Hällgren R, Samuelsson T, Laurent T C, Modig J
Department of Internal Medicine, University Hospital, Uppsala, Sweden.
Am Rev Respir Dis. 1989 Mar;139(3):682-7. doi: 10.1164/ajrccm/139.3.682.
The concentrations of hyaluronan (HA) were measured in bronchoalveolar lavage (BAL) fluid and serum from 12 patients with adult respiratory distress syndrome (ARDS). The median BAL fluid HA concentration was 353 micrograms/L, about six times higher than that seen in control patients (p less than 0.001). The median serum HA value was 619 micrograms/L, which was a 30-fold increase compared with that in the control patients (p less than 0.001). Another connective tissue component, type III procollagen peptide, was not recovered in significant amounts during lavage in patients with ARDS, but it appeared in the bloodstream in increased concentrations (p less than 0.001). Obtained recovery of HA during lavage of patients with ARDS cannot be explained by an enhanced passive leakage from the bloodstream because of increased alveolar-capillary permeability, but rather could reflect a mobilization of HA from lung interstitial tissue because of hydrostatic mechanisms. Alternatively, the appearance of HA in the alveolar space in ARDS might reflect an enhanced lung synthesis of HA. An increased HA production can possibly be mediated, directly or indirectly, by activated complement components, since a significant relationship was seen between increased plasma concentrations of C3a des Arg and BAL fluid HA (r = 0.61; p less than 0.05). The observed accumulation of HA in the small airways in ARDS may be expected to immobilize water and thereby contribute to the interstitial and alveolar edema. The inverse correlation (r = 0.71; p less than 0.01) seen between BAL fluid HA and pulmonary oxygenation index (PaO2/inspired oxygen fraction) supports such a hypothesis.
在12例成人呼吸窘迫综合征（ARDS）患者的支气管肺泡灌洗（BAL）液和血清中测量了透明质酸（HA）的浓度。BAL液中HA浓度的中位数为353微克/升，约为对照组患者的6倍（p<0.001）。血清HA值的中位数为619微克/升，与对照组患者相比增加了30倍（p<0.001）。另一种结缔组织成分，III型前胶原肽，在ARDS患者灌洗过程中未大量回收，但在血液中的浓度升高（p<0.001）。ARDS患者灌洗过程中HA的回收量增加不能用肺泡-毛细血管通透性增加导致的血液被动渗漏增强来解释，而可能反映了由于流体静力机制导致HA从肺间质组织中动员出来。或者，ARDS患者肺泡腔中HA的出现可能反映了肺HA合成增强。HA产生增加可能直接或间接由激活的补体成分介导，因为血浆C3a去精氨酸浓度升高与BAL液HA之间存在显著相关性（r=0.61；p<0.05）。在ARDS患者小气道中观察到的HA积聚可能会固定水分，从而导致间质和肺泡水肿。BAL液HA与肺氧合指数（PaO2/吸入氧分数）之间的负相关（r=0.71；p<0.01）支持了这一假设。
