INTESTINAL MUSCLE CONTRACTILITY DURING ACUTE-PANCREATITIS

Experiments were designed to study the effects of acute pancreatitis, induced by bile duct ligation, on the contractility of longitudinal mu scle from the jejunum of rats. Forty animals were divided randomly int o 5 groups, 8 in each. In three groups, the common bile duct was ligat ed at its entrance into the duodenum (low ligation), and their jejunal longitudinal muscle contractility was studied at 24, 48 or 72 hours a fter operation. In the fourth group, the common bile duct was ligated above the pancreas (high ligation). These animals were studied 72 hour s after operation. In the fifth group, sham operation was performed as a control. At the time of study, two strips of longitudinal muscle we re peeled from a segment of the jejunum from each animal, and were mou nted in organ baths. Muscle contractions in response to carbachol (10( -7)-10(04)M) 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 pancreatit is. Maximal stress to carbachol of intestinal muscle from these animal s decreased progressively with time after operation. Forty-eight and 7 2 hours following low ligation, Maximal stresses in response to carbac hol were 488 +/- 33 g cm-2 and 438 +/- 28 g cm-2, values significantly lower than those after sham operation (611 +/- 24 g cm-2). In contras t, median effective concentrations of carbachol (D-50s) were not signi ficantly different among groups. The response to KCl, although lower t han that to carbachol in each group, did not differ among groups. Anim als with high ligation, although showing signs of bile stasis, did not develop histological evidence of pancreatitis, and maximal stresses t o either carbachol or KCl developed by muscle from these animals did n ot differ significantly from control. We conclude that low ligation wi th the induction of pancreatitis leads to a decreased contractility of the jejunum. Also, the impairment responsible for the decreased contr actility may reside in an excitation-contraction pathway step initiate d by carbachol but not by KCl.