COOK, SPEILLER, SLAUSNER, SINHA, KIKKAWA AND VEITH 
211 
obstructions to the microcirculation. As the 
process progressed, the size of the red cell ag- 
gregates increased so that progressively larger 
arterioles became plugged. Eventually all flow 
in these vessels stopped. The venous side of the 
circulation showed evidence of plasma stream- 
ing and acellularity suggesting that the red cell 
aggregates were becoming caught in the ar- 
terioles and capillaries. The dogs were heparin- 
ized and intravascular thrombosis was not ob- 
served in vivo or in the fixed microscopic 
sections. 
The rejected lungs were grossly heavy and 
dark red. The degree of involvement varied in 
a mosaic distribution similar to the normal sub- 
total perfusion pattern of lungs in resting 
animals.^ On fixed section, the changes were 
most marked in those parts of the lung where 
flow was initially greatest. Serial biopsies re- 
vealed the sequence of events shown in figures 
2-5. Immediately after the cat lungs were first 
perfused with dog blood, the perfused areas 
were found to be massively engorged with 
erythrocyte aggregates (Fig. 3). These aggre- 
gates filled the alveolar capillaries and small 
arterioles. Often these areas of severe erythro- 
cyte aggregate engorgement were adjacent to 
areas that were completely normal. By ten 
minutes this congestive process was widespread 
and became more pronounced. Interstitial and 
intra-alveolar edema were seen at this time 
(Fig. 4). After 15 minutes, the capillary en- 
gorgement had reached its maximum extent and 
severity. In many cases when this was severe, 
it was associated with atelectasis. At this stage, 
interstitial and intra-alveolar hemorrhage were 
seen. Despite the marked engorgement of the 
capillaries, the veins contained only plasma with 
V 
7 
*1 
I 
Figure 2. — Normal cat lung showing thin alveolar septa with a few isolated erythrocytes (arrow) and occasional 
polymorphonuclear leucocytes and monocytes. This biopsy was taken before dog blood entered the cat lung. 
