Pancreaticoduodenal artery (PDA) aneurysm and celiac artery (CA) stenosis are rare diseases in themselves. Interestingly, however, there are more cases documented in the literature in which these two disease entities occurred together than could be coincidental, and CA stenosis has been suggested as the provocative condition in developing PDA aneurysm. This study is aimed at examining the causal relationship between CA stenosis and PDA aneurysm by simulating the splanchnic circulation with an electric circuit. A patient with multiple PDA aneurysms and collaterals with CA stenosis was treated in our institution using hybrid techniques. The patient’s pre- and postoperative status was simulated using an electric circuit, and the two possible scenarios were tested for compatibility: the stenosis-first scenario vs. the aneurysm-first scenario. The simulation was performed in two ways: using Simulink® software (MATLAB® Release 2018b) and actual circuit construction on a breadboard. The stenosis-first scenario showed that as the CA stenosis progresses, the blood flow through PDA increases, favoring the development of an aneurysm and/or collaterals if the artery was already compromised by a weakening condition. On the other hand, the aneurysm-first scenario also showed that if the aneurysm or collaterals developed first, the aneurysm will steal the blood flow through the CA, causing it to collapse if the artery was already compromised by increased wall tension. Contrary to the common belief, this study showed that in patients suffering from concurrent CA stenosis and PDA aneurysm, either condition could develop first and predispose the development of the other. The simulation of splanchnic blood flow with an electric circuit provides a useful tool for analyzing rare vascular diseases that are difficult to provoke in clinical and animal studies.

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Objectives It is unclear whether the improved glucose metabolism in pancreas head cancer (PHC) patients after pancreaticoduodenectomy is due to the anatomical change or the relief of pancreatic duct obstruction. Methods We divided 170 patients into the PHC group (n = 54, 31.8%) and other pathology (non-PHC) group (n = 116, 68.2%). Glucose metabolic function was evaluated using the glucose tolerance index (GTI), and the pancreatic duct obstruction and dilatation was measured using the pancreatic atrophic index (PAI). Results The preoperative GTI was significantly higher in the PHC group (mean [standard deviation {SD}], 0.84 [1.16]) than in the non-PHC group (0.41 [SD, 0.59], P = 0.000). The postoperative GTI decreased significantly in the PHC group but remained unchanged in the non-PHC group. Similarly, the preoperative PAI was higher in the PHC group (0.32 [SD, 0.19]) than in the non-PHC group (0.13 [SD, 0.09], P = 0.000). The postoperative PAI decreased significantly in the PHC group, but not in the non-PHC group. Conclusions The impaired glucose metabolism in PHC can be caused by pancreatic duct obstruction. After pancreaticoduodenectomy, glucose metabolism is improved by the relief of pancreatic duct obstruction, and not by the anatomical change. The patients should be counseled accordingly.