Pancreatic O2 consumption and CO2 output during secretin-induced,exocrine secretion from the pancreas in the anesthetized dog

Secretin stimulates pancreatic water and CO₂ excretion as well as pancreatic blood flow. It has been questioned whether the production (i.e. water and CO₂ excretion) is reflected in the input-output difference of nutrients. In pentobarbital anesthetised dogs, pancreatic exocrine secretion was stimulated by secretin, (Karolinska), 1 U/kg injected as an i.v. bolus. Secretion was maximally increased at 2 min after the secretin shot and returned to a basal value at between 16 and 32 min after secretin. Blood flow was also maximally increased at 2 min, but decreased to the basal value at between 8 and 16 min. O₂ extraction first decreased (at 2 min) and then gradually increased until it was higher than the basal value (at 16 min) and then returned to the basal level (at 32 min). O₂ consumption increased quickly, reached a plateau, lasting from 1 to 16 min, and then decreased to the basal level (32 min). CO₂ transfer from blood to tissue reached a maximum at 4 min and then decreased to the basal value (at between 16 and 32 min). The curves for CO₂ transfer from tissue to pancreatic secretion and for CO₂ in the secretion had the same shape. It is concluded that the curve of production (of water and CO₂ excretion) parallels the curve of O₂ consumption fairly well. The O₂ consumption curve did not correlate either with the blood flow curve or with the O₂ extraction curve. About one quarter of the excreted CO₂ originated from pancreatic metabolism and the remaining three quarters were transferred from blood, through the pancreatic tissue into the secretion. The increase in O₂ consumption was achieved by an increase in blood flow, followed by an increase in O₂ extraction. The release of a vasodilator metabolite by the pancreatic cells upon arrival of the secretin molecules, may explain both the increase in blood flow and the successive increase in O₂ extraction. Therefore these data can be interpreted according to the model for metabolic control of tissue oxygenation.