Experimental acute pancreatitis was produced in 63 mongrel dogs, by introducing staphylococcal toxin into the pancreatic duct. The effects of dexamethasone on survival rate, leucocyte counts, serum amylase, serum lipase, serum trypsin inhibitor, volume and pancreatic enzymes of the intraperitoneal exsudate and pathological findings of the pancreas, liver, kidney and adrenal gland. were observed. The results are summerized as follows: 1) In the 15 control dogs, there was a survival rate of 6.6% and in the fatal cases among them, there was a survival time less than 24 hours. In the 23 dogs treated with dexamethasone or dexamethasone and mycilline, survival rates were 30.7% or 50%, respectively, while in fatal cases, an improvement in survival time was found. Statisticaly significant differences were found between dexamethasone-treated dogs and the control group, as to survival rate and time. In 7 dogs treated with dextran, the survival rate was 14.3%, but the improvement in survival time was significant when compared with the con trol group. 2) As to leucocyte count, serum amylase, serum lipase, serum trypsin inhibitor, and volme and pancreatic enzymes of the intraperitoneal exsudate, there were No significant differences between dexamethasone-treated dogs and the control group. 3) In fatal cases, the pathological findings of the pancreas in treated dogs were identical with those observed in control dogs. In the sacrificed cases, the dextran and dexamethasonetreated dogs, in contrast to the dextran-treated dogs showed, after 12 hours slight pathological changes of the pancreas, liver and kidney, that is, pancreatic hemorrhage and necrosis, congestion of the sinusoid and edema of the Disse's spaces in the liver, and degeneration of the distal uriniferous tubulus in the kidney. 4) Adrenocortical hormones are considered beneficial in acute pancreatitis, probably due to, its anti-shock effect. In the treatment of acute pancreatitis, not only large dosis, of adrenocortical hormones, but an infusion adequate to maintain an effective circulating plasma volume, should be administered promptly, to reverse the hemodynamic deficits of this type of shock.
Six cases with protein-losing enteropathy, four with intestinal lymphangiectasia and two with constrictive pericarditis, were studied clinically with aid of RISA test, 131I-PVP test, peritoneoscopic examination, lymphangiography and thoracic duct cannulation. In the former, it was concluded that the duration of intestinal lymph congestion caused abnormal intestinal protein loss, and that the lymph congestion was attributed to the stenotic lesions of the lymphatic system located between mesenteric lymphatics and thoracic duct. In the latter, it was the primary cause of intestinal protein loss that the elevated venous pressure increased unusually lymph production and disturbed moreover lymph reflex to venous veins. Experimental study was designed to make clear the mechanism of abnormal intestinal protein loss in intestinal lymphangiectasia. The male rats fed on basal diet were injected intravenously with 2μc of 131I-PVP. The fecal excretion of 131I-PVP within 24 hours after injection were determined. When the mesenterial lymphnodes were resected as many as possible, no difference between normal and five days group was found. Abnormal fecal excretion of 131I-PVP were demonstrated in about half numbers of each group from one to seven weeks. That is, about one week duration of lymph congestion seemed to be necessary for giving rise to abnormal intestinal protein loss. After the thoracic duct ligation, abnormal fecal 131I-PVP excretion was seen in each group from one to four weeks. But it was not demonstrated after five weeks, suggesting that the collateral formation of lymph vessles saved the intestine from lymph congestion and abnormal protein loss. In the immunized group with isologous lymphnode homogenate incorporated in Freund's complete adjuvant, abnormal 131I-PVP excretion were shown in four of six animals at five weeks after thoracic duct ligation. The collateral lymph vessles formation was believed to be disturbed by this immunological procedure. Even in the immunized group with Freund's complete adjuvant only, abnormal 131I-PVP excretion were demonstrated at five weeks after thoracic duct ligation. Accordingly, the disturbance of collateral lymph vessles formation was attributed to the lymphatic tissue damage, which was developed presumably on the basic of either specific or non-specific hyper-immune reaction of lymphatic tissue. Besides, some case of the above-mentioned two kinds of immunized groups, who received no ligation of thoracic duct, revealed also abnormal 131I-PVP excretion. It was supporsed that the stenotic lesion of lymphatic tissue and the disturbance of collateral lymph vessles formation were could be originated by these immunological procedures.
There are renewed interests on the role of pancreas in iron absorption, and in particular, on the relationship between pancreatic disease and hemosiderosis. Using ferrous chloride labeled with 59Fe, the author has performed the experimental studies to investigate the relationship between external pancreas function and gastrointestinal iron absorption in dl-ethionine treated rats. The result were summarized as follows; 1. Although the percentage of iron absorbed was decreased with ncreasing dosage, the total quantity was increased continuously in normal rats. 2. Using the fecal recovery method, the absorption rate of iron administered in stomach was higher in dl-ethionine treated rats than in normal rats. 3. It was found that iron absorption, in dl-ethionine treated rats as well as in normal rats, should occur mainly through the pathway of hemosiderin or so-called free iron, and that the pathway of ferritin, which had been regarded as main component of iron transport, did not concerned with the absorption of iron. 4. In dl-ethionine treated rats, iron metabolism of hemosiderin in the gastrointestinal mucosa was activated and iron absorption was increased. The turnover of hemosiderin was remarkable in contrast to that of ferritin. 5. In dl-ethionine treated rats, the absorbed iron from the gastrointestinal tract was largely incorporated into liver and poorly into red blood cells comparing with normal rats. 6. Using a in vivo loop of segmented gastrointestinal tract, iron was more absorbed from duodenum and jejunum in dl-ethionine treated rats than in normal rats. 7. It was revealed that pancreatin had been shown to inhibit intestinal iron absorption in normal and dl-ethionine treated rats and its inhibition was more remarkable in dl-ethionine treated rats. 8. The pH of the gastrointestinal contents did not show any significant difference between in dl-ethionine treated rats and in normal rats. 9. It was found that dl-ethionine treated rats showed the increase of serum iron, hemoglobin and hematocrit, and the increase of hepatic non-hemin iron.