Endocrine Function of the Pancreatic Allograft1

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Abstract
Transplantation of the pancreaticoduodenal allograft was performed in 30 totally pan-createctomized dogs. Ten host dogs served as controls and the remaining 20 were treated with azathioprine to suppress the immune reaction. The control group lived for an average of 10 days (3-20 days) and the immuno-suppressed group for an average of 22 days (7-63 days). In the control group, fasting blood sugar was generally between 60 and 120 mg/100 ml for several days after transplantation, but tended to increase 1-2 days before death. In a majority of the azathioprine-treated group, fasting blood sugar remained within 60 to 120 mg/100 ml throughout their post-transplantation periods. In azathioprine-treated hosts, fasting plasma insulin, determined by radioimmunoassay, tended to increase between the 2nd and 8th days and gradually declined thereafter. Intravenous glucose tolerance (1.0 g/kg) tests were done 13 times on 12 azathioprine-treated hosts. In 4 of 10 tests done between the 7th and 16th post-graft days, glucose tolerance was normal and the peak of plasma insulin reached 100 to 300 [mu]U/ml. In the other 6 tests, glucose tolerance was somewhat impaired and the peak of plasma insulin was less than 75 [mu]U/ml. In 3 tests done at about the 5th week, glucose tolerance was obviously impaired and plasma insulin response was poor, never exceeding 30 [mu]U/ml. Gross and microscopic findings of pancreatic allograft at autopsy revealed either severe necrotic pancreatitis or fibrotic shrinkage of the graft. The latter was found only in azathioprine-treated hosts living longer than 3 weeks. Islet cells with beta granules were recognizable in the latter. The transplanted pancreas deprived of nervous control secretes insulin and is capable of maintaining a normal level of the fasting blood sugar at least for 5 weeks. Glucose tolerance and insulin response deteriorate together gradually in the post-transplantation period, suggesting that the decreased reserve capacity of viable islet cells is unable to control the glucose load.

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