Morphologic and functional evidence of reinnervation of the gastric parietal cell mass after parietal cell vagotomy.

The incidence of recurrent ulceration after parietal cell vagotomy varies greatly and the cause is largely unknown. Whether the vagus nerve can regenerate or reinnervate the gastric parietal cell mass after parietal cell vagotomy was investigated. Careful microscopic dissection of the neurovascular bundle in 130 rats allowed the vagus nerve to be divided to the gastric body with preservation of the antropyloric nerve and gastric vasculature. Gastric secretory tests were performed under basal and stimulated conditions after secretagogue and insulin hypoglycemia stimulation. Rats were killed weekly and the vagal nerve distribution examined by electron microscopy. Stimulated gastric acid output decreased from 164 to 26 mumol/hour immediately after operation (p less than 0.001). One week after parietal cell vagotomy the nerves were swollen with fibroblast infiltration and collagen around axon groups showed degeneration. By the third week after parietal cell vagotomy, the axons were more densely packed with neurofilaments and acid output had increased to 183 mumol/hour. In the fourth and fifth weeks, the enlarged Schwann cell processes had more axons and acid output increased to 262 mumol/hour. By the seventh week, both large and small axons were identified and the acid output was 93 percent higher than the preoperative level (p less than 0.001). The sequential neuropathologic changes of vagus nerve degeneration, regeneration and functional reinnervation of the gastric parietal cell mass after parietal cell vagotomy are shown by this study. If this occurs in man, it may be an important cause of recurrent peptic ulceration after parietal cell vagotomy.