Heard S O, Longtine K, Toth I, Puyana J C, Potenza B, Smyrnios N
Department of Anesthesiology, UMass Memorial Medical Center, Worcester 01655, USA.
Anesth Analg. 1999 Aug;89(2):353-7. doi: 10.1097/00000539-199908000-00020.
Hydrogen peroxide (H2O2) levels are increased in the exhaled breath of patients with the acute respiratory distress syndrome (ARDS). Because liposome-encapsulated prostaglandin E1 (PGE1) downregulates the CD11/CD18 receptor of the neutrophil, thereby limiting endothelial adhesion, the use of this drug should decrease the excretion of H2O2 in the expiratory condensate of patients with ARDS. Patients > 11 yr of age with ARDS (diffuse, patchy infiltrates by chest radiograph; Pao2/fraction of inspired oxygen [P/F] ratio < or = 200 mm Hg; pulmonary capillary wedge pressure < or = 18 mm Hg; and the requirement for mechanical ventilation) were randomized to receive placebo (n = 14) or escalating doses (0.15-3.6 micrograms/kg) of liposomal PGE1 (n = 14) every 6 h for up to 7 days. Condensate was collected every morning from the expiratory tubing that was submerged in an ice saltwater bath (-5 degrees C). H2O2 levels were measured by using a horseradish peroxidase assay. Other data collected included white blood cell count and P/F ratios. There was no significant difference in the concentration of H2O2 in the expiratory condensate between the liposomal PGE1 group and the control group either before (0.99 +/- 0.52 vs 0.93 +/- 0.48 mumol/L) or during treatment (1.04 +/- 0.45 vs 0.76 +/- 0.25 mumol/L). Liposomal PGE1 treatment improved the P/F ratio and decreased the white blood cell count over time. Despite its ability to downregulate the CD11/CD18 neutrophil receptor, liposomal PGE1 did not reduce exhaled H2O2 excretion.
White blood cells (WBC) are thought to be part of the cause of the acute respiratory distress syndrome, a lung disease. WBC in the lung produce hydrogen peroxide, which is exhaled. Liposomal PGE1 inhibits WBC function but was found to have no effect in decreasing exhaled hydrogen peroxide in patients with the acute respiratory distress syndrome.
急性呼吸窘迫综合征(ARDS)患者呼出气体中的过氧化氢(H2O2)水平升高。由于脂质体包裹的前列腺素E1(PGE1)可下调中性粒细胞的CD11/CD18受体,从而限制内皮细胞黏附,因此使用该药物应可减少ARDS患者呼气冷凝物中H2O2的排泄。年龄大于11岁的ARDS患者(胸部X线显示弥漫性、斑片状浸润;动脉血氧分压/吸入氧分数[P/F]比值≤200 mmHg;肺毛细血管楔压≤18 mmHg;且需要机械通气)被随机分为两组,一组接受安慰剂(n = 14),另一组每6小时接受递增剂量(0.15 - 3.6微克/千克)的脂质体PGE1(n = 14),持续7天。每天早晨从置于冰盐水浴(-5℃)中的呼气管道收集冷凝物。使用辣根过氧化物酶测定法测量H2O2水平。收集的其他数据包括白细胞计数和P/F比值。脂质体PGE1组和对照组在治疗前(0.99±0.52对0.93±0.48微摩尔/升)或治疗期间(1.04±0.45对0.76±0.25微摩尔/升)呼气冷凝物中H2O2的浓度均无显著差异。脂质体PGE1治疗可改善P/F比值,并随时间降低白细胞计数。尽管脂质体PGE1能够下调CD11/CD18中性粒细胞受体,但其并未降低呼出的H2O2排泄量。
白细胞(WBC)被认为是急性呼吸窘迫综合征(一种肺部疾病)病因的一部分。肺部的白细胞产生过氧化氢并呼出。脂质体PGE1可抑制白细胞功能,但在降低急性呼吸窘迫综合征患者呼出的过氧化氢方面未发现有效果。