Raff G, Livingston D H, Wang M T, Rameshwar P
Department of Surgery, UMDNJ-New Jersey Medical School, Newark 07103, USA.
J Surg Res. 1995 Jul;59(1):75-9. doi: 10.1006/jsre.1995.1134.
Hemorrhagic shock has been shown to alter bone marrow (BM) myelopoiesis. Isolated hemorrhagic shock is uncommon after trauma and the combined effect of tissue injury and shock on myelopoiesis is unknown. We studied the growth of BM granulocyte-macrophage colony forming units (CFU-GM) following shock and soft tissue injury. Rats were anesthetized and allocated into one of four groups: CONTROL, sham neck dissection; SHOCK, rats were bled to a mean BP of 45 mmHG for 45 min and resuscitated with shed blood and saline; TURP, soft tissue injury was induced by turpentine 0.5 ml/100 g SQ into the hindquarter; SHOCK + TURP, rats received TURP just before SHOCK as described above. Groups (n = 6) were sacrificed 1, 3, and 5 days after treatment. BM cells plated for CFU-GM and splenic macrophages were cultured for IL-1 production. Unstimulated splenic macrophage production of IL-1 alpha was not different for any group except Day 5 turpentine animals. TURP induced a significant increase in CFU-GM on Day 1 compared to that in control (47 +/- 22 vs 21 +/- 11; P < 0.05). SHOCK completely abolished this response to TURP. Both the SHOCK and TURP alone increased CFU-GM on Day 5 compared to that in CONTROL but there was no additive effect in the SHOCK + TURP group. These data show that the BM response to combined soft tissue injury and shock (TURP + SHOCK) appears similar to that of SHOCK alone and that hemorrhagic shock appears to be a significant immunosuppressive factor in the regulation of myelopoiesis following injury.
出血性休克已被证明会改变骨髓（BM）的髓系造血。单纯性出血性休克在创伤后并不常见，组织损伤和休克对髓系造血的联合作用尚不清楚。我们研究了休克和软组织损伤后骨髓粒细胞-巨噬细胞集落形成单位（CFU-GM）的生长情况。将大鼠麻醉后分为四组：对照组，假手术颈部解剖；休克组，大鼠放血至平均血压45 mmHg持续45分钟，然后用自体血和生理盐水复苏；松节油组，通过在后肢皮下注射0.5 ml/100 g松节油诱导软组织损伤；休克+松节油组，大鼠在休克前接受如上所述的松节油处理。每组（n = 6）在治疗后1、3和5天处死。接种用于CFU-GM的骨髓细胞和用于培养白细胞介素-1（IL-1）的脾巨噬细胞。除了第5天的松节油处理组动物外，任何组未刺激的脾巨噬细胞产生的IL-1α没有差异。与对照组相比，松节油组在第1天诱导CFU-GM显著增加（47±22对21±11；P<0.05）。休克完全消除了对松节油的这种反应。与对照组相比，单独的休克组和松节油组在第5天均增加了CFU-GM，但休克+松节油组没有相加效应。这些数据表明，骨髓对软组织损伤和休克联合作用（松节油+休克）的反应似乎与单独休克相似，并且出血性休克似乎是损伤后髓系造血调节中的一个重要免疫抑制因素。
