Respiratory exchanges and acid-base balance during perfusion of ex vivo isolated pancreas.
We used the technique of ex vivo isolated pancreas, perfused with whole heparinized blood. The organ was stimulated by secretin (G.I.H. Stockolm, 0.1-5.0 clinic units/hr), and/or carbamylcholine (100-200 mug/hr). Oxygen consumption was increased under stimulation. This increase was a function of the dose of secretin and also of the bicarbonate output in the juice. Oxygen uptake increased further when carbamylcholine was super-imposed on secretin. This extra increase was independent of hemodynamic conditions of the organ perfusion. Arteriovenous difference in oxygen saturation did not increase when the gland was stimulated. It tended to decrease when the stimulation resulted in a marked vasodilatation. Thus, oxygen needs seemed to be neither the limiting factor of the response to a given stimulation nor the triggering mechanism of functional vasodilatation. Values of pCO2 were spread over a wide range from one experiment to another. However, it could be observed that CO2 efflux into the vein decreased under stimulation by secretin; in most experiments, CO2 efflux was even replaced by an apparent consumption of CO2 during the perfusion of the stimulated gland. Furthermore, arteriovenous pH difference increased following secretin stimulation. This increase was dose-related to secretin. These facts are discussed under the background of theories recently proposed for bicarbonate secretion.
D000136:Acid-Base Equilibrium / Q000187:drug effects; D000818:Animals; D002217:Carbachol / Q000494:pharmacology; D002245:Carbon Dioxide / Q000378:metabolism; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D006439:Hemodynamics; D008954:Models, Biological; D010101:Oxygen Consumption / Q000187:drug effects; D010179:Pancreas / Q000378:metabolism*; D010477:Perfusion; D012633:Secretin / Q000494:pharmacology
D012633:Secretin; D002245:Carbon Dioxide; D002217:Carbachol