CORONARY HEART DISEASE, HAGEMAN FACTOR, HORMONAL CONTROL

本研究的长期目标是深入了解 参与冠心病患者血栓形成的发展 疾病和其他有统计风险的人。 一个可能 血栓形成的原因是“高凝状态”，例如， 血浆中凝血因子滴度异常高。 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， Hageman因子（HF，因子XII）的血浆滴度加倍升高。 冷诱导的凝血因子VII和血浆肾素活性升高 在使用口服避孕药的妇女中观察到的高HF滴度反映了她们的高HF滴度。 最近，心脏病研究报告说，患有冠心病的男性 疾病有高雌激素血症。 由于雌激素增加催乳素 分泌，雌激素和催乳素都可能在提高HF滴度中起作用， 可能是通过影响蛋白质合成。 本项目将研究 参与HF活化、合成和催化的机制，以及 其在血浆中滴度的激素控制。 具体目标是： 1)以确定男性冠心病患者是否有高HF 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 将在新鲜和冷藏血浆中测量因子VII活性， 将与他们的雌二醇和催乳素滴度有关; 2）确定 是否在雌二醇、催乳素和 地塞米松处理的大鼠是由于从头合成或减少 HF的降解、肝灌注技术和体内催化剂 将进行研究; 3）以确定是否抑制 催乳素分泌会降低HF滴度，HF滴度将在 溴隐亭处理的大鼠; 4）确定是否血栓栓塞和 妊娠期高血压并发症与高HF滴度有关， 将对整个妊娠期的妇女进行纵向研究 使用男性冠心病患者研究中的方法; 5） 确定皮质类固醇治疗是否会提高人类HF滴度，HF 将在接受以下治疗的患者中测量凝血剂和抗原滴度： decadron或泼尼松; 6）确定激活的HF-C1酯酶是否 在使用口服避孕药的妇女中形成抑制剂复合物， 血管闭塞性危象期间的镰状细胞患者，交叉 将使用免疫电泳技术。 统计方法 分析将包括学生t检验、皮尔森系数、 相关和多重相关。

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.