[Long term follow-up-study of selective vagotomy with pyloroplasty--physiological and electron microscopical studies of gastrin].

The function of residual G cells after selective vagotomy with pyloroplasty (SV + P) in 24 duodenal ulcer patients was assessed by physiological and electron microscopical studies. We studied the mechanism of gastrin release following insulin-induced hypoglycemia with respect to plasma catecholamines in mongrel dogs. Basal serum gastrin was significantly increased one month after surgery. Integrated gastrin response to meat extract and insulin hypoglycemia stimulation was also increased significantly six months postoperatively. The G cells were still increasing in number six months after SV-P, and G cell hyperplasia became more remarkable after one year. Emiocytotic figures were observed in denervated G cells which were stimulated by meat extract or insulin hypoglycemia. Both serum gastrin and plasma epinephrine began to increase 15 minutes after administration of insulin, peaked at the 45th minute, and decreased thereafter in control dogs and vagotomized dogs. In bilaterally adrenalectomized dogs, both responses were significantly inhibited. In control dogs, the gastrin response was seen under continuous infusion of epinephrine (0.5 micrograms/kg/min). Therefore, our results suggest that regardless of the presence or absence of vagal innervation, gastrin is released from G cells mainly due to epinephrine secreted from the adrenal medulla under insulin-induced hypoglycemia.