To understand ventilator-induced lung injury (VILI) during positive pressur
e ventilation, mechanisms of normal alveolar mechanics must first be establ
ished. Isotropic "baIloonlike" alveolar volume (V-A) change has been viewed
as the prevailing mechanism of normal lung volume (V-L) changes. We hypoth
esized that change in V-L is predominantly caused by alveolar recruitment-d
erecruitment (R/D). Fifteen mongrel dogs were anesthetized and intubated wi
th a tracheal divider. Through a thoracotomy incision, in vivo microscopy o
f subpleural alveoli was performed as the degassed lung was inflated to 80%
TLC, and then deflated to residual volume (RV). Still photomicrographs wer
e evaluated to determine if change in V-L is due to change in VA or R/D Of
alveoli. We noted a steady, significant increase in alveolar recruitment as
V-L increased to 80% TLC (p < 0.05). However, V-A increased significantly,
but only to 20% TLC (p < 0.05). Once recruited, alveoli did not demonstrat
e any further volume change, whereas the lung as a whole maintained a norma
l pressure/volume relationship. In our model, changes in V-L predominantly
are caused by R/D.