FIBRINOLYSIS IN CRITICALLY ILL PATIENTS
FIBRINOLYSIS IN CRITICALLY ILL PATIENTS
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DOI：
10.1164/ajrccm/140.2.287
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发表时间：
1989-08-01
期刊：
影响因子：
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通讯作者：
SALDEEN, T
中科院分区：
文献类型：
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作者：
MOALLI, R;DOYLE, JM;SALDEEN, T
纤维蛋白溶解障碍可能是成人呼吸窘迫综合征（ARDS）的重要原因。内源性纤溶酶原激活物抑制剂（派-1）的病理性增加可能会减弱正常的纤溶作用，并揭示替代的纤溶机制，如弹性蛋白酶诱导的纤维蛋白降解。我们测量了派-1和弹性蛋白酶诱导的纤维蛋白（原）降解产物在69个严重的III型患者在我们的医疗重症监护病房（MICU）和9名健康志愿者。因子VIII相关抗原蛋白（VIII：Ag），一种报告的急性肺损伤标志物，和α-1-蛋白酶抑制剂（α-1-PI），一种急性期反应物，也进行了测量。MICU患者包括24名无已知ABDS风险的对照患者，35名有ARDS风险因素（包括脓毒症、肺炎、吸入性和休克）的患者，12名ARDS患者（包括2名发生ARDS的高危组患者）。血浆派-1测定显色法，弹性蛋白酶诱导肽的一种新的放射免疫分析法，VIII：Ag的免疫电泳，和α-1-Pl的免疫扩散。与正常志愿者相比，MICU对照组患者派-1、VIII：Ag、弹性蛋白酶诱导肽和α-1-PI升高。与MICU对照组相比，ARDS患者派-1和VIII：Ag显著升高;弹性蛋白酶诱导肽和α-1-Pl并不升高。然而，未发生ARDS的高危患者也有高派-1或VIII：Ag。虽然这些数据不能反驳这些化合物在ARDS发病机制中的可能作用，但它们表明派-1和VIII：Ag在许多危重III型患者中可能升高，但可能不是随后发生ARDS的有用标志物。
Impaired fibrinolysis may contribute to development of adult respiratory distress syndrome (ARDS). Pathologic increases in endogenous plasminogen activator inhibitor (PAI-1) may blunt normal fibrinolysis and unmask alternate fibrinolytic mechanisms, such as elastase-induced fibrin degradation. We measured PAI-1 and elastase-induced fibrin(ogen) degradation products in 69 critically III patients in our medical intensive care unit (MICU) and in nine healthy volunteers. Factor VIII-related antigen protein (VIII:Ag), a reported marker of acute lung injury, and alpha-1-protease inhibitor (alpha-1-PI), an acute phase reactant, were also measured. MICU patients included 24 control patients with no known risk of ABDS, 35 patients with risk factors for ARDS including sepsis, pneumonia, aspiration, and shock, and 12 patients with ARDS including two patients from at-risk groups who developed ARDS. Plasma PAI-1 was determined by chromogenic assay, elastase-induced peptides by a new radioimmunoassay, VIII:Ag by immunoelectrophoresis, and alpha-1-Pl by immunodiffusion. When compared to normal volunteers, MICU control patients had elevated PAI-1, VIII:Ag, elastase-induced peptides, and alpha-1-Pl. Patients with ARDS had significantly higher PAI-1 and VIII:Ag than did MICU control patients; elastase-induced peptides and alpha-1-Pl were not higher. However, at-risk patients who did not develop ARDS also had high PAI-1 or VIII:Ag. Although these data cannot refute the possible role of these compounds in the pathogenesis of ARDS, they demonstrate that PAI-1 and VIII:Ag may be elevated in many critically III patients but may not be useful markers for the subsequent development of ARDS.