LIGATION OF PANCREATIC DUCT

Summary Ligation of the pancreatic duct was performed on 34 animals. In 4 of them, the experiment could not be completed. Of the remaining 30 animals, 10 were non‐diabetic (group III A). Five animals were alloxan‐diabetic before operation (group III B), and in 15 the effect of alloxan was tested after ligation, either about 68 days later (group III C a) or 11 days later (group III C b). The controls consisted of 8 animals; 4 of them were untreated (group IV A), and in 4 the left ureter was ligated (group IV D). The alloxandiabetic controls described in Chapter 6 (group IV G b) served as additional controls. An account of the course is given. The general condition of the animals was unaffected, and a postoperative nutritional disturbance was observed in one case only. A gain in weight was recorded in most of the other cases. Transient diastasuria appeared postoperatively. It was maximal during the first 2 days after operation, but disappeared 4 to 6 days after it (Table19). A glucose tolerance test was made postoperatively in 9 animals in group III A; in 8 of them it was entirely within the normal range of variation. In the remaining animal, a completely abnormal curve of “diabetic” type was recorded. In contrast to the others in this group, this animal had transient glycosuria postoperatively (Table I: 8). Glucose tolerance tests made in 5 animals in group III C a after alloxan administration showed signs of decreased tolerance in every case (Table 1: 9, Fig. 51). The diabetic condition of the animals in group III B showed no changes as to glycosuria and insulin requirement after ligation of the duct (Table 21). Complete resistance to the diabetogenic effect of alloxan given in large repeated doses was noted in group III C a, and partial resistance in group III C b (Table 22). Autopsy showed complete exocrine atrophy of the pancreas in all the animals in groups III A, III B and III Ca, with one exception. In this case (in group III A) an extremely small remains of the gland was present in the pyloric region. In group III C b, the exocrine parenchyma exhibited marked regressive changes , although there was not yet complete atrophy. Quantitative analysis of the islet tissue showed a decrease in islet volume of 40 to 55 per cent in group III A in relation to the controls, but a normal alpha cell incidence. In group III B, the islet volume was of the same order of magnitude as in the non‐operated alloxan‐diabetic controls. The alpha cell incidence was much higher than normally, but not fully as high as in the diabetic controls. In group III C a, the islet volume was distinctly greater than in both preceding groups, and as large as in control group IV D. The alpha cell incidence in group III C a was higher than in the other non‐diabetic animals, but lower than in the diabetic animals in group III B (Table 23). In all the duct‐ligated animals, the individual islet size was smaller but the number of islets greater than in comparable controls with functioning exocrine parenchyma. In no case were any signs observed of damage to the liver parenchyma. The lipid and glycogen content of the liver cells was the same as in the controls (Table 12). The results are discussed. They are, on the whole, in agreement with those obtained by BENSLEY, indicating that, in the rabbit pancreas, both regressive and progressive processes in the islet tissue occur after ligation of the pancreatic duct. It was not possible to confirm earlier statements of hyperplasia of the islet tissue after this intervention. The alloxan resistance of duct‐ligated animals also confirms earlier investigations (WALPOLE & INNES). It cannot be explained by supposed islet tissue hyperplasia (DE MOOR), by impairment of the blood supply (ADAMS) or by postulated liver damage, masking diabetes (FERNER). In my opinion, the alloxan resistance is dependent on the “foetal” nature of the islet tissue after ligation of the pancreatic duct (CAPPELLATO & PERISSONOTTO), the absence of active external secretion possibly being an important factor. Support is lent to this view by the results of similar investigations (HUGHES & HUGHES, HULTQUIST & THORELL, SHULTZ & DUKE).