Sinzinger H, Fitscha P, Tiso B
Atherosclerosis Research Group (ATK) Austrian Academy of Sciences, Vienna.
Thromb Res. 1990 Mar 1;57(5):677-84. doi: 10.1016/0049-3848(90)90025-8.
It has been demonstrated that under certain conditions the in-vitro half-life of biologically active PGI2 in plasma is extremely shortened, which may result in-vivo in a local haemostatic imbalance. In 36 patients suffering from acute myocardial infarction a sequential change in in-vitro half-life of synthetic PGI2 was therefore studied during 3 weeks. 21 patients admitted turning out not to develop myocardial infarction served as follow-up controls. During and shortly after the acute episode the plasmatic half-life of PGI2 in-vitro was shortened by about 40%, improving continuously thereafter. No certain influence of either risk factors, sex or age could be discovered. A possible influence of various drugs administered in the hospital period has been excluded in 43 patients with proven coronary artery disease. No such changes occurred during acute angina pectoris attack in 12 patients. It remains to be established, whether the short-lasting destabilisation of PGI2 may be an acute disease-associated finding, or an important pathogenetic factor.
业已证明，在某些情况下，血浆中生物活性前列环素（PGI2）的体外半衰期会极剧缩短，这可能在体内导致局部止血失衡。因此，对36例急性心肌梗死患者在3周内合成PGI2的体外半衰期的连续变化进行了研究。21例入院后未发生心肌梗死的患者作为随访对照。在急性发作期间及发作后不久，PGI2的体外血浆半衰期缩短约40%，此后持续改善。未发现危险因素、性别或年龄有任何确切影响。在43例经证实患有冠状动脉疾病的患者中，已排除住院期间使用的各种药物的可能影响。12例患者在急性心绞痛发作期间未出现此类变化。PGI2的短暂失稳究竟是一种与急性疾病相关的表现，还是一个重要的致病因素，仍有待确定。
