Vadas P, Scott K, Smith G, Rajkovic I, Stefanski E, Schouten B D, Singh R, Pruzanski W
Inflammation Research Group, Wellesley Hospital, University of Toronto, Ontario, Canada.
Life Sci. 1992;50(11):807-11. doi: 10.1016/0024-3205(92)90186-s.
Massive elevations of serum phospholipase A2 activity have been documented in patients with septic shock. Serum PLA2 activity correlated to the degree and duration of circulatory collapse, while purified native PLA2 reproduced hypotension in experimental animals. In a prospective study of patients with septic shock, we have determined the relationship of PLA2 enzyme activity to PLA2 immunoreactivity using radiolabelled E. coli phospholipid substrate and an ELISA specific for group II human nonpancreatic PLA2. In all patients, there was a clear concordance of the two assays. Maximal PLA2 concentration was increased a mean of 554-fold over normal levels. We found no evidence to support the presence of activating or inhibitory proteins. These data confirm that the observed increase in serum PLA2 activity in septic shock is due to intravascular release of group II nonpancreatic PLA2.
脓毒性休克患者血清磷脂酶A2活性有大幅升高的记录。血清PLA2活性与循环衰竭的程度和持续时间相关,而纯化的天然PLA2在实验动物中可导致低血压。在一项针对脓毒性休克患者的前瞻性研究中,我们使用放射性标记的大肠杆菌磷脂底物和针对II型人非胰腺PLA2的酶联免疫吸附测定法(ELISA),确定了PLA2酶活性与PLA2免疫反应性之间的关系。在所有患者中,两种检测方法结果明显一致。PLA2最大浓度比正常水平平均增加了554倍。我们没有发现支持存在激活或抑制蛋白的证据。这些数据证实,脓毒性休克患者血清PLA2活性升高是由于II型非胰腺PLA2的血管内释放所致。