Glauser F L, Egan P, Millen J E, Fischer P, Propst K, Lewis J, Chetty K
Crit Care Med. 1978 May-Jun;6(3):181-4. doi: 10.1097/00003246-197805000-00012.
We observed two patients with aspirin (ASA) ingestion (blood levels of 87 and 56.5 mg/100 ml) who presented with noncardiogenic pulmonary edema (adult respiratory distress syndrome. To determine if ASA had a direct effect on the alveolar epithelial membrane, we established an in vitro isolated lung model and perfused it with platelet free plasma. T1/2 (in minutes), the time for 50% equilibration between the plasma and the saline filled lung, was determined before and after 500 mg salicylate infusion for various molecular weight dextrans. T1/2 decreased significantly (p less than 0.05) as follows: 3000 MW dextran, 2273 +/- 932 to 961 +/- 375; 40,000 MW dextran, 4059 +/- 1550 to 733 +/- 275; 70,000 MW dextran, 11,730 +/- 2750 to 7700 +/- 2230. Histamine levels in plasma and lung liquid did not change significantly with ASA infusion. We conclude that ASA directly increases alveolar epithelial permeability to dextrans less than 70,000 MW.
我们观察了两名服用阿司匹林(ASA)(血药浓度分别为87和56.5mg/100ml)后出现非心源性肺水肿(成人呼吸窘迫综合征)的患者。为了确定ASA是否对肺泡上皮膜有直接作用,我们建立了一个体外离体肺模型,并用无血小板血浆进行灌注。对于不同分子量的右旋糖酐,在输注500mg水杨酸盐前后,测定血浆与充满生理盐水的肺之间达到50%平衡的时间T1/2(分钟)。T1/2显著降低(p<0.05),如下所示:3000MW右旋糖酐,从2273±932降至961±375;40000MW右旋糖酐,从4059±1550降至733±275;70000MW右旋糖酐,从11730±2750降至7700±2230。输注ASA后,血浆和肺液中的组胺水平没有显著变化。我们得出结论,ASA直接增加肺泡上皮对分子量小于70000MW的右旋糖酐的通透性。