The release and degradation of endogenous gastrin was studied using electrical vagal stimulation in the anesthetized dog. A mathematical model was developed to describe the rates of release and degradation of the gastrin hormone.Recently Nilsson et al.(1) reported that endogeneous gastrin is released rapidly into the circulation in response to sham feedings; however, while sham feeding they do not describe in detail the hormone's rate of release.The rate of degradation of endogenous circulating gastrin (as well as for the heptadeca-, penta-and tetrapeptide of the hormone) has been studied and was also found to be rapid (2-7). However, the conditions under which the studies were carried out were not appropriate for detailed measurement.Materials and Methods. Female mongrel dogs weighing 15-25 kg were fasted at least 18 hr prior to receiving 2 mg/kg morphine sulfate subcutaneously. Thirty minutes after receiving the morphine, the dogs were anesthetized with 100 mg/kg chloralose intravenously. A catheter was placed into the portal vein for sampling blood. The pyloric end of the stomach was ligated and an acute gastric fistula was made in the most dependent portion of the stomach. Gastric secretions were collected under vacuum. The cervical vagi were isolated bilaterally and the distal cut ends placed on platinum electrodes. The vagi were stimulated using 7 V, 10-15 Hz and 5 msec duration as the stimulus parameters (8). After a 60-min control period in which blood samples (5 ml vol) were taken at 15-min intervals, the vagi were continuously stimulated for 30 min. With the onset of the stimulus, blood samples were taken from the portal vein at 2.5-niin intervals for the entire period of stimulation. At the end of this period of stimulation, blood samples were taken every 2.5 min for the first 15 min; then a t 5-min intervals for the next 15 min; and finally every 15 min for the next 30 min. The blood was allowed to clot and the serum was stored at -20' until assayed.Gastric acid concentration (mEq/liter ) and output were determined electrometrically by titrating the gastric juice with 0.1 N sodium hydroxide to an endpoint of pH 7.0. Serum gastrin concentrations were determined by the double-antibody radioimmunoassay method of McGuigan (9).Results. Figure 1 shows the changes in circulating serum gastrin levels in response to electrical vagal stimulation. Basal gastrin levels prior to stimulation were 55-71 pg/ml with a mean of 62 t 3 (SEM) pg/ml.Electrical stimulation of the vagus produced a rapid and statistically significant rise in circulating serum gastrin concentrations within 2.5 min of onset of stimulation ( p < 0.05).Average concentrations between 150 and 175 pg/ml were noted during this early period of stimulation. The levels of gastrin remained constant for the next 10 min. At that time gastrin levels appeared to increase further but the rise was not statistically significant
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