Ambrus C M, Ambrus J L, Choi T S, Jung O, Mirand E A, Bartfay-Szabo A
Am J Pediatr Hematol Oncol. 1979 Fall;1(3):251-60. doi: 10.1097/00043426-197923000-00009.
The fibrinolysin system is incomplete in newborn infants. Lack of serum plasminogen in premature newborn has an important role in the pathophysiology of the respiratory distress syndrome since alveolar fibrin deposits cannot be eliminated. Urokinase activated human plasmin has increased the survival rate of infants with respiratory distress syndrome. Plasminogen given I.V. at birth has reduced the incidence and the severity of respiratory distress syndrome, in a randomized double-blind study of 500 premature infants. Death in the plasminogen recipient group occurred only among infants born to mothers with bleeding complications of pregnancy. Plasmin inhibitors measured with a functional assay were the highest in this group of infants, serum plasminogen was the lowest; when activator and purified human plasminogen were added to the serum, fibrinolytic activity was elicited in excess of the plasminogen added. It is suggested that plasminogen and/or plasmin inhibitors may be abnormal fetal variants in infants born to mothers with bleeding complications.
新生儿的纤溶酶系统不完善。早产新生儿血清纤溶酶原缺乏在呼吸窘迫综合征的病理生理学中起重要作用，因为肺泡纤维蛋白沉积物无法清除。尿激酶激活的人纤溶酶提高了呼吸窘迫综合征婴儿的存活率。在一项对500名早产婴儿的随机双盲研究中，出生时静脉注射纤溶酶原降低了呼吸窘迫综合征的发病率和严重程度。纤溶酶原接受组的死亡仅发生在患有妊娠出血并发症的母亲所生的婴儿中。用功能测定法测得的纤溶酶抑制剂在这组婴儿中最高，血清纤溶酶原最低；当向血清中加入激活剂和纯化的人纤溶酶原时，引发的纤溶活性超过了所加入的纤溶酶原。有人提出，纤溶酶原和/或纤溶酶抑制剂可能是患有出血并发症的母亲所生婴儿中的异常胎儿变体。
