Ratnoff W D, Matthay M A, Wong M Y, Ito Y, Vu K H, Wiener-Kronish J, Goetzl E J
Department of Medicine, University of California Medical Center, San Francisco 94143-0724.
J Clin Immunol. 1988 Jul;8(4):250-8. doi: 10.1007/BF00916553.
The human pulmonary edema fluid concentrations of LTC4 and of LTD4 and LTE4, derived peptidolytically from LTC4, were assessed by radioimmunoassays of the mediators resolved by reverse-phase high-performance liquid chromatography. The mean pulmonary edema fluid concentration (+/- SD) of LTD4 of 19.2 +/- 25.6 nM for 12 patients with the adult respiratory distress syndrome and of LTE4 of 192 +/- 309 nM for 10 of the patients were significantly higher (P less than 0.005 and P less than 0.05) than those of 2.2 +/- 2.4 and 11.0 +/- 18.2 nM, respectively, for 10 patients with cardiogenic pulmonary edema, whereas the lower mean concentrations of LTC4 were not significantly different for the two groups. Pulmonary edema fluid from five patients with adult respiratory distress syndrome, one with cardiogenic pulmonary edema, and one with an indeterminate syndrome contained similar concentrations of peptidoleukotriene peptidases. The LTC4 and LTD4 peptidolytic activities in ARDS fluids were 81 and 142 kD, respectively, by gel filtration. The extents of peptidolysis of [3]LTC4 and [3]LTD4 by 100 microliter of pulmonary edema fluid attained respective mean maximum levels of 74.5 +/- 2.9% (N = 5) and 37.7 +/- 10.2% (N = 4) after 30 min at 37 degrees C and were inhibited by serine-borate and by cysteine, respectively. The predominance of LTD4 and LTE4 over LTC4 in states of altered pulmonary vascular pressure and permeability thus is attributable to two distinct peptidases.
通过反相高效液相色谱法分离介质的放射免疫测定法,评估了人肺水肿液中LTC4、LTD4以及从LTC4经肽酶解衍生而来的LTE4的浓度。12例成人呼吸窘迫综合征患者的LTD4平均肺水肿液浓度(±标准差)为19.2±25.6 nM,10例患者的LTE4平均肺水肿液浓度为192±309 nM,显著高于(P<0.005和P<0.05)10例心源性肺水肿患者分别为2.2±2.4 nM和11.0±18.2 nM的浓度,而两组LTC4的较低平均浓度无显著差异。5例成人呼吸窘迫综合征患者、1例心源性肺水肿患者和1例综合征不明患者的肺水肿液中含有相似浓度的肽白三烯肽酶。通过凝胶过滤法测定,ARDS液中LTC4和LTD4的肽酶解活性分别为81 kD和142 kD。100微升肺水肿液对[3]LTC4和[3]LTD4的肽酶解程度在37℃下30分钟后分别达到平均最高水平74.5±2.9%(N = 5)和37.7±10.2%(N = 4),分别被丝氨酸 - 硼酸盐和半胱氨酸抑制。因此,在肺血管压力和通透性改变的状态下,LTD4和LTE4相对于LTC4的优势归因于两种不同的肽酶。