232 
PULMONARY MODELS 
macrophages presumably reflected the incor- 
poration of edema fluid. A variety of crenated 
red cell profiles was observed in the pulmonary 
capillaries. 
Transmission Electron Microscopy 
Edema was evidenced by distended interstitial 
spaces. Collagen fibers were displaced by homo- 
genous areas corresponding to accumulated ede- 
ma fluid. Thickened basement membranes and 
enlarged irregular plasmalemmae characteristi- 
cally defined the areas of intercellular accumula- 
tion of fluid. Intense pinocytotic activity among 
both epithelial and endothelial cells was evident ; 
additionally, some epithelial cells were exten- 
sively vacuolated. Red blood cells were seen in 
pulmonary capillaries, in alveoli and, in rare ob- 
servations, extravasated into the interstitium.^* 
That many of the erythrocytes had been sub- 
jected to osmotic stress was reflected in aber- 
rent red cell profiles ; some of these were swol- 
len while others conformed to the contours of 
adjacent endothelium or exhibited angular 
configurations. The cardinal ultrastructural 
pathologic changes seen were intra-alveolar 
hemorrhage, atelectasis, interstitial edema and 
endothelial swelling (Figure 3). 
Scanning Electron Microscopy 
By scanning microscopy at low magnification, 
the relationships among contiguous alveoli were 
seen. Pulmonary areas corresponding to those in 
which cytopathology was observed by transmis- 
sion or light microscopy showed focal pathology, 
as evidenced by fully opened alveoli adjacent to 
atelectatic areas. Alveoli in control tissues were 
Figure 3. — Transmission electron photomicrograph of lung tissue from group III (continually overloaded) dog. 
Type I epithelial cells are joined at J and show intense pinocytotic activity (p) and vacuolization (v). Marked 
widening of the interstitial space by edema fluid is seen between brackets. Hypoxemia is reflected by swollen mito- 
chondria (m). X 15,000. 
