Neutrophil oxidative burst activation and the pattern of respiratory physiologic abnormalities in the fulminant post-traumatic adult respiratory distress syndrome.
Neutrophil oxidative burst activation and the pattern of respiratory physiologic abnormalities in the fulminant post-traumatic adult respiratory distress syndrome.
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暴发性成人创伤后呼吸窘迫综合征中中性粒细胞氧化爆发激活和呼吸生理异常模式。
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发表时间：
1991
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通讯作者：
J. Stoklosa
中科院分区：
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作者：
A. Rivkind;J. Siegel;M. Littleton;A. De Gaetano;T. Mamantov;F. Laghi;J. Stoklosa
对30例创伤后暴发型成人呼吸窘迫综合征(ARDS)患者中性粒细胞氧化爆发激活(OBA)的作用进行了研究。以中性粒细胞(PMN)化学发光(LE)作为检测OBA的指标。连续观察创伤后8天患者中性粒细胞(Pc)在自身血清(Ps)、正常血清(NS)或Gey‘s液(G)中的变化。用正常中性粒细胞(NC)检测PS的抑制作用。在1×10(6)PMN中加入预调变酵母多糖引发LE，用发光计监测LE的响应，记录LE积分的峰值。7例在前4天内发生ARDS；12例出现脓毒症(TS)，但未发生ARDS，11例患者没有合并创伤(TR)。在48-96小时，所有ARDS均表现为LE增加(P<0.0001)。没有ARDS的患者的LE没有显著增加，尽管他们的平均损伤严重程度(ISS)相同。急性呼吸窘迫综合征的LE反应是通过激活Pc[74%]介导的，仅有少量但显著的附加效应(6%)受ARDS血清(Ps)的影响：LE=0.672(Pc)+0.24[ARDS(Ps)]+1343；N=146，R2 0.733，P<0.0001。但需要血清(Ps或NS)，因为在G中孵育可抑制LE；[Cells+S]大于[Cells+G]，P<0.0001。LE是ARDS的生物学标志，损伤至LE的延迟提示ARDS的发生可能具有重要的治疗意义。ARDS的中性粒细胞激活需要血清，但ARDS的作用主要是由于细胞只有少量的ARDS特异性血清介导的作用。测定呼吸指数(RI)与肺分流(QS/QT)的关系、顺应性(COPL)、净液体平衡(DFLUID)、中性粒细胞(PMN)和血小板(Plat)计数。ARDS患者在48-96小时表现为RI、QS/QT增加，需要增加的FIO2和PEEP随着COMPL、PLAT下降和LE上升而增加。用Bonferroni t-统计量进行方差分析，这些变化均同时显著(P<0.0001或P<0.05)。急性呼吸窘迫综合征患者的死亡率显著增加(P<0.005)，强调了这些生理和生化反应的临床重要性。这些数据表明，PMN、LE和呼吸功能的简单测量是暴发性创伤后ARDS发生的早期生物学标志，可用于预测ARDS的严重程度。
The role of neutrophil oxidative burst activation (OBA) in the development of fulminant post-trauma adult respiratory distress syndrome (ARDS) was studied in 30 patients. Neutrophil (PMN) chemiluminescence (LE) was used as the index of OBA. Serially, for 8 days post-trauma, patient neutrophils (Pc) were studied in their own serum (Ps) normal serum (Ns), or Gey's solution (G). Ps was checked against normal neutrophils (Nc) for inhibition. LE was initiated by the addition of preopsonized zymosan to 1 x 10(6) PMN, the LE response monitored by luminometer, and the peak of the integral of LE recorded. Seven developed ARDS within the first 4 days; 12 patients developed sepsis (TS) but no ARDS, and 11 patients had uncomplicated trauma (TR). All ARDS showed increased LE (P less than 0.0001), at 48-96 hr. Patients without ARDS showed no significant increase in LE, although their mean injury severity (ISS) was the same. The ARDS LE response was mediated by activation of Pc [74%] with only a small but significant additional effect (6%) by ARDS serum (Ps): LE = 0.672 (Pc) + 0.24 [ARDS(Ps)] + 1343; N = 146, r2 0.733, P less than 0.0001. However, sera (Ps or Ns) was required, as incubation in G inhibited LE; [cells + s] greater than [cells + G], P less than 0.0001. LE is a biologic marker of ARDS, and the delay between injury and the LE indicated that initiation of ARDS may have therapeutic importance. Neutrophil activation in ARDS requires sera, but the ARDS effect appears mainly due to cells with only a small ARDS-specific serum-mediated role. The physiologic response to ARDS was evaluated by serial 8-hr studies of blood gases and pH; the respiratory index (RI) to pulmonary shunt (QS/QT) relationship, compliance (COMPL), and net fluid balance (DFLUID) PMN and platelet (PLAT) counts were also measured. Compared with TR and TS, the ARDS patients at 48-96 hr, showed increased RI, QS/QT, and DFluid requiring increased FiO2 and PEEP as COMPL and PLAT fell and LE rose. These changes were all simultaneously significant (P less than 0.05 to P less than 0.0001) by Bonferroni t-statistic applied to ANOVA. The clinical importance of these physiologic and biochemical responses was emphasized by the significantly (P less than 0.005) increased mortality in the ARDS patients. These data suggest that PMN LE and simple measures of respiratory function are early biologic markers of the development of fulminant post-traumatic ARDS and can be used to predict ARDS severity.