Manhart N, Oismüller C, Lassnig A, Spittler A, Sautner T, Götzinger P, Függer R, Roth E
Department of Surgery, AKH University Hospital, Vienna, Austria.
Wien Klin Wochenschr. 1998 Nov 27;110(22):796-801.
Generation of reactive oxygen intermediates (ROI) has been implicated in tissue damage in a variety of disease states including sepsis and trauma. On the other hand, generation of ROI in polymorphonuclear granulocytes (PMN) presents a crucial element in the defence of the host against invading microorganisms. In the present study we investigated the generation of superoxide anions (O2-) and hydrogen peroxide (H2O2) by neutrophils (PMN)5 of 17 critically ill patients treated at a intensive care unit (ICU) after polytrauma (n = 6), heart operation (n = 6) or during septic shock (n = 5) using flow cytometry. O2- production of PMN from ICU patients was significantly lower (p < 0.01) than that in healthy volunteers (HV) during non-receptor mediated stimulation with phorbol-myristate-acetate (PMA) but higher (p < 0.001) during receptor mediated stimulation with formylmethionine-leucine-phenylalanine (FMLP). H2O2 generation of PMN from ICU patients was increased after stimulation with FMLP (p < 0.01) and remained unchanged after stimulation with PMA. Patients in septic shock had lower O2(-)-generation of PMN than did injured patients and patients after heart operations. We conclude that receptor mediated formation of O2- and H2O2 is stimulated in ICU patients. However, in patients in septic shock O2(-)-generation decreases, which potentially might contribute to the immunoparalysis present in septic shock.
活性氧中间体(ROI)的产生与包括败血症和创伤在内的多种疾病状态下的组织损伤有关。另一方面,多形核粒细胞(PMN)中ROI的产生是宿主抵御入侵微生物的关键因素。在本研究中,我们使用流式细胞术调查了17名在重症监护病房(ICU)接受治疗的重症患者的中性粒细胞(PMN)产生超氧阴离子(O2-)和过氧化氢(H2O2)的情况,这些患者分别为多发伤(n = 6)、心脏手术(n = 6)或感染性休克期间(n = 5)。在使用佛波酯-肉豆蔻酸酯-乙酸酯(PMA)进行非受体介导刺激时,ICU患者PMN的O2-产生量显著低于健康志愿者(HV)(p < 0.01),但在使用甲酰甲硫氨酸-亮氨酸-苯丙氨酸(FMLP)进行受体介导刺激时则较高(p < 0.001)。ICU患者PMN经FMLP刺激后H2O2生成增加(p < 0.01),经PMA刺激后保持不变。感染性休克患者PMN的O2-产生量低于受伤患者和心脏手术后患者。我们得出结论,ICU患者中受体介导的O2-和H2O2形成受到刺激。然而,感染性休克患者的O2-产生量降低,这可能是导致感染性休克中免疫麻痹的原因之一。