The immunomodulatory effects of damage control abdominal packing on local and systemic neutrophil activity.
The immunomodulatory effects of damage control abdominal packing on local and systemic neutrophil activity.
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损伤控制腹部填塞对局部和全身中性粒细胞活性的免疫调节作用。
DOI：
10.1097/00005373-200105000-00004
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发表时间：
2001
期刊：
影响因子：
--
通讯作者：
Deitch,EA
中科院分区：
文献类型：
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作者：
Adams,JM;Hauser,CJ;Livingston,DH;Fekete,Z;Hasko,G;Forsythe,RM;Deitch,EA
BackgroundDamage Control剖腹手术（DCL）与腹部填塞已成为司空见惯的重大创伤后，但免疫后果的DCL是unknown.MethodsWe收集了37个流体样本从剖腹手术垫（LPF）从28例DCL后1小时至7天。从8例患者进行了系列包装的样品进行了测定其介质含量和对中性粒细胞（PMN）功能的影响。用荧光法研究了N-甲酰-甲硫氨酰-亮氨酰-苯丙氨酸和佛波酯-肉豆蔻酸酯（PMA）引起的呼吸爆发（RB），以及GRO-α和血小板活化因子对PMN [Ca 2+] i的动员作用。短暂暴露于20% LPF（LPF 20）模拟LPF对腹膜PMN的作用，2% LPF（LPF 2）模拟对PMN的全身作用。采用酶联免疫吸附法检测内毒素（ETX）、GRO-α和白三烯B4。结果LPF使N-甲酰基-甲硫氨酰-亮氨酰-苯丙氨酸诱导的RB从0.4±0.1× 103计数/秒（对照组）增加到0.7±0.1（LPF 2）和1.3±0.3（LPF 20）（p< 0.05），且LPF 2在损伤后较晚时间内活性增加。PMA引发的RB仅由LPF 2引发< 24小时。LPF 2和LPF 20均能显著抑制GRO-α [Ca 2+] i的释放。LPF 2的抑制在< 24小时时最大，48小时后减弱。GRO-α反应的抑制呈剂量依赖性：对照PMN为150±8 nmol/L，LPF 2后为97±19，LPF 20后为59±4（均p< 0.05）。[Ca 1 nmol/L血小板活化因子后的[2+] i通量仅被LPF 20抑制（从181±14 nmol/L至149±15 nmol/L，p< 0.05）。LPF中ETX、GRO-α和白三烯B4的浓度是创伤患者血浆浓度的10 ~ 20倍。结论DCL导致腹膜内ETX和介质积聚，即使培养物是无菌的。LPF暴露引发PMN RB引起的非受体（PMA）或受体偶联激动剂，抵抗受体脱敏。相反，LPF抑制PMN对激动剂的反应，在高介质浓度下进行受体脱敏。在这种情况下，PMN功能障碍可能反映了暴露于浓缩介质后某些细胞功能（如RB）的同时启动和其他（受体依赖性）功能的脱敏。DCL后腹膜介质的产生可能是内毒素驱动的，并可能导致全身炎症反应综合征。DCL用早期止血换取晚期炎症。在规划管理战略时应考虑到这一点。
BackgroundDamage control laparotomy (DCL) with abdominal packing has become commonplace after major trauma, but the immune consequences of DCL are unknown.MethodsWe collected 37 fluid samples from laparotomy pads (LPF) removed from 28 patients 1 hour to 7 days after DCL. Samples from eight patients who underwent serial packing were assayed for their mediator content and effects on neutrophil (PMN) function. Respiratory burst (RB) to N-formyl-methionyl-leucyl-phenylalanine and phorbol myristate acetate (PMA), as well as PMN calcium ([Ca 2+] i) mobilization by GRO-α and platelet-activating factor were studied using dihydrorhodamine and fura-2-acetoxymethyl ester fluorescence. Brief exposure to 20% LPF (LPF20) modeled LPF acting on peritoneal PMNs and 2% LPF (LPF2) modeled the systemic effects on PMNs. Endotoxin (ETX), GRO-α, and leukotriene B4 were assayed by enzyme-linked immunosorbent assay. Data analysis was by analysis of variance with Dunn’s comparisons or the Mann-Whitney test when indicated.ResultsLPF increased N-formyl-methionyl-leucyl-phenylalanine–induced RB from 0.4±0.1× 10 3 counts per second (control) to 0.7±0.1 (LPF2) to 1.3±0.3 (LPF20)(p< 0.05), with LPF2 increasingly active at later times after injury. PMA-elicited RB was primed only by LPF2 from< 24 hours. Both LPF2 and LPF20 markedly suppressed GRO-α [Ca 2+] i flux. Suppression by LPF2 was maximal at< 24 hours, abating after 48 hours. Suppression of GRO-α response was dose dependent: 150±8 nmol/L in control PMNs, 97±19 after LPF2, and 59±4 after LPF20 (all p< 0.05).[Ca 2+] i flux after 1 nmol/L platelet-activating factor was only suppressed (from 181±14 nmol/L to 149±15 nmol/L, p< 0.05) by LPF20. LPF contained ETX, GRO-α, and leukotriene B4 at 10-to 20-fold plasma concentration in trauma patients.ConclusionDCL results in peritoneal ETX and mediator accumulation even when cultures are sterile. LPF exposure primes PMN RB elicited by nonreceptor-(PMA) or receptor-coupled agonists that resist receptor desensitization. Conversely, LPF suppresses PMN responses to agonists that undergo receptor desensitization at high mediator concentrations. PMN dysfunction in such circumstances probably reflects a concomitant priming of some cell functions (eg, RB) and desensitization of other (receptor-dependent) functions after an exposure to concentrated mediators. Peritoneal mediator production after DCL may be ETX driven, and may contribute to systemic inflammatory response syndrome. DCL trades early hemostasis for later inflammation. This should be considered in planning management strategies.