Uyama O, Matsui Y, Shimizu S, Michishita H, Sugita M
Hyogo College of Nursing Art and Science, Akashi, Japan.
Jpn Circ J. 1994 Jun;58(6):409-15. doi: 10.1253/jcj.58.409.
Thromboxane A2 biosynthesis was studied in healthy subjects, in patients in whom the extent of carotid atherosclerosis was determined, and in patients receiving chronic aspirin treatment, to determine what factors activate platelets to develop carotid atherosclerosis. Urinary 11-dehydrothromboxane B2, a major metabolite of thromboxane A2, was measured by radioimmunoassay after purification by reverse-phase HPLC. The extent of carotid atherosclerosis was determined by real-time B-mode ultrasonography. The severity of carotid atherosclerosis in each subject was evaluated by plaque score, which was computed by summing the maximum thickness of plaque measured in millimeters. Urinary excretion of 11-dehydrothromboxane B2 in healthy subjects was higher (P < 0.01) in cigarette smokers (1063 +/- 244 ng/g creatinine) than in non-smokers (815 +/- 183 ng/g creatinine). Aspirin significantly suppressed 11-dehydrothromboxane B2 excretion (266 +/- 114 ng/g creatinine). In the 24 patients in whom the plaque score was measured, multivariate analysis indicated a significant positive correlation between urinary excretion of 11-dehydrothromboxane B2 and plaque score, age, smoking and hypercholesteremia. Our results indicate that risk factors such as age, hypercholesteremia, atherosclerosis and smoking activate platelets in vivo to develop carotid atherosclerosis.
在健康受试者、已确定颈动脉粥样硬化程度的患者以及接受慢性阿司匹林治疗的患者中研究血栓素A2的生物合成，以确定哪些因素会激活血小板从而引发颈动脉粥样硬化。血栓素A2的主要代谢产物尿11 - 脱氢血栓素B2，经反相高效液相色谱法纯化后，采用放射免疫分析法进行测定。通过实时B型超声检查确定颈动脉粥样硬化的程度。通过斑块评分评估每个受试者颈动脉粥样硬化的严重程度，斑块评分通过将以毫米为单位测量的斑块最大厚度相加得出。健康受试者中，吸烟者尿11 - 脱氢血栓素B2的排泄量（1063±244 ng/g肌酐）高于不吸烟者（815±183 ng/g肌酐）（P<0.01）。阿司匹林显著抑制了11 - 脱氢血栓素B2的排泄（266±114 ng/g肌酐）。在测量了斑块评分的24名患者中，多因素分析表明尿11 - 脱氢血栓素B2的排泄量与斑块评分、年龄、吸烟和高胆固醇血症之间存在显著正相关。我们的结果表明，年龄、高胆固醇血症、动脉粥样硬化和吸烟等危险因素在体内激活血小板，从而引发颈动脉粥样硬化。
