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SUMMARYThe recently reported vagal nerve stain leucomethylene blue was assessed in 20 patients as an intraoperative aid to attaining complete vagotomy. Of 101 stained specimens removed at surgery, only 30 (30%) contained nerve tissue. Four of 17 postoperative insulin tests were positive by Hollander's criteria. The dye technique was found to be an unreliable method of ensuring complete vagotomy at the time of surgery.Due to the high incidence of incomplete vagotomy (Davies, 1956;Ross and Kay, 1964;Johnston, Thomas, Checketts, and Duthie, 1967) there is a need for a simple and reliable intraoperative method for achieving complete vagal section. Lee (1969) recently described a selective nerve stain, leucomethylene blue', which he claimed reliably stained small vagal fibres. The present report describes our experience with the dye in 20 patients. Material and MethodsFor this study 20 patients undergoing vagotomy for peptic ulcer disease were selected at random over a three-month period. The operations were performed by 14 different surgeons but the stain was applied and the specimens removed in each instance by one of the authors (M.L.F.).The technique employed was similar to that described by Lee with the exception that the left gastric artery was not divided. After dissection of the peritoneum and division of both main vagal trunks, leucomethylene blue was applied to the bared anterior and posterior surfaces of the oesophagus using a cotton swab. Considerable

This study was performed to determine the effects of vagotomy on the gastric mucosal resistance to ethanol injury that develops in the rat in response to prolonged mild restraint. The resistance to ethanol injury up to 4 days after cessation of chronic mild restraint (CMR) was also examined. Intragastric administration of ethanol/acid to rats previously subjected to 10 days of CMR produced significantly (P less than 0.0001) less damage than to the mucosae of control rats. While previous exposure to CMR appeared to prevent the necrotic gastric damage induced by ethanol, damage to the surface epithelium was not prevented. When similar experiments were performed on CMR and control rats that had truncal vagotomy, the extent of ethanol/acid injury in the two groups was not significantly different. Intragastric administration of ethanol/acid to 8-day CMR rats produced 91% less (P less than 0.005) gastric damage than in control rats. When ethanol was administered 2 days after cessation of CMR, the gastric injury was still significantly less (P less than 0.01) than in control rats. However, when ethanol was administered 4 days after cessation of CMR, the resulting damage was not significantly different from that of control mucosae. These studies suggest that intact vagal innervation may be necessary for adaptation of the gastric mucosa to chronic mild restraint. These adaptive changes are still present up to 4 days after cessation of the restraint procedure.