Loewen G M, Holm B A, Milanowski L, Wild L M, Notter R H, Matalon S
Department of Medicine, State University of New York, Buffalo 14214.
J Appl Physiol (1985). 1989 Mar;66(3):1087-92. doi: 10.1152/jappl.1989.66.3.1087.
We have previously demonstrated that instillation of a calf lung surfactant extract (CLSE) in rabbits after exposure to 100% O2 for 64 h mitigates the progression of lung pathology after return to room air (J. Appl. Physiol. 62: 756-761, 1987). In the present study, we investigated whether we could prevent or reduce the onset and development of hyperoxic lung injury by sequential instillations of CLSE during the hyperoxic exposure. Rabbits were exposed to 100% O2. CLSE (125 mg, approximately 170 mumol of phospholipid) was suspended in 10 ml of sterile saline and instilled intratracheally into their lungs, starting at 24 h in O2, a time at which no physiological or biochemical injury was detected, and at 24-h intervals thereafter. Control rabbits breathed 100% O2 and received either equal volumes of saline or no instillations at all. CLSE-instilled rabbits had higher arterial PO2 (Pao2) values throughout the exposure period and survived longer when compared with saline controls [120 +/- 4 vs. 102 +/- 4 (SE) h; n greater than or equal to 10; P less than 0.05]. At 72 h in O2, CLSE-instilled rabbits had significantly higher lavageable alveolar phospholipid levels (12.5 +/- 1.5 vs. 5 +/- 1 mumol/kg) and total lung capacities (41 +/- 2 vs. 25 +/- 3.5 ml/kg) and lower levels of alveolar protein (24 +/- 3 vs. 52 +/- 8 mg/kg), minimum surface tension (2 +/- 1 vs. 26.1 dyn/cm), and lung wet-to-dry weights (5.9 +/- 0.2 vs. 6.5 +/- 0.3). After 72 h in O2, lungs from both CLSE- and saline-instilled rabbits showed evidence of diffuse hyperoxic injury. However, atelectasis was less prominent in the former. We concluded that instillation of CLSE limits the onset and development of hyperoxic lung injury to the alveolar epithelium of rabbits.
我们之前已经证明,在兔暴露于100%氧气64小时后给予小牛肺表面活性物质提取物(CLSE),可减轻恢复至室内空气后肺病理变化的进展(《应用生理学杂志》62: 756 - 761, 1987)。在本研究中,我们调查了在高氧暴露期间通过序贯给予CLSE是否能够预防或减少高氧性肺损伤的发生和发展。将兔暴露于100%氧气中。将CLSE(125毫克,约170微摩尔磷脂)悬浮于10毫升无菌盐水中,并于氧气暴露24小时时开始经气管内注入兔肺,此时未检测到生理或生化损伤,此后每隔24小时注入一次。对照兔呼吸100%氧气,接受等量盐水注入或根本不进行注入。与盐水对照相比,注入CLSE的兔在整个暴露期间动脉血氧分压(Pao2)值更高,存活时间更长[120±4 vs. 102±4(SE)小时;n≥10;P<0.05]。在氧气暴露72小时时,注入CLSE的兔可冲洗出的肺泡磷脂水平显著更高(12.5±1.5 vs. 5±1微摩尔/千克),肺总量更高(41±2 vs. 25±3.5毫升/千克),肺泡蛋白水平更低(24±3 vs. 52±8毫克/千克),最小表面张力更低(2±1 vs. 26.1达因/厘米),肺湿重与干重比值更低(5.9±0.2 vs. 6.5±0.3)。在氧气暴露72小时后,注入CLSE和盐水的兔的肺均显示出弥漫性高氧损伤的迹象。然而,前者肺不张不太明显。我们得出结论,注入CLSE可限制兔肺泡上皮高氧性肺损伤的发生和发展。