Fontes B, Moore E E, Moore F A, Koike K, Carl V, Banerjee A
Department of Surgery, Denver General Hospital, Colorado 80204-45007, USA.
J Surg Res. 1995 Jun;58(6):599-604. doi: 10.1006/jsre.1995.1094.
Our previous work has implicated platelet activating factor (PAF)-induced neutrophil (PMN) priming and increased CD11b/CD18 receptor expression in the pathogenesis of lung injury following gut ischemia/reperfusion (I/R). In this model CD11b blockade abrogates lung injury but does not alter PMN priming or pulmonary leukosequestration. We, therefore, hypothesized that PAF-stimulated PMN priming and CD11b expression are insufficient to promote lung PMN sequestration. Normal rat PMNs, labeled with 51Cr, were incubated with PAF (10 ng/ml) to induce priming for superoxide (O2-) generation and enhance CD11b expression. Gut I/R animals underwent superior mesenteric artery occlusion for 45 min. 51Cr-labeled PMNs (2 x 10(7)) were injected iv. Study groups, consisting of (a) normal/control, (b) sham/laparotomy, and (c) gut I/R, were given either normal or PAF-treated PMNs. PAF-primed PMNs had increased 2- release and CD11b expression, but did not sequester in the lungs of normal rats. However, following gut I/R PAF-treated PMNs sequestered in the pulmonary bed. These data suggest that PAF priming for O2- generation and increased CD11b expression are insufficient alone to promote PMN sequestration in the lung. Rather, additional factors generated by gut I/R are necessary for this process.
我们之前的研究表明，血小板活化因子（PAF）诱导的中性粒细胞（PMN）预激以及CD11b/CD18受体表达增加，在肠道缺血/再灌注（I/R）后肺损伤的发病机制中起作用。在该模型中，阻断CD11b可消除肺损伤，但不会改变PMN预激或肺内白细胞扣押。因此，我们推测PAF刺激的PMN预激和CD11b表达不足以促进肺内PMN扣押。用51Cr标记的正常大鼠PMN与PAF（10 ng/ml）孵育，以诱导超氧化物（O2-）生成的预激并增强CD11b表达。肠道I/R动物接受肠系膜上动脉闭塞45分钟。静脉注射51Cr标记的PMN（2×10^7）。研究组包括（a）正常/对照组、（b）假手术/剖腹术组和（c）肠道I/R组，分别给予正常或PAF处理的PMN。PAF预激的PMN的O2-释放和CD11b表达增加，但在正常大鼠肺中不发生扣押。然而，在肠道I/R后，PAF处理的PMN在肺床中发生扣押。这些数据表明，PAF诱导的O2-生成预激和CD11b表达增加单独不足以促进肺内PMN扣押。相反，肠道I/R产生的其他因素对此过程是必需的。
