To examine the relation between variations in the calcium level in the cytoplasm of liver remaining after hepatectomy following the application of ischemia and hepatocellular damage, we measured the calcium level in the cytoplasm of the liver with an X-ray microanalyzer. the effect of administration of a calcium antagonist was also examined. Using male Wistar rats we blocked the blood flow to the right lobe and caudate lobe of the liver for 60 min and then resected the left lobe in this experiment. The calcium antagonist was slowly administered in one shot through the portal vein before ischemia. There was no difference in the 7-day survival rate between animals given the antagonist and those not receiving it, but postoperative early deaths were decreased. The calcium level of the cytoplasm of liver, which had risen slightly during ischemia, was increased markedly during re-prefusion, but decreased thereafter. The serum GOT level was increased up to 2 hr after the release of ischemia. In the animals receiving the drug, the rise in the calcium level in the cytoplasm of liver and that in serum GOT were inhibited significantly. It was considered that administration of a calcium antagonist relieved hepatocellular damage by inhibiting the rise in the calcium level in the cytoplasm of the remaining liver and contributed to the decrease in postoperative early deaths.

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There is mounting evidence that gallstone formation after surgery for gastric cancer is caused by dysfunction of the gallbladder due to vagotomy. In order to evaluate the effect of vagotomy on gallbladder function, the author analyzed patients who underwent surgery for gastric cancer in our department and experimental models of guineapigs after vagotomy. The clinical study demonstrated that the postprandial contractile activity of the gallbladder was markedly impaired after gastrectomy with extended dissection of lymphnodes, which can not be performed with preservation of vagal innervation to the gallbladder. This finding emphasizes that vagotomy promotes the development of gallstone. In contrast, the physiological functioning of the gallbladder was well preserved after vagus-preserving gastrectomy. These results indicate that preservation of vagal innervation to the gallbladder may be highly significant in preventing the development of gallstone after surgery for gastric cancer. Vagotomy produced the formation of gallstone-like substance in the gallbladder in 27.5% of guinea pigs at 8 weeks after operation. The results of this study concerning the mechanism by which gallbladder function is regulated shows that the postpranidal contractile activity of the gallbladder may be mainly attributable to the vagus nerve. In addition, the author observed that vagotomy reduced the postprandial rhythmic contraction of the gallbladder in the experimental model of the guinea pig. These results led to the conclusion that vagotomy is critically involved in gallstone formation after surgery for gastric cancer.

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