COOK, SPEILLER, SLAUSNER, SINHA, KIKKAWA AND VEITH 213 
Figure 4. — After ten minutes, focal congestion has become diffuse and marked. Although no atelectasis has oc- 
curred, there is both interstitial and intra-alveolar edema. 
is probably related to the subtotal perfusion 
pattern which normally occurs in the lung.^ 
Hyperacute rejection of renal allografts has 
been characterized by the presence of conges- 
tion, endothelial distruction, focal vascular 
thrombosis, hemorrhage, and platelet and 
leukocyte plugging of capillaries, arterioles, 
and occasionally venules.^ '^'^'ii On the basis of 
our study, it would appear that the primary 
event in hyperacute rejection of the lung 
is erythrocyte aggregation. This aggregation 
seems to be an important factor in causing 
the cessation of blood flow, and in our studies 
was noted before any other alterations in the 
microsvasculature could be observed either by 
histologic study or by in vivo microscopy. Al- 
though preformed recipient antibodies have 
been implicated in other forms of hyperacute 
rejection, it is difficult to see how these anti- 
bodies could lead directly to the erythrocyte ag- 
gregation in the xenograft models in our stud- 
ies.*'^*^ All donor blood was removed from our 
xenografts prior to their transplantation. 
Therefore, after establishment of the recipient 
circulation to the xenograft, only recipient 
antibody could be present in large amounts. For 
this to agglutinate recipient red cells, it must 
first damage some element of the donor lung 
and we observed no morphologic evidence of 
injury to graft structures such as endothelium 
early in the hyperacute xenograft rejection 
process. 
The red cell aggregation was not modified by 
heparinization, and thrombosis was not ob- 
served. Thus, simple intravascular coagulation 
was not a primary event in the hyperacute re- 
jection process in our studies. Since neither 
erythrocytes nor their aggregates adhered to 
