CORONARY HEART DISEASE, HAGEMAN FACTOR, HORMONAL CONTROL

这项研究的长期目标是深入了解这一机制 参与男性冠心病患者血栓形成的发生 疾病和其他处于统计风险中的个人。一个可能的 血栓形成的原因是“高凝状态”，例如， 血浆中凝血因子的异常高滴度。在使用口服的女性中 含有雌激素化合物的避孕药以及孕妇， 血浆Hageman因子效价(HF，FXII)加倍升高。 寒冷诱导的凝血因子VII和血浆肾素活性的升高 在使用口服避孕药的妇女中观察到的情况反映了她们的高HF滴度。 最近，弗雷明翰心脏研究报告称，患有冠心病的男性 疾病有高雌激素血症。因为雌激素会增加催乳素 分泌，雌激素和催乳素都可能在提高HF效价方面发挥作用， 可能是通过影响蛋白质的合成。这项计划将研究 参与HF的激活、合成和分解代谢的机制以及 血浆中对其滴度的荷尔蒙控制。具体目标是： 1)确定男性冠心病患者是否患有高心衰 滴度，以及他们的血浆是否表现出增强的冷激活 凝血因子VII和前肾素、HF凝血剂和抗原滴度、血浆肾素和 将在新鲜和冷藏的血浆中测量凝血因子VII活性 会与她们的雌二醇和催乳素效价有关；2)测定 无论在雌二醇、催乳素和 地塞米松处理的大鼠因从头合成或减少 HF的降解、肝脏灌流技术和体内分解代谢 将进行研究；3)确定是否抑制了 分泌催乳素会降低HF滴度，HF滴度将在 溴隐亭治疗的大鼠；4)确定血栓栓塞剂和 妊娠高血压并发症与高血压病病毒滴度有关 将对怀孕期间的妇女进行纵向研究 在男性冠心病研究中使用的方法；5) 确定皮质类固醇治疗是否提高了人类的HF滴度 接受治疗的患者将测定凝血剂和抗原滴度 6)以确定激活的HF-C1酯酶 在使用口服避孕药的妇女中形成抑制物复合体 血管闭塞危象中的镰状细胞患者，交叉 将使用免疫电泳法。数理统计方法 分析将包括学生t检验，皮尔逊系数 相关性和多重相关性。

The long-term goal of this study is to gain insight into the mechanisms involved in the development of thrombosis in men with coronary heart disease and other individuals who are at statistical risk. A possible cause of thrombosis is a state of "hypercoagulability", for example, abnormally high titers of clotting factors in plasma. In women using oral contraceptives containing estrogenic compounds, as well as pregnant women, the plasma titer of Hageman factor (HF, factor XII) is doubly elevated. The cold-induced increase in factor VII and plasma renin activities observed in women using oral contraceptives reflect their high HF titers. Recently, the Framingham Heart Study reported that men with coronary heart disease have hyperestrogenemia. Since estrogens increase prolactin secretion, both estrogen and prolactin may play a role in raising HF titer, possibly by affecting protein synthesis. This project will study the mechanisms involved in HF activation, synthesis and catabolism, as well as the hormonal control of its titer in plasma. The specific objectives are: 1) to determine whether men with coronary heart disease have high HF titers, and whether their plasmas manifest enhanced cold-activation of factor VII and prorenin, HF coagulant and antigen titers, plasma renin and factor VII activities will be measured in fresh and cold-stored plasmas and will be related to their estradiol and prolactin titers; 2) to determine whether the high HF titer observed in estradiol, prolactin and dexamethasone-treated rats is due to de novo synthesis or decreased degradation of HF, liver perfusion techniques and in vivo catabolism studies will be performed; 3) to determine whether the inhibition of prolactin secretion will reduce HF titer, HF titer will be measured in bromocriptine-treated rats; 4) to determine whether the thromboembolic and hypertensive complications of pregnancy are related to high HF titer, a longitudinal study of women throughout their pregnancy will be performed using methods in the study of men with coronary heart disease; 5) to determine whether corticosteroid therapy raises HF titer in humans, HF coagulant and antigen titers will be measured in patients receiving decadron or prednisone; 6) to determine whether an activated HF-C1 esterase inhibitor complex is formed in women using oral contraceptives and in sickle cell patients during vaso-occlusive crises, crossed immunoelectrophoretic techniques will be used. Statistical methods of analyses will include the Student's t test, Pearson's coefficient of correlation and multiple correlation.