oedematous pancreatitis in rats: non-parallel changes in pancreatic morphology and amylase release in vitro

Pancreatic morphology and amylase release from isolated pancreatic acimn in response to caerulein was studied in the course of an experimental bile induced acute pancreatitis without acinar necrosis. The inflammation was induced by retrograde microinfusion of 25 RI bile into the rat bile pancreatic duct. A dissociation between functional and structural findings was seen. One hour after the bile injury, there was a transient change in acinar cell function. The response to stimulation by caerulein was reduced by 50%, whereas the sensitivity to caerulein was normal. There was oedema and an initial leucocyte infiltration of the gland. Six hours, one day, three days, and seven days after the bile injury, there was an acute interstitial oedematous pancreatitis with a modest polymorphonuclear leucocyte infiltration of the interstitium and widespread acinar vacuolisation. Morphological changes were most pronounced at the third postoperative day. Acinar amylase release, however, was normal both in terms of sensitivity and responsiveness to stimulation. These results show that bile injury may result in an initial disturbance of acinar celi function. Normal acinar amylase release prevailing in the course of the inflammation suggests that disturbance of the acinar amylase secretory response is not a primary stimulant of the inflammation before the development ofacinar necrosis. (Gut 1994; 35: 1127-1131) caerulein stimulation of rat pancreatic exocrine secretion, changes in acinar digestive enzyme release in vitro were seen: pancreatic acini were less sensitive to muscarinic agonist stimulation and showed a decrease in the maximal secretory capacity.2 It was proposed that changes in acinar stimulus secretion coupling may also be important in other forms of acute pancreatitis and perhaps even in the human disease.3 In the early period of bile induced acute pancreatitis, however, no data exist to support this hypothesis. To date, studies on acinar cell function in bile induced acute pancreatitis have been hampered by the lack of non-destructive models of the disease. We studied the relation between the development of morphological inflammatory lesions of the pancreas and of amylase release from isolated pancreatic acini in a model of bile induced acute pancreatitis without significant acinar necrosis that uses retrograde microinfusion of bile into the rat bile pancreatic duct.