The aim of our study was to determine whether the discrepancy in the data reported on the effect of atropine on food-induced intestinal hyperemia results from a difference in experimental materials and methods. In the first two series of experiments, atropine (0.5 mg/kg iv) was given before or during intraluminal perfusion of digested food plus bile through a long jejunal loop (62% of the total small intestine) at 4 ml/min for 60 min while measuring the portion of the blood flow through the superior mesenteric artery (SMA) that perfused the loop. Atropine per se had no effect on jejunal blood flow. Before atropine food increased flow 31.5 +/- 10.1% and after atropine flow increased 54.8 +/- 11.0 and 66.0 +/- 28.0% above controls in the first and second series, respectively. Atropine also increased net fluid volume absorption. In the third series, food alone and food plus bile were placed into the lumens of the two adjacent jejunal segments. Atropine had no effect on the increases in flow and oxygen uptake produced by food alone but enhanced the hyperemia produced by food plus bile without affecting the increase in oxygen uptake. Our results suggest that the previously reported inhibition of increased SMA flow by atropine is due to the inhibitory effect of atropine on gastrointestinal motility and inhibition of pancreatic blood flow. In conclusion, food-induced jejunal hyperemia does not result from a direct vasodilator action of the cholinergic nerves.