AbstractExperiments were designed to study the effects of acute pancreatitis, induced by bile duct ligation, on the contractility of longitudinal muscle from the jejunum of rats. Forty animals were divided randomly into 5 groups, 8 in each. In three groups, the common bile duct was ligated at its entrance into the duodenum (low ligation), and their jejunal longitudinal muscle contractility was studied at 24, 48 or 72 hours after operation. In the fourth group, the common bile duct was ligated above the pancreas (high ligation). These animals were studied 72 hours after operation. In the fifth group, sham operation was performed as a control. At the time of study, two strips of longitudinal muscle were peeled from a segment of the jejunum from each animal, and were mounted in organ baths. Muscle contractions in response to carbachol (10‐7‐10‐4m) and to KCL (30 mM) were measured, correlated to the cross‐sectional area of the muscle strips, and expressed as stress. Animals with low ligation developed histological evidence of acute pancreatitis. Maximal stress to carbachol of intestinal muscle from these animals decreased progressively with time after operation. Forty‐eight and 72 hours following low ligation, Maximal stresses in response to carbachol were 488 ± 33 g cm‐2and 438 ± 28 g cm‐2, values significantly lower than those after sham operation (611 ± 24 g cm‐2). In contrast, median effective concentrations of carbachol (D‐50s) were not significantly different among groups. The response to KCl, although lower than that to carbachol in each group, did not differ among groups. Animals with high ligation, although showing signs of bile stasis, did not develop histological evidence of pancreatitis, and maximal stresses to either carbachol or KCl developed by muscle from these animals did not differ significantly from control. We conclude that low ligation with the induction of pancreatitis leads to a decreased contractility of the jejunum. Also, the impairment responsible for the decreased contractility may reside in an excitation‐contraction pathway step initiated by ca