Effects of nitric oxide synthesis inhibition on mesenteric perfusion in young pigs

We tested the hypothesis that nitric oxide (NO) modulates postprandial hyperemia in young pigs. To test this hypothesis, we studied five groups of 3-wk-old pigs: group 1: milk fed, N(G)-monomethyl-L-arginine (L-NMMA) and L-arginine (L-Arg) treated (n = 10); group 2: milk fed, placebo treated (n = 8); group 3: water fed, L-NMMA and L-Arg treated (n = 6); group 4: water fed, placebo treated (n = 4); and group 5: fasted sham fed, L-NMMA and L-Arg treated (n = 6). After catheter placement and electromagnetic flow probe instrumentation of the mesenteric artery, systemic blood pressure and mesenteric artery blood flow were measured during preprandial baseline, postprandial, and postprandial intra-arterial L-NMMA- and L-Arg-infused study periods. The same measurements were made in the milk- and water-fed placebo-treated groups except that diluent replaced the L-NMMA and L-Arg infusions. In the milk- and water-fed placebo-treated groups, a significant (analysis of variance, P < 0.05), postprandial hyperemia was observed. The change in blood flow was greater (P < 0.05) in the milk-fed group than in the water-fed group. Inhibition of NO synthesis with L-NMMA diminished (P < 0.05) the hyperemic responses to both water and milk feeding and resulted in a decrease (P < 0.05) in mesenteric artery perfusion in the fasted sham-fed state. We conclude that, in young pigs, NO is a modulator of mesenteric vascular tone in both the postprandial and fasted states.

Adenosine plays a role in food-induced jejunal hyperemia

The aim of this study is to determine the role of adenosine in postprandial hyperemia in the jejunum of anesthetized dogs. The effect of two adenosine antagonists, aminophylline and 8-phenyltheophylline, on the vascular responses to intra-arterial infusion of adenosine and luminal placement of food was determined. The effect of aminophylline on the food-induced hyperemia was found to be dependent on motility. Aminophylline had no effect on the hyperemia when motility was high but inhibited the hyperemia when motility was low. Vasodilations produced by intra-arterial infusions of adenosine, however, were attenuated by aminophylline regardless of the level of motility. The more potent and specific adenosine antagonist, 8-phenyltheophylline, also inhibited both adenosine- and food-induced vasodilations. This inhibition occurred whether the intestinal motility was high or low. In conclusion, adenosine receptor blockade inhibits jejunal food-induced hyperemia, and adenosine may play a role in the hyperemia. The effect of aminophylline was complicated by motility.