214 
PULMONARY MODELS 
Figure 5. — After fifteen minutes, there is massive capillary and precapillary engorgement with partial occlusion 
of small arterioles by erythrocyte aggregates. The veins are distended with plasma, but nearly devoid of cells. 
There is also marked atelectasis, and interstitial and intra-alveolar hemorrhage. 
the vascular endothelium, our studies do not 
implicate primary endothelial damage in the 
process although it could have occurred. What 
we saw was a very rapid me.^hanical plugging 
of capillaries and then arterioles by the dense 
erythrocyte aggregates. This was followed, as 
rejection progressed, by interstitial and intra- 
alveolar edema, hemorrhage, and atelectasis. In 
no instance, either on in vivo microscopy or his- 
tologic examination, could we find evidence that 
either platelets or leukocytes were initiating 
the process. Although it is possible that small 
numbers of platelets may be surrounded by the 
erythrocyte aggregates, this was not demon- 
strated by light microscopy. 
Of particular interest were our previously re- 
ported studies of lungs in intact cats after dog 
blood or plasma infusion.^ Infusion of whole 
dog blood into the cat produced changes in the 
cat lungs on in vivo microscopy and histologic 
examination identical to those seen in xeno- 
grafted cat lungs. Almost identical changes oc- 
curred when cell-free dog plasma was infused 
into the cat lung. When the dog plasma was 
first absorbed repeately with cat erythrocytes, 
the process did not occur. After an hour there 
were essentially no intravascular changes. This 
is consistent with the findings of Linn, Moberg 
and their co-workers that absorption of xeno- 
geneic plasma by donor red cells or antigen de- 
layed the manifestations of hyperacute rejec- 
tion.*-^ The findings also suggest that anti-cat 
antibody initated the erythrocyte agglutination 
process in our infusion model.- In addition, our 
infusion studies show that the presence of a 
foreign erythrocyte is not necessary for the 
