Perfused Pancreas Preparation Research Articles

Effect of fasting on insulin removal by liver of perfused liver-pancreas.

Using in situ perfused rat liver-pancreas preparations, the hepatic clearance of biphasically released endogenous insulin was studied using livers of fed and fasted rats. Hepatic insulin extraction was determined by subtracting the mean endogenous insulin output found in the posthepatic vena cava effluent of liver pancreas preparations from the amount of insulin found in the prehepatic portal effluent of perfused pancreas preparations. All pancreas perfusions and liver-pancreas perfusions were subjected to the same plasma glucose stimulus (250 mg/dl) for 40 min. In the fed state, no significant hepatic extraction of insulin occurred. The biphasic pattern of insulin appearance in the posthepatic vena cava effluent, which ranged from less than 1 to 21 ng/ml, was unaffected by passage through the liver. In contrast, when rats were fasted for 24 h, approximately 50% of the insulin released into the portal vein was removed by their livers during one transhepatic passage. After a 48-h fast, insulin extraction capacity decreased relative to the capacity observed for livers of 24-h fasted rats.

Pancreatic polypeptide, glucagon and insulin secretion from the isolated perfused canine pancreas.

The release of pancreatic polypeptide (PP) by gut hormones, acetyl choline and adrenaline was investigated in an isolated perfused pancreas preparation. PP was potently released by 1 nmol/1 caerulein (186 +/- 12%, p is less than 0.001) and gastric inhibitory peptide (GIP) (211 +/- 31%, p is less than 0.005) as well as by 1 mumol/1 acetyl choline (1097 +/- 59%, p is less than 0.001). A significant two-fold release of PP was also evoked by 1 nmol/1 vasoactive intestinal peptide (VIP) (129 +/- 38%, p is less than 0.02 and gastrin (108 +/- 25% p is less than 0.01). Insulin release, induced by high glucose concentration was enhanced by both GIP (210 +/- 38%, p is less than (0.01) and VIP (48 +/- 5%, p is less than 0.001). In addition GIP enhanced the release of glucagon by 179 +/- 18% (p is less 0.001) at 1.4 mmol/1 glucose and by 127 +/- 24% (p is less than 0.005) at 8.3 mmol/1 glucose. Thus no simple inter-relationship appears to exist between the control of the three circulating islet hormones.

Discrepancies in the response of the insulin secreting cells of the dog and rat to different adrenergic stimulating agents

Our experiments were carried outin vitro on different isolated and perfused pancreas preparations: adult rat pancreas, newborn dog pancreas, uncinate process and splenic portion of adult dog pancreas. The perfusion liquid contained 1.5 g/l glucose. 1) L-isoprenaline (0.05 µM), a stimulating agent of the β-adrenergic receptors, provoked only a slight and brief stimulation of insulin secretion from the rat pancreas. At the same concentration, this substance provoked a considerable stimulation of the insulin secreting cell of the newborn dog pancreas and a still much more marked response from the uncinate process and the splenic portion of adult dog pancreas. The effects of salbutamol (0.09 µM), a stimulating agent of the β-adrenergic receptors, were comparable to those of isoprenaline. The effects of isoprenaline and salbutamol on these preparations were suppressed by propranolol. 2) As to the effects of L-adrenaline on these different preparations, the following results have been recorded: a) Adrenaline (0.011 µM) inhibited insulin secretion by rat pancreas; this effect was suppressed by phenoxybenzamine; it was not modified by propranolol. — b) Adrenaline (0.011 µM) exerted an inhibitory effect on newborn dog pancreas, but only temporarily. Phenoxybenzamine inversed the effects of adrenaline and allowed the appearance of stimulation of insulin secretion; propranolol accentuated the inhibitory effect of adrenaline. — c) On the uncinate process of the adult dog pancreas adrenaline (0.011 µM) provoked a biphasic effect: brief and strong rise of insulin secretion followed by slight inhibition. Phenoxybenzamine enhanced the adrenaline-induced stimulation and transformed the inhibition of the second phase into strong stimulation. Propranolol suppressed the stimulatory effect of adrenaline which then had only an immediate and strong inhibitory effect. Adrenaline at 0.055 µM concentration provoked an extremely brief hypersecretion peak which was less intense than that recorded when using the 5-times weaker concentration; this peak was followed by strong and lasting inhibition.