[Surgery and postoperative care of aged patients with diseases of the liver, biliary tract, and pancreas].
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Biomedical subjects
Publications and source records attributed to A Kashii.
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Comparative studies were performed on changes in endocrine and exocrine responses of the pancreas after partial hepatectomy, partial pancreatectomy or combination of these procedures in rats, in order to clarify the effect of the combined operation on the remnant pancreatic parenchyma. Three days after partial (60%) pancreatectomy with partial (70%) hepatectomy, endocrine function was better preserved than after partial pancreatectomy alone, suggesting that hypersecretion of insulin initiated by partial hepatectomy may ameliorate the defective glucose-induced insulin secretion following partial pancreatectomy. Further, exocrine function in terms of amylase output was relatively well maintained 3 days after partial pancreatectomy + partial hepatectomy as compared with partial pan after partial pancreatectomy + partial hepatectomy as compared with partial pancreatectomy alone.
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The effect of obstructive jaundice on pancreatic amylase secretion was studied in isolated pancreatic acini prepared from bile duct ligated rats (7 days postoperatively), sham operated rats being used as control. Obstructive jaundice caused increase in pancreatic wet weight, pancreatic protein content and pancreatic amylase content by 27.9%, 40.1% and 33.2%, respectively. In acini prepared from obstructive jaundice group, compared with acini from sham operation group, responsiveness to cholecystokinin (CCK) and carbachol was decreased when amylase release was expressed as the percentage of total amylase activity initially present in acini. However, sensitivity to both secretagogues was unchanged when expressed as the percentage of maximally stimulated amylase release. The dose-response curves to Ca2+ ionophore for amylase release were similarly shaped in both groups. These results suggested that a pancreatico-trophic effect, compared with altered responsiveness of pancreatic acini, should play a major role in hypersecretion in obstructive jaundice.
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Insulin responses to oral glucose loads were studied in patients with obstructive jaundice and compared with those of other liver diseases (fatty liver, chronic hepatitis and liver cirrhosis), pancreatic diseases, and definite diabetes mellitus. Compared with their corresponding glucose intolerance, high insulin responses were characteristic in fatty liver, chronic hepatitis and liver cirrhosis, and insulin responses and insulinogenic index decreased in chronic hepatitis and liver cirrhosis as glucose intolerance progressed. In obstructive jaundice with the pancreatic ducts stenotic or obstructed, insulin responses were suppressed in comparison with their corresponding glucose intolerance, and also insulinogenic index were below 0.5 in most of the cases. However, in obstructive jaundice with the pancreatic ducts intact, high insulin responses were observed in almost half of the cases with insulinogenic index above 0.5, and insulin response and insulinogenic index decreased as glucose intolerance progressed. While most cases of fatty liver, chronic hepatitis and liver cirrhosis with insulinogenic index above 0.5 were distributed in non-diabetes zone in sigma BS-sigma IRI plane (Kosaka's), those with insulinogenic index below 0.5 were distributed in intermediate zone. Most cases with obstructive jaundice with pancreatic ducts stenotic or obstructed, had insulinogenic index below 0.5 and were distributed in diabetes zone. However, half of cases with obstructive jaundice with pancreatic ducts intact, had insulinogenic index above 0.5 and their distribution in non-diabetes zone, while the other half had insulinogenic index below 0.5 and their distribution in diabetes zone. Therefore, it may be concluded that insulin responses increase at the early stage of obstructive jaundice mainly under influence of liver dysfunction itself, but that insulin response is suppressed at later stage of obstructive jaundice as pancreatic islets are affected.
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This time trend of hemodynamics and mitochondrial functions were studied to determine whether the ligation of the hepatic artery would result in an antitumor effect on 3'-methyl-4-dimethylaminoazobenzene-induced hepatic carcinoma in rats. The studies revealed that the hepatic tumors were nourished predominantly by the artery and less by the portal vein; the size of the vascular beds in the hepatic tumors decreased as compared with those in the non-tumor area; and as the tumors grew larger, the artery became less predominant and the size of vascular beds decreased further. The mitochondria in the tumor were characterized by impaired growth, impaired oxidative phosphorylation, and by the low activity and nucleotide specificity of membrane bound ATPase. Hepatic dearterialization enhanced ischemia in the tumors and was accompanied by intensified impairment of the aerobic energy production, resulting in necrosis of the tumor. The effects of the dearterialization tended to decrease after the 5th day following the operation. In view of the gross findings upon relaparotomy and the recovery of hemodynamics and mitochondrial functions, this tendency appeared to be chiefly attributed to the increasing collateral circulation.
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