Smith E B, Ashall C
Atherosclerosis. 1985 May;55(2):171-86. doi: 10.1016/0021-9150(85)90096-6.
In samples of human aortic intima fibrin/fibrinogen degradation products (FDP) were assayed by isoelectric focussing/immunoelectrophoresis as a possible measure of endogenous fibrinolysis, and plasminogen concentration was assayed by rocket immunoelectrophoresis as a possible marker for fibrinolytic potential. No consistent differences were found between normal intima and different types of atherosclerotic lesion, but there was marked variation between patients, and multiple samples from the same aorta showed similar levels. There was no significant correlation with age, sex, or time after death. Low concentrations of FDP and failure to recover measureable amounts of plasminogen from intima were highly associated with death in patients who had suffered a recent myocardial infarction. In aortas from which 3 or more samples of intima and lesions were obtained (n = 16), no FDP were found in 3 (total of 12 samples); all of these were from patients who died following myocardial infarction. Low levels were present in the 4th patient with myocardial infarction. No plasminogen was found in 10 of 11 aortas from patients dying after myocardial infarction (total of 46 samples with no plasminogen), but it was present in 10 of 17 aortas from patients dying of other causes (X2 = 7.6, P less than 0.01). Where both were assayed, FDP were not found in any samples which did not contain plasminogen. Low levels of FDP and absence of plasminogen were associated with increased involvement with atherosclerosis. There was no relation between intimal and serum plasminogen levels, and prothrombin and low density lipoprotein were present in all samples from which no plasminogen was recovered. The results indicate that in some patients, particularly those dying after myocardial infarction, there is decreased fibrinolysis and fibrinolytic potential in the arterial intima, and this may result in increased intimal accumulation of fibrin.
在人主动脉内膜样本中，通过等电聚焦/免疫电泳法检测纤维蛋白/纤维蛋白原降解产物（FDP），作为内源性纤维蛋白溶解的一种可能指标；通过火箭免疫电泳法检测纤溶酶原浓度，作为纤维蛋白溶解潜力的一种可能标志物。在正常内膜与不同类型的动脉粥样硬化病变之间未发现一致的差异，但患者之间存在显著差异，且同一主动脉的多个样本显示出相似的水平。与年龄、性别或死亡时间无显著相关性。FDP浓度低以及未能从内膜中检测到可测量量的纤溶酶原与近期发生心肌梗死的患者死亡高度相关。在获取了3个或更多内膜和病变样本的主动脉（n = 16）中，12个样本中的3个未检测到FDP；所有这些样本均来自心肌梗死后死亡的患者。第4例心肌梗死患者中FDP水平较低。在心肌梗死后死亡患者的11个主动脉中的10个（共46个未检测到纤溶酶原的样本）未发现纤溶酶原，但在死于其他原因患者的17个主动脉中的10个发现了纤溶酶原（X2 = 7.6，P小于0.01）。在同时检测两者的情况下，不含纤溶酶原的任何样本中均未发现FDP。FDP水平低和纤溶酶原缺失与动脉粥样硬化的累及增加相关。内膜和血清纤溶酶原水平之间无关联，在未检测到纤溶酶原的所有样本中均存在凝血酶原和低密度脂蛋白。结果表明，在一些患者中，尤其是心肌梗死后死亡的患者，动脉内膜中的纤维蛋白溶解和纤维蛋白溶解潜力降低，这可能导致内膜中纤维蛋白的积累增加。
