Fu Z, Costello M L, Tsukimoto K, Prediletto R, Elliott A R, Mathieu-Costello O, West J B
Department of Medicine, University of California, San Diego, La Jolla 92093-0623.
J Appl Physiol (1985). 1992 Jul;73(1):123-33. doi: 10.1152/jappl.1992.73.1.123.
We previously showed that when pulmonary capillaries in anesthetized rabbits are exposed to a transmural pressure (Ptm) of approximately 40 mmHg, stress failure of the walls occurs with disruption of the capillary endothelium, alveolar epithelium, or sometimes all layers. The present study was designed to test whether stress failure occurred more frequently at high than at low lung volumes for the same Ptm. Lungs of anesthetized rabbits were inflated to a transpulmonary pressure of 20 cmH2O, perfused with autologous blood at 32.5 or 2.5 cmH2O Ptm, and fixed by intravascular perfusion. Samples were examined by both transmission and scanning electron microscopy. The results were compared with those of a previous study in which the lung was inflated to a transpulmonary pressure of 5 cmH2O. There was a large increase in the frequency of stress failure of the capillary walls at the higher lung volume. For example, at 32.5 cmH2O Ptm, the number of endothelial breaks per millimeter cell lining was 7.1 +/- 2.2 at the high lung volume compared with 0.7 +/- 0.4 at the low lung volume. The corresponding values for epithelium were 8.5 +/- 1.6 and 0.9 +/- 0.6. Both differences were significant (P less than 0.05). At 52.5 cmH2O Ptm, the results for endothelium were 20.7 +/- 7.6 (high volume) and 7.1 +/- 2.1 (low volume), and the corresponding results for epithelium were 32.8 +/- 11.9 and 11.4 +/- 3.7. At 32.5 cmH2O Ptm, the thickness of the blood-gas barrier was greater at the higher lung volume, consistent with the development of more interstitial edema. Ballooning of the epithelium caused by accumulation of edema fluid between the epithelial cell and its basement membrane was seen at 32.5 and 52.5 cmH2O Ptm. At high lung volume, the breaks tended to be narrower and fewer were oriented perpendicular to the axis of the pulmonary capillaries than at low lung volumes. Transmission and scanning electron microscopy measurements agreed well. Our findings provide a physiological mechanism for other studies showing increased capillary permeability at high states of lung inflation.
我们之前的研究表明，当麻醉兔的肺毛细血管暴露于约40 mmHg的跨壁压力（Ptm）时，血管壁会发生应力性破裂，同时伴有毛细血管内皮、肺泡上皮或有时所有层的破坏。本研究旨在测试在相同的Ptm下，高肺容积时应力性破裂是否比低肺容积时更频繁发生。将麻醉兔的肺充气至20 cmH₂O的跨肺压，以32.5或2.5 cmH₂O的Ptm灌注自体血，然后通过血管内灌注进行固定。通过透射电子显微镜和扫描电子显微镜对样本进行检查。将结果与之前一项将肺充气至5 cmH₂O跨肺压的研究结果进行比较。在较高肺容积时，毛细血管壁应力性破裂的频率大幅增加。例如，在32.5 cmH₂O的Ptm下，高肺容积时每毫米细胞内衬的内皮破裂数为7.1±2.2，而低肺容积时为0.7±0.4。上皮的相应数值分别为8.5±1.6和0.9±0.6。两者差异均具有统计学意义（P＜0.05）。在52.5 cmH₂O的Ptm下，内皮的结果分别为20.7±7.6（高容积）和7.1±2.1（低容积），上皮的相应结果分别为32.8±11.9和11.4±3.7。在32.5 cmH₂O的Ptm下，较高肺容积时气血屏障的厚度更大，这与更多间质性水肿的形成一致。在32.5和52.5 cmH₂O的Ptm下，可见上皮细胞因上皮细胞与其基底膜之间水肿液的积聚而出现气球样变。在高肺容积时，破裂往往更窄，且与低肺容积相比，垂直于肺毛细血管轴的破裂较少。透射电子显微镜和扫描电子显微镜测量结果吻合良好。我们的研究结果为其他显示高肺膨胀状态下毛细血管通透性增加的研究提供了一种生理机制。
