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目的：探讨心血管病患者阿司匹林抵抗(AR)与炎症的关系。方法：采用比浊法测定110例冠心痛服用阿司匹林患者及20例健康对照组花生四烯酸(AA)、二磷酸腺苷(ADP)诱导的血小板聚集率,判断阿司匹林抵抗(AR)、阿司匹林半抵抗(ASR)和阿司匹林敏感(AS)患者；放免法测定6-酮-前列腺素PGE_(1α)(6-Keto-PGF_(1α)))及血栓素B_2(TXB_2)。结果：研究对象中AR占2.72%；ASR占7.27%,其中ADP诱导者5.45%,AA诱导者1.82%；AR与ASR合计9.99%；而AS占90.01%。对各组患者TXB_2、6-Keto-PGF_(1α)以及TXB_2/6-Keto-PGF_(1α)研究发现,阿司匹林抵抗、以及阿司匹林抵抗和半抵抗患者血浆TXB_2、、TXB_2/6-Keto-PGF_(1α)较阿司匹林敏感患者显著升高；而6-Keto-PGF_(1α)差异无统计学意义。结论：血浆TXB_2以及TXB_2/6-Keto-PGF_(1α)对阿对司匹林抵抗有预测和筛查价值。
Objective: To investigate the relationship between aspirin resistance (AR) and inflammation in cardiovascular patients. Methods: Turbidimetric method was used to determine the platelet aggregation rate induced by arachidonic acid (AA) and adenosine diphosphate (ADP) in 110 patients with coronary heart disease taking aspirin and 20 healthy controls. The aspirin resistance (AR), aspirin half (ASR) and aspirin sensitive (AS) patients. The levels of 6-Keto-PGF_ (1α) and thromboxane B_2 (TXB_2) were determined by radioimmunoassay. Results: AR accounted for 2.72%, ASR accounted for 7.27%, of which ADP induced 5.45%, AA induced 1.82%, AR and ASR combined 9.99%, while AS accounted for 90.01%. The study of TXB_2, 6-Keto-PGF_ (1α) and TXB_2 / 6-Keto-PGF_ (1α) in each group showed that aspirin resistance and TXB_2, TXB_2 / 6-Keto-PGF_ 1α) were significantly higher than those in aspirin-sensitive patients, while there was no significant difference in 6-Keto-PGF_ (1α). CONCLUSION: Plasma TXB_2 and TXB_2 / 6-Keto-PGF_ (1α) have predictive and screening values for aspirin resistance.