Effects of gastric inhibitory polypeptide on leucine- and arginine-stimulated insulin release.

Insulin release stimulated by single amino acids, with and without gastric inhibitory polypeptide (GIP), was studied in vivo in anesthetized rats and in vitro in collagenase-digested isolated rat pancreatic islets. Insulin release in vivo during a 15-min intravenous infusion of leucine (0.97 mM) or arginine (0.97 mM) with GIP (17 ng/min) was greater than with infusion of either amino acid or GIP alone. Serum immunoreactive GIP was in the physiological range, and serum glucose showed no significant change in these studies. In contrast, insulin release did not occur with valine infused alone or with GIP. Insulin release in vitro by isolated islets was greater during a 45-min incubation period with leucine (5-20 mM) or arginine (20 mM) plus GIP (10 ng to 10 micrograms/ml) than with either amino acid alone. This effect that occurred in the absence of glucose could not be demonstrated with low concentrations of leucine (1.5 mM) or with 20 mM valine. In vitro insulin release during paired perfusion studies of isolated islets was greater with leucine (20 mM) plus GIP (50 ng/min) than with leucine alone, and augmentation of insulin release by GIP was demonstrable in both the early and late phases of insulin release. From these results it is concluded that insulin release is greater, both in vivo and in vitro, after leucine or arginine plus GIP than with either amino acid or GIP alone. This effect appears to be specific for the insulinotropic amino acids tested, does not appear to be glucose dependent, and can be demonstrated in both the early and late phases of insulin release.

Breath hydrogen reflects canine intestinal ischemia.

The relationship between breath hydrogen excretion and intestinal ischemia was investigated in nine mechanically ventilated dogs under pentobarbital anesthesia. An ileal segment was isolated in situ, ligated at each end, and insufflated with hydrogen. Expired air was collected at intervals. Blood volume was reduced 30% by three successive equivalent hemorrhages 10 min apart. Local bowel ischemia was produced by clamping the blood supply to the isolated segment for 10 min. Graded hemorrhage produced step-wise reductions in breath hydrogen concentration, to 77 +/- 13, 66 +/- 15, and 35 +/- 8% (mean +/- S.E.) of baseline after the first, second, and third hemorrhages, respectively. These reductions correlated highly (r = 0.84; P less than 0.01) with declines in mean aortic blood pressure. Occlusion of blood supply caused a significant (P less than 0.025) decrease in breath hydrogen concentration and excretion to 39 +/- 14% of baseline. Termination of occlusion was followed within 2 min by a 7-fold increase in breath H2 concentration above the original baseline, probably reflecting reactive hyperemia. Breath hydrogen measurements appear to reflect functional (hemorrhagic shock-induced) and mechanical (vascular occlusion induced) enteric ischemia in dogs.