Influence of Neural Blockages and Proglumide on Rat Pancreatic Enzyme Secretion in Response to Intraluminal Fatty Acid

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Abstract
Effects of neural blockages on pancreatic enzyme secretion in response to infusion fatty acid into the lumen were investigated using anesthetized rats, equipped with bile-pancreatic and duodenal cannulae, to evaluate the relative contribution of the neural and the hormonal mediations in the pancreatic response. Oleate (0.2 ml) was injected as a bolus into the rat duodenum, and the trypsin output in bile-pancreatic juice was monitored to determine the pancreatic enzyme secretion response with continous return of bile-pancreatic juice to the intensine. When anticholinergic agents such as atropine sulfate and scopolamine were administered, although basal level in pancreatic enzyme secretion fell, the increase of pancreatic enzyme secretion from the basal level after stimulation by oleate was not significantly different from that of the control (no blockage). However, the ganglion blocker, hexamethonium, inhibited the pancreatic enzyme secretion in response to oleate by 94%. An adrenergic blocker, guanethidine, also led to as much of a decresae as the ganglion blocker-induced decrease. Adrenergic .alpha.- and .beta.-blockers partially, but not completely, inhibited the enzyme secretion. Adrenergic blockage also suppressed the basal level in pancreatic enzyme secretion. On the other hand, a specific CCK antagonist, proglumide, significantly inhibited pancreatic enzyme secretion induced by oleate in the presence of scopolamine. These observations suggest that pancreatic secretion in response to oleate is primarily mediated by CCK and that adrenergic modulation may play an important role in the CCK-mediate pancreatic enzyme secretion in response to oleate, although interpretation of these results may have some restriction related to anesthesia.