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J P Pascal

Publications and source records attributed to J P Pascal.

At least 109 records · Page 6Linked to original sources

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.

Acid-Base Equilibrium↗

Role of cholinergic mechanisms in the response to secretin of isolated canine pancreas.

The effects of carbamylcholine (CCH, 100 mug per hr) and of atropine (0.25, 1.0, and 10.0 mg per hr) on the response of the exocrine pancreas to secretin (0.1, 0.5, and 5.0 clinic units per hr) were studied using the isolated canine pancreas perfused with whole heparin-treated blood. CCH induced a sharp decrease in D50 (dose of secretin which elicits half the calculated maximal response) but no increase in maximal response to secretin. Experiments performed under different haemodynamic conditions show that this potentiating effect (synergism) is partly due to vasomotor modifications and chiefly to the action of CCH on the receptor of secretin. Although this work indicates that cholinergic tone is not necessary for secretin-induced hydrelatic response to occur, it evidences that this cholinergic tone plays a major role in modulating the pancreatic response to submaximal doses of secretin. It has also been found that large doses of atropine (10 mg per hr) were necessary to achieve a complete inhibition of enzymatic response to CCH. Even at these high doses, however, enzymatic response to secretin and cholecystokinin-pancreozymin were not significantly inhibited.

Animals↗

Relationships between blood flow and secretion in the isolated perfused canine pancreas.

1. Stimulation by a continuous intra-arterial infusion of secretin caused a marked vasodilatation in the pancreato-duodenal preparation or in the isolated pancreas perfused with whole heparinized blood. There was no difference in the vasomotor effects of two unequally purified preparations of secretin. The fact that the vasodilatation was still observed when the duodenum was removed proved that the haemodynamic effect of secretin was initiated in the pancreas itself.2. The secretory response of the pancreas to a given dose of secretin was larger when the blood pressure was kept constant by increasing the blood flow than when the blood pressure was allowed to fall by maintaining the blood flow at a fixed value. It is concluded that the vasodilatation plays a role in the functional regulation of the pancreatic response to secretin.3. The correlation between blood flow and arterial pressure on the one hand, and the secretory response to secretin on the other, was not mediated by the control of respiration since there was no variation in oxygen uptake in response to a variation in the blood flow. This correlation was still observed when the venous blood was discarded and therefore could not be explained by variations in the rate of recirculation of secretin. It was observed too in experiments where the duodenum was removed, the pancreas alone being introduced into the perfusion apparatus, which indicated that this effect was not mediated by a control of the release of secretin by the duodenum.

Arteries↗