The effect of terbutaline on exocrine function in the denervated canine pancreas.

This study was designed to evaluate the effects of the beta adrenergic agonist, terbutaline, on pancreatic exocrine secretion in the denervated canine pancreas. In vitro assessment was performed by evaluating the effect of terbutaline on 10(-8) OP-CCK stimulated amylase release of pancreatic tissue slices incubated at 37 degrees C in Krebs-bicarbonate media. In vivo assessment was accomplished in animals with pancreatic autografts and functioning pancreaticocystostomies, by evaluating the effect of intravenous terbutaline (0.075 mg/kg over 15 min) on the basal, and OP-CCK (125 ng/kg/hr)--stimulated, rate of secretion of urinary (autograft) amylase and bicarbonate. Incubation of tissue slices with terbutaline had no significant effect on OP-CCK-stimulated amylase release. The intravenous terbutaline infusion resulted in a decrease in the basal rate of amylase (U/min) and bicarbonate (mmol/min) secretion, with the bicarbonate inhibition being significantly decreased, when compared with controls (0.073 +/- .04 vs. 000 +/- .00; P less than 0.05). Following the terbutaline infusion, there was also a significant decrease in OP-CCK-stimulated amylase (140.3 +/- 23.3 vs. 24.6 +/- 11.9; P less than 0.005) and bicarbonate release (.069 +/- .03 vs. .003 +/- .001; P less than 0.05). This inhibition persisted until the study was terminated 3 hr after the terbutaline infusion. These studies demonstrate that terbutaline causes a significant and prolonged decrease in autograft exocrine secretion--and, as a result, may have a therapeutic role in reducing the exocrine complications associated with pancreatic transplantation. The mechanism of action of this agent in the denervated pancreas requires further elucidation.