘要
目的观察高血压患者阿司匹林抵抗(AR)发生率,并探讨阿司匹林抵抗的影响因素和可能机制。方法分别以致聚剂花生四烯酸(AA)、二磷酸腺苷(ADP)诱导,测定108名未经治疗的高血压患者服用阿司匹林前及每日服用阿司匹林100mg,1周后的全血的血小板聚集电阻抗值。根据对阿司匹林反应分为阿司匹林抵抗:环氧化酶型阿司匹林抵抗(COX型AR);环氧化酶旁路型阿司匹林抵抗(COX-AP型AR);阿司匹林敏感(AS),同时测定服药前的血常规及血纤维蛋白原浓度。结果高血压患者108例,总的阿司匹林抵抗发生率为55.5%,其中COX-AP型发生率为44.4%,COX型发生率为11.1%。COX-AP型和COX型AR患者服用阿司匹林后ADP诱导的的血小板聚集值均明显高于服药前[(9.0±2.7)vs(6.4±2.9)ohm,P<0.05;(6.7±2.4)vs(5.7±2.5)ohm,P<0.05]。COX型和COX-AP型阿司匹林抵抗患者的血小板、白细胞、中性粒细胞计数明显高于阿司匹林敏感者[(215.5±20.0)/(213.5±44.3)vs(189.1±61.8)×109L-1,P<0.05];[(6.20±0.5)/(6.5±1.5)vs(5.6±1.2),P<0.05];[(3.5±0.1)/(3.8±1.6)vs(3.1±0.8)×109L-1,P<0.05]。结论高血压患者存在阿司匹林抵抗,其发生机制与启动血小板聚集的途径异常有关。环氧化酶旁路的存在且功能代偿性增强是高血压患者发生阿司匹林抵抗的主要机制;环氧化酶途径异常是另一次要机制。血液中血小板、白细胞、中性粒细胞等数量增加可能对阿司匹林抵抗的发生有影响。
Objective To investigate the incidence of aspirin resistance in hypertension patients and explore its mechanisms. Methods Platelet aggregation function induced by adenosine diphosphate（ADP）and arachidonic acid （AA） was determined by whole blood impedance method in 108 hypertension patients after taking aspirin （≥ 7 d, 100 mg/d）. Based on the response to aspirin, patients were categorized into： （1） Cyclooxygenase type aspirin resistance（COX-AR）; （2）Cyclooxygenase alternative pathway type aspirin resistance （COX-AP-AR） and aspirin sensitiveness （AS）. Blood routine, numbers of platelet and fibrinogen were determined. Results Incidence of aspirin resistance in patients with hypertension was 55.5 %, including 44.4 % COX-AP type AR and 11.1% COX type AR. Platelet aggregation impedance induced by ADP for COX-AP type AR and COX type AR hypertension patients after taking aspirin was higher than before administration respectively [（9.0 ± 2.7） vs （6.4 ± 2.9） ohm, P〈0.05]; [（6.7±2.4） vs （5. 7±2.5）ohm, P〈0. 05]. Blood platelet （Cox type：215.5±20.0; Cox-AP 213.5±44.3 vs AS：189.1±61.8×10^9L^-1, P〈0.05）, leucocytes （Cox type： 6.2±0.5; Cox-AP：6.6±1.5 vs AS：5.6±1.2×10^9L^-1, P〈0.05）, neutrophils （Cox type：3.3±0.1; Cox-AP： 3.8±1.6 vs AS： 3. 1±0.8 10^9L^-1 , P〈0.05）. Conclusion Aspirin resistance in patients with hypertension is related to the disorder of platelet aggregation pathway. The pathway of platelet aggregation-cyclooxygenase bypass and its enhancement is the principal mechanism for aspirin resistance; Thrombocytosis, leukocytosis and neutrophilic leukocytosis are associated with aspirin resistance.
出处
《中华高血压杂志》
CAS
CSCD
北大核心
2007年第5期367-371,共5页
Chinese Journal of Hypertension
关键词
高血压
血小板聚集性
阿司匹林抵抗
Hypertension
Platelet aggregation function
Aspirin resistance
