抄録
Effect of the infusion of acetylcholine on the secretion of gut glucagon immunoreactivity (gut GI) that was measured using C-terminal specific glucagon antiserum after pancreatectomy, and gut glucagon-like immunoreactivity (gut GLI) that was obtained by subtracting GI from total glucagon-like immunoreactivity (total GLI) which was measured using non-specific glucagon antiserum, was investigated in sixteen pancreatectomized dogs untreated with insulin, in order to demonstrate whether the secretion of gut GI and gut GLI is influenced by the parasympathetic nervous system.
During the infusion of acetylcholine at a rate of 10μm/kg/min, gut GI in the femoral venous blood showed a significant increase from the basal value of 181±22pg/ml to a maximum of 569±107pg/mI at 30min (p<0.01), and “true gut GI secretion increment” in the portal venous blood showed a maximum significant increase of 916±144% at30min from the basal value (p<0.001). However, gut GLI showed no significant change. One shot administration of atropine at a rate of 15μg/kg could significantly inhibit the stimulatory effect of acetylcholine on gut GI (p<0.05-0.001).
It is concluded that the parasympathetic nervous system might play an important role in the control mechanism of the release of gut GI, but not of gut GLI in pancreatectomized dogs untreated with insulin.
