The Japanese Journal of Gastroenterological Surgery

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Twenty dogs orally given acrylamide developed an esophageal achalasia-like lesion, and esophageal motility and axonal degeneration of the vagus nerve were investigated electrophysiologically and electron microscopically. From 7 weeks after the start of acrylamide administration, vomiting, diarrhea and weight loss were observed in addition to neurological distrubances such as ataxia and muscle weakness of the hind limbs. The largest transverse diameter of the lower esophagus was 16.8±1.85 mm in the control group and was significantly (p<0.01) increased to 28.9±2.26 mm in the late stage of administration in the treated group. Lower esophageal sphincter pressure (LESP) was significantly (p<0.01) increased to 29.6±4.4 cmH₂O in the treated group. By a set of electrodes stimulating the cervical vagus nerve, the percentage of the fall values [(LESP-LESP with vagal stimulation) /LESP) ×100%] was decreased significantly in the treated group. The coefficient of variation of the R-R interval in ECGs was 1.49±1.09% in the control group and was significantly (p<0.05) decreased to 0.77±0.45% in the treated group. In the histologic examination, no changes in the esophageal ganglionic cells were observed in the treated group. Axonal degeneration of the vagus nerve in the treated group was revealed by electron microscopy. From these observations it seems mandatory to seek the cause of esophageal achalasia not only in the esophageal ganglionic cells but also in the central to peripheral nervous system.

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In the specialty of the gastroenterological surgery, surgeons are often confronted with treating disease states of the liver in which the circulation is acutely or chronically impaired, and in some cases surgical procedures which result in circulation derangement have to be instituted. In this study, new simplified computer simulation models were built to analyze 1) liver circulation with the hepatic artery or portal vein ligated, 2) graded arterialization of the portal vein with the hepatic artery ligated, and 3) splanchnic and hepatic circulation in portal hypertension, all of which would be encountered in clinical and research settings with relative frequency. All simulations were performed with the general purpose simulator PSpice. By altering the main determinants of the hepatic circulation, such as arterial pressure, intrahepatic, splanchnic vascular resistance and/or shunt resistance, most of the hemodynamic changes induced by liver diseases or by surgical procedures can be simulated well.

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