F. K. MERKEL 
379 
Figure 7. — The histopathology of the rejecting canine 
allograft. This is acute rejection characterized by a 
round cell invasion of the gland including the islets 
of Langerhans (IL), widening of the interlobular fis- 
sures and disruption of the acinar tissue. These fea- 
tures are common to renal transplantation and 
indicate that endocrine tissue is not immune from 
immunologic attack. 
tion reaction two weeks after the operation. 
This was directed against the pancreas, the duo- 
denum and the kidney, and was characterized 
by oliguria, elevated blood urea nitrogen and 
creatinine, elevated blood sugar, fall in circula- 
tory plasma insulin, and a decrease in the amy- 
lase content and volume of the duodenal juice. 
Figure 8. — Budding off of new beta cells in the trans- 
planted canine pancreas. This is occurring under the 
influence of steroids used to prevent rejection. Note 
the beta cells (B) arise from the epithelium of the 
pancreatic duct (PD). 
Figure 9. — Fibrosis appearing in biopsy taken 55 days 
after transplantation of this canine pancreas. 
The duodenal mucosa became grossly edema- 
tous, hemorrhagic, and sloughed. A massive 
hemorrhage from the stoma occurred requiring 
transfusion and iced saline lavage of the duo- 
denal segment. Biopsies showed a round cell in- 
filtrate and mucosal slough of the duodenal seg- 
ment. With appropriate anti-rejection therapy, 
both renal and pancreatic function improved 
and the mucosa of the stoma regenerated. The 
FASTING BLOOO GLUCOSE 7 DAYS AFTER PANCREATIC ISCHEMIA 
0 30 60 90 lao IM 
DURATION OF ISCHEMIA - MINUTES 
Figure 10. — Fasting blood sugar levels after varying 
periods of normothermic ischemia to the isolated 
pancreas segment in the dog. Note that no abnormal- 
ity is seen until 120 minutes. 
