Zimmerman J J
Crit Care Med. 1986 Sep;14(9):761-7. doi: 10.1097/00003246-198609000-00001.
Inhibition by prostaglandin E1 (PGE1) of superoxide anion (O2-.) production by isolated intact human neutrophils (PMNs) was investigated utilizing initial-velocity enzyme kinetics. Lag time, linearity, rate, and extent of reaction were simultaneously examined. Dose-response data indicate progressive PGE1-induced suppression of O2-. synthesis by activated PMNs with a Ki value of 0.50 and 0.98 mumol/L for initial velocity and extent of reaction, respectively. There were no significant dose-related trends for either lag time or linearity for reactions with PGE1 concentrations less than 10(-6) mol/L; however, at concentrations of 10(-8) mol/L and greater, the length of reaction was progressively shortened. PGE1 inhibition of PMN-induced O2-. production does not involve PMN activation/desensitization since PGE1 itself cannot stimulate O2-. generation. Moreover, PGE1 does not function as a free-radical scavenger. These data indicate the clinical feasibility of utilizing PGE1 to titrate PMN-induced synthesis of active oxygen metabolites, in order to attenuate PMN-associated host autoinjury.
利用初速度酶动力学研究了前列腺素E1（PGE1）对分离的完整人中性粒细胞（PMN）产生超氧阴离子（O2-.）的抑制作用。同时检测了延迟时间、线性、速率和反应程度。剂量反应数据表明，PGE1可逐渐抑制活化的PMN合成O2-，初速度和反应程度的Ki值分别为0.50和0.98μmol/L。对于PGE1浓度低于10（-6）mol/L的反应，延迟时间或线性均无明显的剂量相关趋势；然而，在10（-8）mol/L及更高浓度下，反应时间逐渐缩短。PGE1对PMN诱导的O2-.产生的抑制作用不涉及PMN的活化/脱敏，因为PGE1本身不能刺激O2-.的产生。此外，PGE1不起自由基清除剂的作用。这些数据表明，利用PGE1滴定PMN诱导的活性氧代谢产物合成以减轻PMN相关的宿主自身损伤具有临床可行性。
